FitSugar

Sanya Richards Goes For Gold, Again!

FitSugar — Mon, 04 Aug 2008 03:30:00 -0700

If you don't already know the name Sanya Richards, then it's about time you learned about this 23-year-old amazing athlete.

Sanya Richards already achieved Olympic gold in Athens in 2004, but things have changed since then. In 2006 Richards was diagnosed with Behcet's Syndrome - a rare disease resulting from inflammation of the blood vessels, which causes pain, swelling, and stiffness of the joints (among other things). Despite her painful illness, Richards finished first in the 400-meter race during the US trials, and she's expected to medal in this Olympics.

I'm always thoroughly impressed with athletes just from their stamina and strength, but when they overcome hurdles that would make most of us throw the towel in, I'm in awe. Cheer on Sanya at the Olympics in Beijing that begin Aug. 8 - yay!

Source

Gout

FitSugar — Wed, 08 Oct 2008 17:35:16 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Types of Gout:

There are two types of gout -- primary and secondary.

Primary gout: The cause is usually unknown. However, primary gout is likely the result of a combination of genetic, hormonal, and dietary factors.
Secondary gout: Secondary gout is caused by medications or medical conditions that cause an increase in the serum (blood) levels of uric acid.

Risk Factors:

Risk factors for gout include:

Advancing age
Male gender
Family history of the condition
Obesity
Use of certain drugs, including diuretics, aspirin, cyclosporine, or levodopa
Drinking a large amount of alcohol, particularly beer
Exposure to lead
Organ transplants
Thyroid problems

Symptoms of a Gout Attack:

Symptoms of a gout attack include:

Severe pain at and around the joint
- May feel like "crushing" or a dislocated bone
- Walking and the weight of bed sheets may be unbearable
- Usually takes 8 - 12 hours to develop
- Occurs late at night or early in the morning and may wake you up
Swelling that may extend beyond the joint
Red, shiny, tense skin over the affected area, which may peel after a few days
Chills and mild fever, loss of appetite, and feelings of ill health

Research News

A large study found that people with gout are at an increased risk of having metabolic syndrome. Metabolic syndrome is a collection of problems, such as abdominal obesity, high blood pressure, and low "good" cholesterol. This syndrome increases a person's risk of heart disease and diabetes.

Introduction

Gout is a painful and common type of arthritis. About 1 in 100 people develop gout. The condition is usually associated with a long-lasting, abnormally high amount of uric acid in the blood, called chronic hyperuricemia.

The rate of gout has increased in recent decades, not only in America but also in other developed countries. The increase is possibly due to dietary and lifestyle changes, greater use of medications that cause hyperuricemia, and aging populations. Gout is very uncommon in developing countries.

Click the icon to see an animation about gout.

Metabolism of Purines. The process leading to hyperuricemia and gout begins with the metabolism of purines, nitrogen-containing compounds that are important for energy. Purines can be divided into two types:

Endogenous purines are manufactured within human cells.
Exogenous purines are obtained from foods.

The process of breaking down purines results in the formation of uric acid in the body. Most mammals have an enzyme called uricase, which breaks down uric acid so it can be easily removed from the body. Because humans lack uricase, uric acid is not as easily removed, and can build up in body tissues.

Uric Acid and Hyperuricemia. Purines in the liver produce uric acid. The uric acid enters the bloodstream, and most of it eventually goes through the kidneys and is excreted in the urine. The remaining uric acid travels through the intestines, where bacteria help break it down.

Normally these actions keep the level of uric acid in the blood plasma (the liquid part of the blood) at a healthy level, which is below 6.8 mg/dL. But under certain circumstances, the body produces too much uric acid or removes too little. In either case, concentrations of uric acid increase in the blood. This condition is known as hyperuricemia.

If concentrations of uric acid reach 7 mg/dL and above, needlelike crystals of a salt called monosodium urate (MSU) form. As MSU crystals build up in the joints, they trigger inflammation and pain, the characteristic symptoms of gout.

Symptoms

The specific symptoms of gout depend on the stage of the disease. Gout is often divided into four stages:

Asymptomatic hyperuricemia
Acute gouty arthritis
Intercritical gout
Chronic tophaceous gout

Asymptomatic means there are no symptoms. Asymptomatic hyperuricemia is considered the first stage of gout. MSU levels slowly increase in the body. This stage lasts for an average of 30 years.

Note: Hyperuricemia does not inevitably lead to gout. In fact, less than 20% of cases develop the full-blown arthritic gout disease.

Acute gouty arthritis occurs when the first symptoms of gout appear. Sometimes the first signs of gout are brief twinges of pain (petit attacks) in an affected joint. These attacks can precede the actual full-blown condition by several years.

MSU crystals form at normal body temperature when the concentration of uric acid in the blood reaches 7 mg/dL. At lower temperatures, MSU crystals form at lower concentrations of uric acid. Since blood temperature falls the further blood gets from the heart, gout strikes the toes and fingers first.

Symptoms of acute gouty arthritis include:

Severe pain at and around the joint
- May feel like "crushing" or a dislocated bone
- Walking and the weight of bed sheets may be unbearable
- Usually takes 8 - 12 hours to develop
- Occurs late at night or early in the morning and may wake you up
Swelling that may extend beyond the joint
Red, shiny, tense skin over the affected area, which may peel after a few days
Chills and mild fever, loss of appetite, and feelings of ill health

Most often symptoms start in one joint.

Monoarticular Gout. Gout that occurs in one joint is called monoarticular gout. About 60% of all first-time monoarticular gout attacks in middle-aged adults occur in the big toe. This occurrence is known as podagra. Symptoms can also occur in other locations, such as the ankle or knee.

Polyarticular Gout. If more than one joint is affected, the condition is known as polyarticular gout. Multiple joints are affected in only 10 - 20% of first attacks. Older people are more likely to have polyarticular gout. The most frequently affected joints are the foot, ankle, knee, wrist, elbow, and hand. The pain usually occurs in joints on one side of the body and it is usually, although not always, in the lower legs and the feet. People with polyarticular gout are more likely to have a slower onset of pain and a longer delay between attacks. People with polyarticular gout are also more likely to experience low-grade fever, loss of appetite, and a general feeling of poor health.

An untreated attack will typically peak 24 - 48 hours after the first appearance of symptoms, and go away after 5 - 7 days. However, some attacks last only hours, while others persist as long as several weeks.

Intercritical gout is the term used to describe the periods between attacks. The first attack is usually followed by a complete remission of symptoms, but, if left untreated, gout nearly always returns. Over two-thirds of patients will have at least one further attack within 2 years of the first attack. By 10 years, over 90% of the patients are likely to have repeat attacks.

Chronic Tophaceous Gout and Tophi. After several years, persistent gout can develop into a condition called chronic tophaceous gout. This long-term condition often produces tophi, which are solid deposits of MSU crystals that form in the joints, cartilage, bones, and elsewhere in the body. In some cases, tophi break through the skin and appear as white or yellowish-white, chalky nodules that have been described as looking like crab eyes.

Click the icon to see an image of tophi gout.

Without treatment, tophi develop about 10 years after the initial onset of gout, although the occurence can range from 3 to 42 years. Tophi are more likely to appear early in the course of the disease in older people. In the elderly population, women appear to be at higher risk for tophi than men. Certain people, such as those who are receiving cyclosporine after a transplant, have a high risk of developing tophi.

Development of Chronic Pain. When gout remains untreated, the intercritical periods typically become shorter and shorter, and the attacks, although sometimes less intense, can last longer. Over the long term (about 10 - 20 years) gout becomes a chronic disorder characterized by constant low-grade pain and mild or acute inflammation. Gout may eventually affect several joints, including those that may have been free of symptoms at the first appearance of the disorder. In rare cases, the shoulders, hips, or spine are affected.

Location of Tophi. Tophi generally form in the following locations:

Curved ridge along the edge of the outer ear
Forearms
Elbow or knee
Hands or feet -- older patients, particularly women, are more likely to have gout in the small joints of the fingers.
Around the heart and spine (rare)

Tophi are generally painless. However, they can cause pain and stiffness in the affected joint. Eventually, they can also erode cartilage and bone, ultimately destroying the joint. Large tophi under the skin of the hands and feet can give rise to extreme deformities.

Uric Acid Nephrolithiasis (Kidney Stones). Persons who have kidney stones that formed from uric acid are more likely to have higher levels of uric acid in their blood than in their urine. This suggests that gout is responsible for this type of kidney stones. Uric acid stones and other forms of kidney stones are present in 10 - 25% of patients with primary gout, a rate of more than 1,000 times that of the general population. In gout caused by other conditions (called secondary gout), the reported rate reaches 42%.

Click the icon to see an image of nephrolithiasis.

Not all of the kidney stones in patients with gout are made of uric acid. Some are made from calcium oxalate, calcium phosphate, or substances combined with uric acid. Uric acid stones can also form when you do not have gout or hyperuricemia.

Chronic Uric Acid Interstitial Nephropathy. Chronic uric acid interstitial nephropathy occurs when crystals slowly form in the structures and tubes that carry fluid from the kidney. It is reversible and not likely to injure the kidneys.

Kidney Failure. Sudden overproduction of uric acid can occasionally block the kidneys and cause them to fail. This occurrence is very uncommon but can develop after any of the following:

Chemotherapy for leukemia or lymphoma
Severe heat stress from vigorous exercise
Epileptic seizures
Corticosteroid therapy for severe allergic reactions

Causes and Risk Factors

Gout is classified as either primary or secondary, depending on what causes the high levels of uric acid in the blood (hyperuricemia).

More than 99% of primary gout cases are referred to as idiopathic, meaning that the cause of the hyperuricemia cannot be determined. Primary gout is most likely the result of a combination of genetic, hormonal, and dietary factors. Secondary gout is caused by drug therapy or by medical conditions other than a metabolic disorder.

The following factors increase your risk for gout:

Advancing age
Male gender
Family history of the condition
Obesity
Use of certain drugs, including diuretics ("water pills"), aspirin, cyclosporine, or levodopa
Drinking a large amount of alcohol, particularly beer
Exposure to lead
Organ transplants
Thyroid problems
Other serious illness

Each risk factor is discussed in more detail below.

Middle-Aged Adults. Gout usually occurs in middle-aged men, peaking in the mid-40s. It is most often associated in this age group with obesity, high blood pressure, unhealthy cholesterol levels, and heavy alcohol use.

Elderly. Gout can also develop in older people, when it occurs equally in men and women. In this group, gout is most often associated with kidney problems and the use of diuretics. It is less often associated with alcohol use.

Children. Except for rare inherited genetic disorders that cause hyperuricemia, gout in children is rare.

Men. Men are significantly at higher risk for gout. In males, uric acid levels rise substantially at puberty. In about 5 - 8% of American men, levels exceed 7 mg/dL (indicating hyperuricemia). However, gout typically strikes after 20 - 40 years of persistent hyperuricemia, so men who develop it usually experience their first attack between the ages of 30 and 50.

Women. Before menopause, women have a significantly lower risk for gout than men, possibly because of the actions of estrogen. This female hormone appears to facilitate uric acid excretion by the kidneys. (Only about 15% of female gout cases occur before menopause.) After menopause the risk increases in women. At age 60 the incidence is equal in men and women, and after 80, gout occurs more often in women.

According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, up to 18% of people with gout have a family history of the condition. Some people with a family history of gout have a defective protein (enzyme) that interferes with the way the body breaks down purines.

Researchers report a clear link between body weight and uric acid levels. In one Japanese study, overweight people had two to more than three times the rate of hyperuricemia as those who maintained a healthy weight. Children who are obese may have a higher risk for gout in adulthood.

Thiazide diuretics are "water pills" used to control hypertension. The drugs are strongly linked to the development of gout. In fact, 75% of patients who develop gout at an older age report the use of diuretics.

Several other medications can increase uric acid levels and raise your risk for gout. These include:

Aspirin -- low doses of aspirin reduce uric acid excretion and increase the chance for hyperuricemia. This may be a problem for older people who take baby aspirin (81 mg) to protect against heart disease.
Niacin (used to treat cholesterol problems)
Pyrazinamide (used to treat tuberculosis)

Drinking excessive amounts of alcohol can raise your risk of gout. Beer is the kind of alcohol most strongly linked with gout, followed by spirits. Moderate wine consumption does not appear to increase the risk of developing gout.

Alcohol use is highly associated with gout in younger adults. Binge drinking particularly increases uric acid levels. Alcohol appears to play less of a role among elderly patients, especially among women with gout.

Alcohol increases uric acid levels in the following three ways:

Providing an additional dietary source of purines (the compounds from which uric acid is formed)
Intensifying the body's production of uric acid
Interfering with the kidneys' ability to excrete uric acid

Chronic occupational exposure to lead is associated with build-up of uric acid and a high incidence of gout.

Kidney transplantation poses a high risk for renal insufficiency and gout. In addition, other transplantation procedures, such as heart and liver, increase the risk of gout. The procedure itself poses a risk of gout, as does the medication (cyclosporine) used to prevent rejection of the transplanted organ. Cyclosporine also interacts with indomethacin, a common gout treatment.

The kidneys are responsible for removing waste from the body, regulating electrolyte balance and blood pressure, and stimulating red blood cell production.

Treatment of several other conditions can cause significant elevations of uric acid in the blood, and therefore a gout attack. These conditions include:

Leukemia
Lymphoma
Psoriasis

Triggers

Triggers are events or conditions that can set off a gout attack. Certain risk factors, including a purine-rich diet, are also considered a trigger. Triggers include:

Joint injury
Overindulging in alcohol or purine-rich foods
Over-strenuous exercise
Severe illness or infection
Stress
Sudden weight loss
Surgery
Using certain drugs

Hot and humid weather may also be strongly associated with recurrent gout attacks. Such weather can cause sweating and, ultimately, dehydration, which has long been recognized as a potential trigger for gout attacks.

Drinking more water and fluids when it's warm outside could help persons with gout prevent future attacks.

Diagnosis

The first step in diagnosing the disease is to determine which joints are affected. A physical examination and medical history can help confirm or rule out gout. For example, gout is more likely if arthritis first appears in the big toe.

The speed of the onset of pain and swelling is also important. Symptoms that take days or weeks (rather than hours) to develop probably indicate a disorder other than gout.

Abnormal enlargements in joints that had been affected by previous injury or osteoarthritis are possible signs of gout. This is particularly significant in older women who take diuretics ("water pills").

A blood test is usually done to measure uric acid levels and detect hyperuricemia. A low level of uric acid in the blood makes a diagnosis of gout much less probable, and a very high level increases the likelihood of gout, especially if patient has symptoms of gout. Nevertheless, uric acid levels in the blood during an attack of gout can be within or below the normal range, and the presence of hyperuricemia does not necessarily mean someone has gout. However, most doctors feel that closer monitoring of blood uric acid levels in people with gout may help reduce gout flares.

Synovial fluid examination is the most accurate method for diagnosing gout. The synovial fluid is the lubricating liquid that fills the synovium (the membrane that surrounds a joint and creates a protective sac). The fluid cushions joints and supplies nutrients and oxygen to the cartilage surface that coats the bones. This exam also helps detect gout during intercritical periods.

The health care provider uses a needle attached to a syringe to draw out fluid from the affected joint. This is called aspiration. Local anesthesia is not used because it can reduce the effectiveness of the procedure. However, the procedure is usually only mildly uncomfortable. Afterwards, there can be some minor discomfort in the area where the needle was inserted, but it usually goes away quickly.

The fluid sample is sent to a laboratory for analysis. Testing can reveal the presence of monosodium urate (MSU) crystals, which will nearly always confirm a diagnosis of gout. The laboratory can also test the sample for infection.

The procedure itself can cause infection, though this occurs in less than 0.1% of patients. Aspiration sometimes eases the patient's symptoms by reducing swelling and pressure on the tissue surrounding the joint.

Synovial fluid analysis is a method to look at the fluid that cushions a joint. It is done to help diagnose and treat joint-related problems such as gout.

It is sometimes helpful to gauge the amount of uric acid found in a patient's urine, particularly if the patient is young and has pronounced hyperuricemia that might be related to a metabolic disorder. If uric acid in the urine exceeds a particular value, further tests for an enzyme defect or other identifiable cause of gout should be performed. Greater-than-normal amounts of uric acid in the urine also mean that the patient is more likely to develop uric acid kidney stones.

Typically, a 24-hour urine test is performed. The patient discards the first urination sample on the day of the test. Afterward all urine passed over the next 24 hours is collected into a special container, including the first urination on the morning of day two. The container is delivered to the patient's health care provider or sent directly to the laboratory.

The urine is collected during an intercritical period, after the patient has been placed on a purine-reduced diet. The patient is also asked to temporarily stop using alcohol and any medications that can interfere with the test. The patient should not change any of his or her usual eating or drinking patterns when performing this test.

Click the icon to see an image of a uric acid test.

X-Rays. For the most part, x-rays do not reveal any problems during the early stages of gout. Their usefulness lies in assessing the progress of the disorder in its chronic phase and identifying other health problems with symptoms similar to gout. Tophi can be seen on x-rays before they become apparent on physical examination.

Advanced Imaging Techniques. Advanced imaging techniques being investigated for identifying tophi include computed tomography (CT), magnetic resonance imaging (MRI), and Doppler ultrasonography.

As part of the diagnosis, other disorders that produce gout-like symptoms or cause hyperuricemia should be ruled out. In general, it is easy to distinguish acute gout that occurs in one joint from other arthritic conditions. The two disorders that may confuse this diagnosis are pseudogout and septic arthritis. Pseudogout is a condition most likely to be confused with gout.

Chronic gout can often resemble rheumatoid arthritis. Several other conditions may at some point in their course resemble gout.

Pseudogout (also called calcic gout and calcium pyrophosphate dihydrate deposition disease) is a common inflammatory arthritis among older adults. It is very similar to gout, but is caused by deposits of calcium pyrophosphate dihydrate crystals in and around the joints.

Although symptoms of pseudogout resemble gout in some ways, there are differences:

The first attack typically strikes the knee. Other joints commonly affected are the shoulders, wrists, and ankles. At least two-thirds of cases affect more than one joint during a first attack. Pseudogout may involve any joint, although the small joints in the fingers or toes are not commonly affected.
The symptoms of pseudogout also appear more slowly than those of gout, taking days rather than hours to develop.
Pseudogout is more likely to first develop in elderly people, particularly those with osteoarthritis. (It affects 10 - 15% of people over 65.)

Pseudogout is more likely to occur in the autumn while gout attacks are most common in the spring.

Conditions that are associated with a higher risk for pseudogout in elderly patients include underlying acute medical conditions, trauma, or surgery. Medical conditions associated with pseudogout include hypothyroidism, diabetes, gout, and osteoarthritis. Liver transplantation also may increase the risk.

There is no cure for pseudogout. It is a progressive disorder that can eventually destroy joints. Treatments for pseudogout are similar to those for gout and are aimed at relieving the pain and inflammation and reducing the frequency of attacks.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for treating inflammation and pain from pseudogout.
For acute attacks in large joints, fluid aspiration alone or with corticosteroids may help.
Colchicine may be used for acute attacks.
Magnesium carbonate may help dissolve crystals, but existing hard deposits may remain.
Surgery may be required for joint replacement.

Rheumatoid Arthritis. Rheumatoid arthritis can distort the joints of the finger and cause inflammation and pain that may mimic gout. In older people, it is particularly difficult to distinguish chronic gout from rheumatoid arthritis. A proper diagnosis can be made with a detailed medical history, laboratory tests, and identification of MSU crystals.

Osteoarthritis. Gout can coincide and be confused with osteoarthritis in older people, particularly when it occurs in arthritic finger joints in women. In general, gout should be suspected if the joints in the fingertips are unusually enlarged.

Click the icon to see an image of osteoarthritis.

Infections. Joint infections can have features that resemble gout. A correct diagnosis is critical for appropriate treatment. For example, some cases of gout have been confused with infection after joint replacement. On the other hand, joint infection not associated with surgery might indicate sepsis, which is a widespread and potentially life-threatening bacterial infection that can cause inflamed joints, chills, and a spiking fever. The severity of the fever and a high white blood cell count in the joint fluid helps diagnose a septic infection, while urate crystals in the joint are a good indicator of gout.

Charcot Foot. Between 1 - 2.5% of people with diabetes have Charcot foot or Charcot joint (medically referred to as neuropathic arthropathy). This condition is caused by problems in the nerves in the feet. Early changes may resemble gout, with the foot becoming swollen, red, and warm. Recognition and treatment of this condition is very important. A seriously affected foot can become deformed. The bones may crack, splinter, and erode, and the joints may shift, change shape, and become unstable.

Bunions. A bunion is a foot deformity that usually occurs at the head of the first of five long bones (the metatarsal bones) that extend from the arch and connect to the toes, and may be confused with gout. The first metatarsal bone is the one that attaches to the big toe. A bunion begins to form when the big toe is forced in toward the rest of the toes, causing the head of the first metatarsal bone to jut out and rub against the side of the shoe. The underlying tissue becomes inflamed, and a painful bump forms. As this bony growth develops, the bunion is formed as the big toe is forced to grow at an increasing angle towards the rest of the toes.

Click the icon to see an illustrated series detailing bunion removal.


Disease	Specific Subtypes
Osteoarthritis
Infectious Arthritis	Lyme disease, septic arthritis, bacterial endocarditis, mycobacterial and fungal arthritis, viral arthritis, osteomyelitis
Postinfectious or Reactive Arthritis	Reiter syndrome (a disorder characterized by arthritis and inflammation in the eye and urinary tract), rheumatic fever, inflammatory bowel disease
Pseudogout
Rheumatic Autoimmune Diseases	Rheumatoid arthritis, systemic vasculitis, systemic lupus erythematosus, scleroderma, Still's disease (also called juvenile rheumatoid arthritis)
Fibromyalgia
Other Diseases	Chronic fatigue syndrome, hepatitis C, familial Mediterranean fever, cancers, AIDS, leukemia, bunions, Whipple's disease, dermatomyositis, Behcet's disease, Henoch-Schonlein purpura, Kawasaki's disease, erythema nodosum, erythema multiforme, pyoderma gangrenosum, pustular psoriasis

Treatment: Acute Gout Attack

Acute attacks of gout and long-term treatment of gout and hyperuricemia require different approaches. Treatment usually involves medication. After the first attack, some health care providers advise their patients to keep a supply of medications on hand so that self-medication can begin at the first sign of symptoms of a second acute attack. There are also specific treatments for conditions associated with gout, including uric acid nephropathy and uric acid nephrolithiasis.

Many patients do not require medications. During the period between gout attacks, patients are advised to avoid foods high in purines and to maintain a healthy weight. Patients should also avoid alcohol and reduce any stress.

Drug treatments for acute attacks of gout are aimed at relieving pain and reducing inflammation. They should be started as early as possible.

Medications used in the treatment of gout include:

NSAIDs (nonsteroidal anti-inflammatory drugs)
Colchicine
Corticosteroids

Powerful forms of nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs of choice for an acute attack in younger, healthy patients with no serious health problems, particularly problems that affect the kidneys, liver, or heart. Usually indomethacin is prescribed for 2 - 7 days.

There are dozens of NSAIDs available. Over-the-counter NSAIDs include:

Low-dose Ibuprofen (Motrin IB, Advil, Nuprin)
Naproxen (Aleve)
Ketoprofen (Actron, Orudis KT)

Prescription NSAIDs include:

Ibuprofen (Motrin)
Naproxen (Naprosyn, Anaprox)
Flurbiprofen (Ansaid)
Diclofenac (Voltaren)
Tolmetin (Tolectin)
Ketoprofen (Orudis, Oruvail)
Dexibuprofen (Seractil)
Indomethacin (Indocin)

Indomethacin (Indocin) is typically the first choice of treatment for patients who have no medical conditions that would interfere with its use. Usually 2 - 7 days of high-dose indomethacin is enough to treat a gout attack. The first dose of indomethacin usually begins to act against the pain and inflammation within 24 hours and often much sooner.

Ibuprofen, naproxen, sulindac, or NSAIDs are good alternatives, particularly for elderly patients who might experience confusion or bizarre sensations with indomethacin. (Aspirin is an NSAID, but is associated with a higher risk for gout and should be avoided.)

Regular use of even over-the-counter NSAIDs can cause certain health problems, such as:

Ulcers and gastrointestinal bleeding
Increased blood pressure -- people with hypertension, severe vascular disease, kidney, or liver problems and those taking diuretics must be closely monitored if they need to take NSAIDs.
Delayed emptying of the stomach, which could interfere with the actions of other drugs. The elderly are at special risk.
Dizziness
Tinnitus (ringing in the ear)
Headache
Skin rash
Depression
Confusion or bizarre sensation (in some higher-potency NSAIDs, notably indomethacin)
Kidney damage

NSAIDs can cause kidney problems, especially in the elderly and those with kidney disease. When caught early enough, these problems generally resolve if the drugs are stopped. Any sudden weight gain or swelling should be reported to a physician. Anyone with kidney disease should avoid these drugs.

Patients with diabetes who take hypoglycemics by mouth may need to adjust their medication dosage if they also take NSAIDs, because of possible harmful interactions between these classes of drugs.

Some studies reported that ibuprofen (but not other NSAIDs) may reduce the heart-protective effects of low-dose aspirin. Additional research is needed to confirm these findings.

Long-term use of NSAIDs is a common cause of ulcers. NSAID-related bleeding and stomach problems may be responsible for over 100,000 hospital admissions and over 15,000 deaths each year. Because there are usually no gastrointestinal symptoms from NSAIDs until bleeding begins, health care providers cannot predict which patients taking these drugs will develop bleeding.

Those at high risk for NSAID-related bleeding include the elderly, anyone with a history of an ulcer or gastrointestinal bleeding, patients with serious heart conditions, those who drink too much alcohol, and persons on certain medications, such anticoagulants (blood thinners), corticosteroids, or bisphosphonates (drugs used for osteoporosis).

Preventing NSAID-Related Ulcers. Switching to alternative pain relievers is the first step in preventing or healing ulcers caused by NSAIDs. If people cannot change drugs, they should use the lowest NSAID dose possible.

In addition, medications are available that may help prevent ulcers in people who need to take NSAIDs. Proton-pump inhibitors (PPIs) are the first drug of choice for preventing ulcers in high-risk individuals. They have been shown to reduce NSAID-ulcer rates by as much as 80% compared with no treatment. Types of these drugs include omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), rabeprazole (AcipHex ), and pantoprazole (Protonix). Prevacid is the first proton-pump inhibitor specifically approved for protecting against ulcers in chronic NSAID users.

Arthrotec is a combination of an ulcer-protective drug called misoprostol and the NSAID diclofenac. It too may reduce the risk for gastrointestinal bleeding.

Colchicine is a derivative of the autumn crocus (also called the meadow saffron). It has been used against gout attacks for centuries. It is highly effective, although it is no longer the first drug of choice because of its frequent, unpleasant, and sometimes very serious side effects.

Colchicine may be given to a healthy adult within 48 hours of an attack. It should not be used by elderly patients or those with kidney, liver, or bone marrow disorders. It can also affect fertility and should not be used during pregnancy. The drug can cause gastrointestinal side effects at high dose, including nausea, vomiting, diarrhea, and abdominal cramps. Low doses do not pose as high a risk for gastrointestinal symptoms, and can prevent further attacks, including attacks in patients who are starting anti-hyperuricemic therapies.

Colchicine may be taken by mouth or given by an intravenous line. Those who take it by mouth need doses every hour until either symptoms improve or side effects develop. Improvement should be seen by the tenth dose. It usually eliminates the pain of an acute attack within 48 hours. The intravenous route has some serious side effects, however, and poses an increased risk for injury to the kidney, liver, central nervous system, and bone marrow.

The antibiotic erythromycin, or H2 blockers such as famotidine (Pepcid AC), cimetidine (Tagamet), or ranitidine (Zantac) may intensify the gastrointestinal side effects of colchicine.

Warning Note: Overdose of colchicine can be dangerous, and there have even been reports of death. The drug may also suppress blood cell production and cause nerve and muscular injury in certain people, sometimes even in those not taking high doses.

Corticosteroids may be used in patients who cannot tolerate NSAIDs and they may be particularly beneficial for elderly patients. Injections into an affected joint provide effective relief for many patients, but this is not useful for patients who have multiple affected joints. Steroids taken by mouth may be used for patients who cannot take NSAIDs or colchicine and who have gout in more than one joint. Corticosteroids include triamcinolone and prednisone.

Treatment: Preventing Attacks

After an acute attack some patients remain at high risk for another attack for several weeks during the intercritical period. Such patients include those with kidney insufficiency or those with congestive heart failure who are on diuretics. Low doses of colchicine or NSAIDs may be used to during this period for prevention of another attack. They should be taken in low doses for 1 - 2 months after an attack, or for longer periods in patients who have experienced frequent attacks.

Antihyperuricemic medications reduce levels of uric acid in the body. The decision whether to use an antihyperuricemic medicine and at what point is not entirely clear. Some health care providers do not prescribe them if hyperuricemia is mild, or until a patient has had two gout attacks. Others prescribe them immediately after a single attack. Most of the time, antihyperuricemic therapy means taking a drug routinely throughout life, which many people find difficult.

Experts do not recommend treatment for hyperuricemia that causes no symptoms. Asymptomatic hyperuricemia often does not lead to gout or other health problems. In addition, the drugs used to treat it are expensive and carry certain risks. In unusual circumstances treatment may be justified, for example in patients with very high uric acid levels that threaten the kidney or those with a personal or strong family history of gout, kidney stones, or kidney damage.

Before treatment, some experts recommend a 24-hour urine collection sample in patients with frequent gout attacks to determine whether they are over-producers or under-excreters of uric acid. Also, before starting one of these drugs, any previous acute attack should be completely controlled and the joints should not be inflamed. Some health care providers prefer to wait about a month after an attack.

Low doses of NSAIDs or colchicine are used during several months after introducing anti-hyperuricemic therapies to prevent gout attacks. It should be noted that NSAIDs, particularly aspirin and similar drugs, reduce the effectiveness of uricosurics. These are drugs given to under-excreters of uric acid (see below). Patients taking uricosurics should avoid NSAIDs, if possible.

Long-term treatment of hyperuricemia may be recommended for people who have:

A risk for tophaceous gout
Had more than two or three acute attacks of gout in the past
Unusually severe attacks, or attacks that affect more than one joint
Joint damage from gout, as shown on x-rays
Hyperuricemia caused by an identifiable inborn metabolic deficiency

Uricosurics. These drugs prevent the kidney from reabsorbing uric acid, and therefore increase the amount excreted in the urine. They are appropriate when gout is caused by under-excretion of uric acid, which occurs in about 80% of gout cases. They are not used for patients with reduced kidney function or those with tophaceous gout. Uricosurics are usually the choice for preventing gout in the following patients:

Those under 60 years of age
Those with normal diets
Those who have normal kidney function
Those who have no risk of kidney stones

Uricosuric drug candidates should produce no more than 700 - 800 mg of uric acid in the urine over a 24-hour period.

Probenecid (Benemid, Probalan) and sulfinpyrazone (Anturane) are the standard uricosurics. A more potent uricosuric, benzbromarone, may work for people with severe tophaceous gout and kidney impairment when other drugs do not. In some studies, benzbromarone was equal to or even more effective than allopurinol, another type of antihyperuricemic drug. Because benzbromarone can cause liver failure in some patients, it is available in the U.S. only with special authorization. A uricosuric combined with allopurinol may be beneficial in some cases.

Probenecid is taken two to three times a day, and sulfinpyrazone begins at twice a day and increases to three or four times daily. The initial doses should be low and gradually increased. Probenecid combined with colchicine is more effective than probenecid alone, but everyone responds differently, so the dose should be carefully individualized.

The possible side effects of probenecid and sulfinpyrazone include skin rashes, gastrointestinal problems, anemia, and kidney stone formation. To help reduce acidity and the risk for kidney stones, patients should drink plenty of fluids (ideally water, not caffeinated beverages). Sodium bicarbonate supplemented by acetazolamide can also reduce acidity and the risk for stones.

NSAIDs, particularly aspirin, as well as other salicylate drugs, interfere with uricosuric drugs and reduce effectiveness. Patients who require minor pain relief should instead take acetaminophen (Tylenol). Uricosurics interact with many other drugs, and a patient should be sure to inform their health care provider of all medications they are taking.

People who take these drugs should have normal kidney function. This therapy may not be as beneficial in many elderly patients, who often have some kidney insufficiency.

Allopurinol (Lopurin, Zyloprim). Allopurinol blocks uric acid production. It is the drug most often used in long-term gout treatment for older patients and those who overproduce uric acid.

Allopurinol is taken by mouth once a day in doses of 100 - 600 mg, depending on the patient's response to treatment. When it is first used, allopurinol can trigger further attacks of gout. Therefore, during the first months (or longer) of therapy, the patient also takes an NSAID or colchicine to reduce that possibility.

Allopurinol has positive effects on "bad" cholesterol levels, so it may be better than other drugs for patients with both gout and coronary artery disease.

Side effects, which can be severe, include:

Rash
Diarrhea
Headache
Fever
Leukopenia (a reduction in the number of white blood cells)
Thrombocytopenia (a reduction in the number of platelets)
Cataracts

In rare cases, the rash can become severe and widespread enough to be life threatening (this condition is called toxic epidermal necrolysis, or TEN). Allergic individuals who experience only a mild rash may be able to build up their tolerance for the drug by undergoing a desensitization process.

Allopurinol interacts with certain other drugs, such as azathioprine.

Puricase (PEG-Uricase). This is an experimental drug that has been shown to rapidly reduce excess uric acid. If approved, it may help those who have failed other treatments.

It should be noted that many drugs used for gout can also precipitate acute gout symptoms and so should not be used until symptoms have subsided. The patient should then start treatment with small doses that gradually increase.

Hypertensive Agents. People with gout have a higher risk for high blood pressure. Some of the drugs used to treat hypertension, such as thiazide diuretics, can increase the risk for gout attacks. Newer agents, such as losartan (an angiotensin II receptor antagonist), and amlodipine (a calcium channel blocker), may have beneficial effects on both high blood pressure and gout.

Febuxostat. Febuxostat is the first drug to emerge in many decades as a potential new treatment for chronic gout. It may prove to be an alternative for patients who are allergic to allopurinol. The drug is awaiting approval from the U.S. Food and Drug Administration (FDA).

Other Treatments

Surgery. Large tophi that are draining, infected, or interfering with the movement of joints may need to be surgically removed. When infection is present, the procedure carries a high risk for complications. People most likely to have surgery also tend to have other medical conditions that might worsen their outlook. In one study, experts suggested that better preventive measures, such as the use of allopurinol, could reduce the need for surgery.

Several other surgical procedures are available for relieving pain and improving the function of affected joints. It is sometimes necessary to replace joints.

Hot and Cold Therapy. Rest and protecting the affected joint with a splint can also promote recovery. One study reported that applying ice packs for 30 minutes four times daily significantly reduced pain. However, a different study recommended applying warm water continuously and moving the joint. The theory behind this advice was that the pain in a gout attack is due to grinding from the crystals and that warmth would help dissolve the crystals and relieve pain.

Lifestyle Changes

Any activities that increase energy demands on the body also increase metabolism of purines, which produces uric acid. Avoiding stress and staying healthy are important for the prevention of attacks.

Because uric acid levels are only mildly affected by diet, dietary therapy does not play a large role in the prevention of gout. Still, people who have had an attack of gout may benefit from reducing their intake of purine-rich foods, particularly if they eat unusually large quantities of such foods.

While meat and certain types of seafood and shellfish do produce high levels of purines in the blood, research has suggested that not all purine-rich foods are associated with gout. Eating a moderate amount of purine-rich vegetables (spinach, cauliflower, mushrooms, legumes) does not appear to increase the risk of gout.

Dairy products, especially low-fat products (low-fat yogurt and skim milk), may actually protect against gout. Researchers have also found that taking 500 mg a day of vitamin C significantly reduces uric acid levels. They are investigating whether vitamin C can be used to prevent or treat gout.

Foods to Avoid:

Organ meats (liver, kidneys, sweetbreads)
Red meat (beef, pork, lamb)
Meat extracts (soup, broth, gravies)
Seafood (anchovies, sardines, herring, fish roe, canned tuna fish, shrimp, lobster, scallops, mussels)
Yeast products (beer and baked goods)

A supervised weight-loss program may be a very effective way to reduce uric acid levels in overweight patients. Crash dieting, on the other hand, is counterproductive because it can increase uric acid levels and may cause an acute attack.

Drinking plenty of water and other nonalcoholic beverages helps remove MSU crystals from the body.

Alcohol should be avoided, since it promotes purine metabolism and uric acid production. It also may reduce excretion of uric acid. Heavy drinking, especially binge drinking of beer or distilled spirits, should be avoided.

People with gout should also attempt to avoid activities that cause repetitive joint trauma, such as wearing tight shoes.

Travel is an example of an activity that increases the risk for gout. It not only increases stress, but eating and drinking patterns may change. Before traveling, patients should discuss preventive measures with their health care providers. The doctor may prescribe a prednisone tablet to be taken immediately at the first sign of a gout attack. In most cases, this stops the episode.

Complications

Properly treated gout rarely poses a long-term health threat, though it can be a cause of short-term pain and incapacity for thousands of Americans.

Left untreated, gout can develop into a painful and disabling chronic disorder. Persistent gout can destroy cartilage and bone, causing irreversible joint deformities and loss of motion. Survey results released in 2006 show that two-thirds of persons with gout consider the pain of attacks among the worst they've ever experienced. An estimated 75% of those surveyed said flare-ups made walking very difficult, and about 70% reported trouble putting on shoes or playing sports.

Tophi are firm chalky, gritty clumps of uric acid crystals that build up in tissue surrounding a joint. If gout is not treated, tophi can grow to the size of golf balls and can destroy bone and cartilage in the joints, similar to the process in rheumatoid arthritis. If they lodge in the spine, tophi can cause serious damage including compression, although this is very rare. In extreme cases, joint destruction results in complete disability.

Kidney Stones. Kidney stones occur in 10 - 40% of gout patients, and can occur at any time after the development of hyperuricemia. Although the stones are usually composed of uric acid, they may also be mixed with other materials.

Kidney stones result when urine becomes too concentrated, and substances in the urine crystallize to form stones. Symptoms occur when the stones begin to move down the ureter and cause intense pain. Kidney stones may form in the pelvis or calyces of the kidney or in the ureter.

Kidney Disease. About 25% of patients with chronic hyperuricemia develop progressive kidney disease, which sometimes ends in kidney failure. It should be noted, however, that many experts believe that chronic hyperuricemia is unlikely to be a common cause of kidney disease. In most cases, the kidney disease comes first and causes high concentrations of uric acid.

Gout is found in higher rates in people with high blood pressure, coronary artery disease, and heart failure. Hyperuricemia, in fact, has been associated with a higher risk of death from heart conditions. A large study published in 2007 found an association between gout and having the metabolic syndrome -- a collection of problems, such as abdominal obesity, high blood pressure, high triglycerides levels, and low "good" cholesterol levels. This syndrome increases a person's risk of heart disease and diabetes.

A study published in the August 2006 journal Arthritis & Rheumatism found that gout increases the risk of heart attacks in men with no previous history of heart problems. According to some studies, hyperuricemia may be associated with heart disease, but there is not enough data to confirm such an association.

Click the icon to see an image of coronary artery blockage.

The following are some conditions that are associated with long-term gout:

Cataracts
Dry eye syndrome
Complications in the lungs (in rare cases, uric acid crystals occur in the lungs)

Resources

www.niams.nih.gov -- National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.rheumatology.org -- American College of Rheumatology
www.arthritis.org -- The Arthritis Foundation
www.gouteducation.org -- The Gout & Uric Acid Education Society

References

Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-15.

Huang HY, Appel LJ, Choi MJ et al. The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum. 2005 Jun;52(6):1843-7.

Krishnan E, Baker JF, Furst DE, Schumacher HR. Gout and the risk of acute myocardial infarction. Arthritis Rheum. 2006 Aug;54(:2688-96.

Underwood M. Diagnosis and management of gout. BMJ. 2006;332(7553):1315-9.

Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1301-11.

Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1312-24.

Zhang YQ, Chaisson CE, Chen CA, McAlindon TE, Hunter DJ. High Humidity and High Temperature Increase the Risk of Recurrent Gout Attacks: The Online Case-crossover Gout Study. Presentation Number 707. American College of Rheumatology Annual Scientific Meeting, Washington, DC, November 2006.

Review Date:
1/21/2008
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

A.D.A.M. Copyright

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997-2010 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

adam.com

Uveitis

admin — Wed, 03 Sep 2008 17:53:43 -0700

Overview

Definition
Alternative Names
Causes, incidence, and risk factors
Symptoms
Signs and tests
Treatment
Expectations (prognosis)
Complications
Calling your health care provider
Prevention

Illustrations

Eye

Visual field test

HEALTH GUIDE REFERENCE FROM A.D.A.M

Definition

Uveitis is an inflammation (swelling and irritation) of the the uvea. The uvea is the layer of the eye between the sclera and the retina. This layer includes the iris, ciliary body, and the choroid.

Alternative Names

Iritis; Pars planitis; Choroiditis; Chorioretinitis; Anterior uveitis; Posterior uveitis

Causes, incidence, and risk factors

Uveitis is an inflammation inside the eye, affecting the uvea. The uvea provides most of the blood supply to the retina. Causes of uveitis can include autoimmune disorders, infection, or exposure to toxins. However, in many cases the cause remains unknown.

The most common form of uveitis is anterior uveitis, which involves inflammation in the front part of the eye. This form of uveitis is usually limited to the iris. Therefore, this condition is often called iritis (inflammation of the iris). The inflammation may be associated with autoimmune diseases such as rheumatoid arthritis or ankylosing spondylitis, but most cases occur in healthy people and do not indicate an underlying disease. The disorder may affect only one eye and is most common in young and middle-aged people. A history of an autoimmune disease is a risk factor.

Pars planitis is inflammation of the pars plana, a narrow area between the iris and the choroid. Pars planitis usually occurs in young men and is generally not associated with any other disease. However, there have been a few case reports of an association with Crohn's disease, and some experts suggest a possible association with multiple sclerosis. For this reason, these experts recommend that those over 25 years old diagnosed with pars planitis receive an MRI of their brain and spine.

Posterior uveitis affects the back portion of the uveal tract, and involves primarily the choroid. This is called choroiditis. If the adjacent retina is also involved it is called chorioretinitis. Posterior uveitis may follow a systemic infection or occur in association with an autoimmune disease.

The inflammation causes spotty areas of scarring on the choroid and retina that result in areas of vision loss. The degree of vision loss depends on the amount and location of scarring. If the central part of the retina, called the macula, is involved, central vision becomes impaired.

Uveitis, affecting one or both eyes, can be associated with any of the following:

Toxoplasmosis
Histoplasmosis
Tuberculosis
Sarcoidosis
Syphilis
AIDS
CMV retinitis or other cytomegalovirus infection
Trauma
Ulcerative colitis
Rheumatoid arthritis
Kawasaki disease
Herpes zoster infection
Ankylosing spondylitis
Behcet syndrome
Psoriasis
Reiter syndrome

Symptoms

Redness of the eye
Blurred vision
Sensitivity to light
Dark, floating spots in the vision
Eye pain

Note: Symptoms may develop rapidly.

Signs and tests

A complete medical history and eye examination should be performed. If there is suspicion of an associated systemic disease, a physical examination and laboratory tests may be needed to look for underlying causes.

Treatment

Iritis is usually mild. Pain caused by spasm of the pupil constriction muscle is relieved by drops to dilate the pupil. Dark glasses may be helpful. Steroid eye drops or ointment may be needed. More severe cases require a search for an underlying cause.

Pars planitis is often treated with steroid eye drops, but may be treated with oral steroids or another type of medication to suppress the immune system.

Choroiditis requires determination of the underlying cause, and treatment of the underlying disease. The underlying disease may be serious. Additional specialists in infectious disease or autoimmunity may be needed for such diseases as syphilis, tuberculosis, AIDS, sarcoidosis, or Behcet's syndrome.

For systemic infectious diseases, corticosteroids are often used along with antibiotic therapy. For autoimmune diseases, various forms of suppression of the immune system may be required.

Expectations (prognosis)

In anterior uveitis, most attacks last from a few days to weeks with treatment, but relapses are common. In posterior uveitis, the inflammation may last from months to years and may cause permanent vision damage, even with treatment.

Complications

Glaucoma
Cataracts
Fluid within the retina
Retinal detachment
Vision loss

Calling your health care provider

Call for an appointment with your health care provider if you have symptoms of uveitis. If eye pain or reduced vision are present, this condition is more urgent than if symptoms are very mild.

Prevention

Treating any underlying disorders may help to prevent uveitis for some people with existing systemic diseases.

Review Date: 8/8/2006

Reviewed By: Paul B. Griggs, MD, Department of Ophthalmology, Virginia Mason Medical Center, Seattle, WA. Review provided by VeriMed Healthcare Network.

A.D.A.M. Copyright

adam.com

Source Doc: 1_001005

Cataracts

FitSugar — Wed, 08 Oct 2008 17:35:39 -0700

In This Report

Highlights
Introduction
Causes
Symptoms
Prognosis
Risk Factors
Prevention
Diagnosis
Treatment
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Medical Societies Issue Tamsulosin (Flomax) Warning

In August 2006, the American Society of Cataract and Refractive Surgery (ASCRS), the American Academy of Ophthalmology, and the American Urological Association (AUA) issued a joint warning concerning Tamsulosin (Flomax). The societies advised patients to be sure to inform their eye surgeons if they are taking this drug. Tamsulosin is frequently prescribed to treat prostate enlargement.

The ACSRS has developed specific cataract surgery techniques for cataract patients who take this drug. Recent research suggests that these new techniques produce successful surgical outcomes.
The AUA warns that while men are primarily at risk, more women may be at risk in the future as Tamsulosin is increasingly being prescribed for urinary retention.

Cost of Cataracts

Cataracts cost the United States nearly $7 billion a year in medical services and pharmaceutical costs, according to a 2006 report in the Archives of Ophthalmology.

Can Statins Reduce Cataract Risk?

Statin drugs, which are used to manage cholesterol levels, are associated with a lower risk of nuclear cataract -- the most common type of age-related cataract -- according to a 2006 study in the Journal of the American Medical Association. Researchers think that the antioxidant properties of statins may account for this association.

Cataract Surgery

A new surgical technique, phacoviscocanalostomy, works well for patients who have both glaucoma and cataracts, suggests a 2006 study in the Journal of Cataract and Refractive Surgery.
Newer methods of administering local anesthesia are resulting in fewer complications than older methods, indicates a 2006 study in the British Journal of Ophthalmology.

Intraocular Lenses (IOLs)

The Tecnis ZM001 IOL helped produce better reading clarity and reading speed than several other newer multifocal IOLs, according to a 2006 comparison study. Multifocal IOLs are used for patients who need correction for both farsightedness and nearsightedness.

Introduction

A cataract is an opacity, or clouding, of the lens of the eye.

The lens of an eye is normally clear. If the lens becomes cloudy or is opacified, it is called a cataract.

The prevalence of cataracts increases dramatically with age. It typically occurs in the following way:

The lens is an elliptical structure that sits behind the pupil and is normally transparent. The function of the lens is to focus light rays into images on the retina (the light-sensitive tissue at the back of the eye).
In young people, the lens is elastic and changes shape easily, allowing the eyes to focus clearly on both near and distant objects.
As people reach their mid-40s, biochemical changes occur in the proteins within the lens, causing them to harden and lose elasticity. This causes a number of vision problems. For example, loss of elasticity causes presbyopia, or far-sightedness, requiring reading glasses in almost everyone as they age.
In some people, the proteins in the lens, notably those called alpha crystallins, may also clump together, forming cloudy (opaque) areas called cataracts. They usually develop slowly over several years and are related to aging. In some cases, depending on the cause of the cataracts, loss of vision progresses rapidly.
Depending on how dense they are and where they are located, cataracts can block the passage of light through the lens and interfere with the formation of images on the retina, causing vision to become cloudy.

Click the icon to see an image of eye anatomy.

Cataracts can form in any of three parts of the lens and are named by their location.

Nuclear cataracts. These form in the nucleus (the inner core) of the lens. This is the most common variety of cataract associated with the aging process.
Cortical cataracts. These form in the cortex (the outer section of the lens).
Posterior subcapsular cataracts. These form toward the back of a cellophane-like capsule that surrounds the lens. They are more frequent in people with diabetes, who are overweight, or those taking steroids.

Causes

Although older age is the primary risk factor for cataracts, experts are still not certain about the exact biologic mechanisms that tie cataracts to aging.

Researchers have been focusing on particles called oxygen-free radicals as a major factor in the development of cataracts. They cause harm in the following way:

Oxygen free radicals (also called oxidants) are molecules produced by natural chemical processes in the body. Toxins, smoking, ultraviolet radiation, infections, and many other factors can create reactions that produce excessive amounts of these oxygen free radicals.
Oxidants are missing an electron, so they are unstable and tend to chemically bind with other molecules in the body. When oxidants are overproduced, these chemical reactions can be very harmful to nearly any type of cell in the body. At times these reactions can even effect genetic material in cells.
Cataract formation is one of many destructive changes that can occur with overproduction of oxidants, possibly in concert with deficiencies of an important protective anti-oxidant called glutathione.
Glutathione occurs in high levels in the eye and helps clean up these free radicals. One theory posits that in the aging eye, barriers develop that prevent glutathione and other protective antioxidants from reaching the nucleus in the lens, thus making if vulnerable to oxidation.

Sunlight and Ultraviolet Radiation. Sunlight consists of ultraviolet (referred to as UVA or UVB) radiation, which penetrates the layers of the skin. Both have destructive properties that can promote cataracts. The eyes are protected from the sun by eyelids and the structure of the face (overhanging brows, prominent cheekbones, and the nose). Long-term exposure to sunlight, however, can overcome these defenses.

UVB radiation produces the shorter wavelength, and primarily affects the outer skin layers. It is the primary cause of sunburn. It is also the UV radiation primarily responsible for cataracts. Long-term exposure to even low levels of UVB radiation can eventually cause changes in the lens, including pigment changes, which contribute to cataract development. (UVB also appears to be responsible for macular degeneration, an age-related disorder of the retina.) Some scientists suggest that global warming and ozone depletion may increase people’s exposure to UVB, leading to a greater incidence of cataracts.
UVA radiation is composed of longer wavelengths. They penetrate more deeply and efficiently into the inner skin layers and are responsible for tanning. The main damaging effect of UVA appears to be the promotion of the release of oxidants.

Radiation Treatments. Cataracts are common side effects of total body radiation treatments, which are administered for certain cancers.

Electromagnetic Waves. Questions have been raised about the hazards of low-level radiation from computer screens. To date, no study has demonstrated an association between cataract development and video display terminals. It is a good idea, in any case, to sit at least a foot away from the front of a screen.

Cataracts are one of the many ill effects caused by smoking. Many studies have implicated smoking in the development of nuclear cataracts. The major damaging effects of cigarette smoke appear to be enhancement of free oxygen radicals, the chemical byproducts in the body that can damage cells, including those in the eye.

Corticosteroids. Long-term use of oral steroids is a well-known cause of cataracts. Studies have been conflicting, however, over whether inhaled and nasal-spray steroids increase the risk for cataracts. Information on cataract risk from inhaled steroids is important because they are commonly used by asthma patients, and steroid spray use is increasing among allergy sufferers. Studies have suggested a higher risk for cataracts among middle-aged and elderly patients treated with beclomethasone (Beclovent, Vanceril). However, newer inhaled steroids are available, and their effects on the eye are unclear. In children, cataracts are rare, and the benefits of inhaled steroids for asthma far outweigh any small additional risk.

Other Medications Associated with Cataracts.

Psoralens, a class of drugs used along with light therapy to treat skin disorders, such as psoriasis
Antipsychotic medications such as chlorpromazine (Thorazine)
Glaucoma medications

Many others drugs have been weakly associated with cataracts, including allopurinol, tamoxifen, amiodarone, tricyclic antidepressants, potassium-sparing diuretics (but not other diuretics), thyroid hormone, tetracyclines, sulfamidase, and mepacrine. According to a 2006 study in the Journal of the American Medical Association, statin drugs (used for managing cholesterol) may possibly reduce the risk for nuclear cataracts.

Click the icon to see an animation about cataracts.

Glaucoma. Glaucoma and its treatments, including certain drugs (notably miotics) and filtering surgery, pose a high risk for cataracts. The glaucoma drugs posing a particular risk for cataracts including demecarium (Humorsol), isoflurophate (Floropryl), and echothiophate (Phospholine).

Uveitis. Uveitis is chronic inflammation in the eye, which is often caused by an autoimmune disease or response. Often the cause is unknown. It is a rare condition that carries a high risk for cataracts.

A number of medical conditions appear to be associated with a higher risk for cataracts either because of a direct effect or because of the medications used for them, or both. They include the following:

Diabetes. Cataracts in patients with diabetes appear to form when high levels of blood sugar react with proteins in the eye to form byproducts that accumulate in the lens (sugar cataracts).
High blood pressure (hypertension).
Autoimmune diseases including rheumatoid arthritis, psoriasis, multiple sclerosis, systemic lupus erythematosus, Behcet's disease, and others.

Rarely, about 1 in every 10,000 births, a baby is born with cataracts (called congenital cataracts).

Inherited disorders are often involved in the development of congenital cataracts in children. Such cataracts are most often due to inborn abnormalities in the structure or shape of the lens, including its capsule. Dozens of variations can affect the lens causing, susceptibility to cataracts. Researchers are also investigating genetic factors that may cause mutations in alpha crystallins -- major proteins in the lens, which form cataracts. (Genetic factors also may play a role in some adult cataract cases. The exact hereditary predispositions have yet to be established.)
Infection during pregnancy can lead to cataracts.
Pregnant women who abuse alcohol or drugs increase the risk for cataracts (along with other more serious birth defects) in their infants.

Surgery in children with early-onset cataracts can help correct this problem in many cases, but it should be performed as soon as possible for full benefit. Experts recommend routine examination of the face of a fetus during ultrasound for abnormalities.

Symptoms

During the early stages, cataracts have little effect on vision. The symptoms of a cataract may include:

Cloudy vision, double vision, or both may be the first signs.
Images may take on a yellowish tint as color vibrancy diminishes.
Reading may become difficult over time because of a reduced contrast between letters and their background.
Sensitivity to bright lights may make it difficult or impossible to drive at night because of glare from the headlights of oncoming cars. (People with diffuse cataracts in the rear walls of their lenses are particularly prone to glare sensitivity because bright light tends to scatter in their lenses.)
In very advanced cases, the pupil, which is normally black, looks milky or yellowish. The patient's vision is reduced to being able only to distinguish light from dark.

This photograph shows a cloudy white lens (cataract) over the pupil. Cataracts are a leading cause of decreased vision in older individuals, but children may have congenital cataracts. With new surgical techniques, the cataract can be removed, a new lens implanted, and the person can usually return home the same day.

Nuclear Cataracts. Cataracts of the lens nucleus are most commonly associated with aging. Symptoms include:

Hazy distance vision and increasing glare.
Progressive nearsightedness and the need for frequent changes in eyeglass prescriptions. This effect may even temporarily counteract age-related farsightedness and provide a temporary improvement in overall vision in some people. The improvement fades when the cataract advances sufficiently to overwhelm the inherent farsightedness. Eventually, as the cataracts grow worse, stronger glasses can no longer correct the patient's vision.

Click the icon to see an image of normal, near, and farsighted vision.

Cortical Cataracts. Cortical cataracts usually start on the outside of the cortex (the outer area of the lens).

They have very little initial effect on vision.
Glare can develop as these cataracts increase and approach the center of the lens.
Problems with distance vision, contrast sensitivity, and clarity may occur as the cataracts progress further.

Posterior Subcapsular Cataracts. Posterior subcapsular cataracts typically start near the center of the back part of the capsule surrounding the lens. These cataracts often advance rapidly. For many patients, major impairment of eyesight, including near-vision problems and glare, develops within several months.

Prognosis

Some cataracts stop progressing after a certain point. Cataracts are never reversible, however, even after eliminating factors, (such as drugs or illnesses), which might have promoted their development. If extensive and progressive cataracts are left untreated they can cause blindness. In fact, cataracts are the leading cause of blindness among adults age 55 and older. About 20.5 million Americans have at least one cataract. By 2020, that number is expected to jump to 30.1 million.

Fortunately, cataracts nearly always can be successfully removed with surgery. However, surgery is unavailable in certain parts of the world, leaving millions at risk for vision loss. Even in the U.S., where surgery has greatly reduced the risk of blindness, tens of thousands still lose their sight and millions more have poor vision because of cataracts. Cataracts also exact a financial burden. According to 2006 data, cataracts cost the U.S. nearly $7 billion each year in medical services and drug treatments.

In a 2001 study, cataracts were associated with a significantly higher mortality rate in older women, although not older men. These higher rates did not seem to be caused by certain health risks (for example, diabetes) that are often associated with both cataracts and lower survival rates. A 2004 study published by scientists in Italy appears to confirm the association between shortened lifespan and cataracts, especially cataracts confined to the lens nucleus and those that had already required surgery. A few other studies have also linked cataracts and vision impairment with poorer survival, regardless of accompanying health problems. One study reported that even middle-aged people with cataracts, particularly those in ethnic minority groups, had lower survival rates than their peers, perhaps because of premature aging.

Effect on Survival by Location of the Cataract. Some studies have suggested poorer survival specifically in patients with nuclear or mixed cataracts but not in those with cataracts in the cortex or capsule. Not all studies have found these differences. In any case, nuclear cataracts are highly associated with smoking and diabetes, although some studies have found lower survival rates in patients with nuclear cataract regardless of these health risks.

A 2002 study reported twice the rate of automobile accidents in patients who do not have cataract surgery compared to those who had surgery. This finding, however, is obscured by the possibility that patients who choose not to have surgery may have other health problems that put them at risk for accidents. Also, driving skills decline with age in nearly everyone. Cataract surgery, then, is no insurance against age-related accidents.

Reduced vision ranks third only behind arthritis and heart disease as a cause of impaired function in older people. Extensive cataracts can compromise the ability to earn a living, read, drive, or live independently. Although vision loss has been associated with a number of major adverse effects, few studies have reported on the effect of vision on daily activities.

Both blurred vision and problems in seeing contrasts contribute to impaired activity. The degree of these impairments, however, may have different effects on disability depending on individual tasks and needs. For example, even a slight loss in vision sharpness and contrast can impair the ability to recognize faces or slow down reading speed. For those who read very quickly, this may not be significant, but it could be very disabling for slower readers. In one study, people under age 65 rated blurred vision as reducing their quality of life more than any other chronic medical problem except shortness of breath.

Nevertheless some people who have small cataracts can see well enough around the clouded areas to live normally. But for many people, cataracts are extensive enough to interfere greatly with daily activities.

Risk Factors

Aging is the primary risk factor for cataracts, but other factors are also involved.

Nearly everyone who lives long enough will develop cataracts to some extent. A major study reported that:

About 40% of people age 55 - 64 years had some opaque areas in their lenses, and 5% had fully-developed cataracts.
About 70% of people age 65 - 74 years had opaque areas, and 18% had cataracts.
More than 90% of people age 75 - 84 years had opaque areas, and almost 50% had cataracts.

One study indicated that posterior subcapsular cataracts are the most common type in people under 70 years old, while nuclear and mixed cataracts are most common in people over age 80. The risk for nuclear cataracts also increases with age.

Women face a higher risk than men. Women who started menstruating late are at an even higher risk.

Eye Features. People who are nearsighted and those with brown eyes may be at higher than average risk. (Not all studies, however, report a higher risk in people with darker eyes.)

Obesity and Height. Studies are now reporting obesity as a risk factor for cataracts, notably posterior subcapsular cataracts, which form toward the back of the lens. A study of 17,150 people found a specifically higher rate of cataracts in overweight people who are tall and whose fat distribution is primarily in the abdomen.

A 9-year population study, published in 2004, revealed that African Americans have nearly twice the risk of developing cataracts than do Caucasians. Analysis of the 3,000 participants also demonstrated for the first time that the risk of cortical cataracts is 3 times higher in African Americans than Caucasians. Earlier studies also identified a higher cataract risk in the black population, suggesting that it may be due to other medical illnesses, particularly diabetes. It has long been known that African Americans are much more likely to become blind from cataracts and glaucoma than Caucasians, mostly due to lack of treatment.

Hispanic Americans are also at increased risk for cataracts. In fact, cataracts are the leading cause of visual impairment among Hispanics. A 2005 study found that cataracts were about 3 times more common in Hispanic patients age 65 - 84 years than in similarly aged white or African Americans. (The study evaluated Hispanic patients of Mexican descent.) As with African Americans, Hispanic patients often face barriers to access to care.

People with certain medical conditions, notably diabetes, are at high risk for cataracts, either because of a direct effect of the disease, its treatments, or both.

Autoimmune Diseases and Conditions Requiring Steroid Use. Medical conditions requiring high use of corticosteroids (commonly called steroids) pose a particularly high risk. Many of these medical conditions are autoimmune diseases, including rheumatoid arthritis, psoriasis, multiple sclerosis, systemic lupus erythematosus, Behcet's disease, and others.

Diabetes and People with High Blood Glucose Levels. People with diabetes type 1 or 2 are at very high risk for cataracts and are much more likely to develop them at a younger age. They also have a higher risk for nuclear cataracts than nondiabetics. Cataract development is significantly related to high levels of blood sugar (called glycemia), and cataracts in people with diabetes are sometimes referred to as so-called sugar cataracts. Even people without diabetes but with higher-than-normal blood sugar levels are at high risk for cataracts. Some doctors now recommend that children with diabetes undergo an eye exam to check for cataracts at the time they are diagnosed.

Insulin is a hormone produced by the pancreas that is necessary for cells to be able to use blood sugar.

Exposure to even low-level UVB radiation from sunlight increases the risk for cataracts. A 2003 study published provided new evidence supporting the link between sun exposure and nuclear cataracts. The risk was highest among those who had significant sun exposure at a young age. Additional studies suggesting risk associated with sunlight exposure report:

The closer people live to the equator the greater the chance for cataracts. As suggested by a study in Southern France, sunlight exposure in these climates also increases the risk for severe cortical or mixed cataracts. In this study, even wearing sunglasses did not reduce the risk for these cataracts, although it did for posterior subcapsular cataracts.
People whose jobs expose them to sunlight for prolonged periods are at higher risk. People in southern climates whose occupations, such as fishing or oyster farming, exposed them to very intense sunlight were at high risk for all cataracts, including posterior subcapsular cataracts. (People in more northern climates with similar occupations may not have as high a risk.)
Occupational exposure to very intense artificial light, such as arc welding, increases the risk for cataracts.

Smokers. A study of nearly 18,000 doctors showed that those who smoked 20 or more cigarettes a day had approximately twice the risk of developing cataracts. Smokers are at particular risk for cataracts located in the nuclear portion of the lens, which limit vision more severely than cataracts in other sites. Quitting smoking may reverse some of this damage.

Alcohol Users. Chronic drinkers are at high risk for a number of eye disorders, including cataracts. Alcohol has been implicated in cataract development in a number of studies. Wine provided the least risk, and the more moderate the drinking the lower the risk. Alcohol may work directly on the proteins in the lens itself and indirectly by affecting absorption of nutrients important to the lens.

Long-term environmental lead exposure may increase the risk of developing cataracts according to a study published in the Journal of the American Medical Association. Researchers assessed bone lead levels in 795 men aged 60 years and older. Because lead tends to accumulate over time in the skeleton, the researchers measured lead levels in the men’s shin bones. Men with the highest levels of lead were three times more likely to have cataracts than men with the least amount of lead.

A poor diet may deprive the body of amino acids and B vitamins that are essential for eye health. A French study of elderly adults found that lower blood levels of the protein albumin were associated with an increased risk of cataracts.

Other conditions that can trigger the process leading to cataracts include:

Physical injury to the eye (such as a hard blow, cut, or puncture)
Chemical burns
Electrical shock injuries
Chronic exposure to intense heat or cold

Prevention

Although cataracts are not completely preventable, their occurrence can be delayed. Quitting smoking, avoiding overexposure to sunlight, drinking alcohol in moderation, and eating plenty of fresh fruits and vegetables can delay the formation of cataracts. No evidence exists that using eye drops or ointments or performing eye exercises will stem the onset of cataracts.

The simplest and most effective way to protect against ultraviolet (UV) radiation is to stay out of the sun. A hat and cover-up should be worn outside, particularly when the sun is most intense (10 AM - 3 PM). A wide-brimmed hat can reduce eye exposure to UVB radiation by 30 - 50%. Because the sun's rays are highly reflective, sitting in the shade or under an umbrella by itself does not guarantee protection.

Clothing that blocks or screens the harmful rays of the sun (UVA and UVB), in combination with wide-brimmed hats, sunglasses, and sunscreen, all help prevent damage to the eyes and skin. Any one of these by itself, even the sunscreen, may not be enough to prevent sun damage.

Note: Avoidance of the sun should not be taken to extremes. Some sunshine is desirable. Moderate sun exposure provides an important source of vitamin D, which is essential for healthy bones. There is a link between lack of sun exposure and depression (known as seasonal affective disorder, or SAD).

Click the icon to see an image of vitamin D.

Sunglasses. Protective sunglasses do not have to be expensive. Sunglasses are classified into three categories based on UVA and UVB protection:

Cosmetic purpose sunglasses block at least 70% UVB and up to 60% UVA. People should avoid these glasses if they have any risk for cataracts or eye problems.
General purpose sunglasses block at least 95% UVB and a minimum of 60% UVA. At the very least, people should purchase general purpose sunglasses that are labeled "Meets ANSI Z80.3 General Purpose UV Requirements." Labels should indicate that sunglasses block UV radiation up to 400 nm.
Special purpose sunglasses block at least 99% UVB and a minimum of 60% UVA rays. These are the optimal sunglasses for people at risk for cataracts. Ideally they should have the Skin Cancer Foundation's Seal of Recommendation for Sunglasses. Special purpose glasses should wrap around the head and block light coming from above, below, and both sides of the glasses. They should also fit snugly on the nose.
Lenses that are simply dark but not coated with UV-absorbing material may actually increase the risk of cataracts because the pupil widens to compensate for the shaded glass. This may allow more harmful ultraviolet waves to enter. Polarized glasses cut glare but have no effect on UV radiation. Mirror finishes without additional processing for UV blockage are also not fully protective. There is some controversy over whether blue light is harmful to the eyes. Some people prefer amber lenses, which block out the blue spectrum.

Antioxidant vitamins C and E. Because of the role oxidants may play in cataract formation, researchers are investigating the benefits of antioxidant vitamins and other food chemicals. Vitamins C, E, and riboflavin (a B vitamin), for example, are helpful in preserving levels of glutathione, an enzyme that helps protect against oxidation in the eye. Low levels of vitamin C in the lens of the eye have been particularly strong predictors of cataracts. Some evidence also suggests that ultraviolet B radiation interacts with deficiencies in certain antioxidants, such as vitamin E and zinc, to increase damage in the corneas and lenses of the eye.

Evidence on the benefits of supplements of vitamin E or C, or vitamin-rich foods, is conflicting. For example, in two identically constructed trials in the US and Britain, the American group derived apparent benefits from vitamins E, C, and beta carotene while the British group reported very little cataract protection. A 2005 study suggested that long-term use of vitamin E supplements may slow cataract development. However, in a major on-going American study called the Age-Related Eye Disease Study (AREDS), researchers reported no difference in the incidence of cataracts after 7 years in people who took the antioxidant vitamins compared to those who took sham vitamins.

High doses of vitamins may have harmful effects. It is always wise, in any case, to pursue a healthy diet that is low in fats, high in complex carbohydrates, and rich in fruits and vegetables.

B vitamins. Some studies report some protection from a number of B vitamins, including vitamins B1 (thiamin) B2 (riboflavin), B3 (niacin) and B12 (folate). Riboflavin, for example, plays a critical role in the production of glutathione, an enzyme that helps protect against oxidation in the eye. All forms of vitamin B are widely available in dairy products, fortified grains, and meat.

Carotenoids. Carotenoids are a group of more than 700 fat soluble nutrients that produce the colors in foods such as carrots, pumpkins, sweet potatoes, tomatoes, and other deep green, yellow, orange, and red fruits and vegetables. Many are proving to be very important for health. Different carotenoids may be more beneficial then others. They include:

Xanthophylls are compounds that form a particular category of carotenoids. The xanthophylls lutein and zeaxanthin are found in the lenses of the eye and may be of significant importance for people at risk for cataracts. Some evidence indicates supplements of xanthophyll-rich foods may help retard the aging process in the eye and protect against cataracts. In fact, some experts suggest that the higher risk of cataracts in women compared to men may be partly due to a lesser ability to transport these carotenoids from the blood into the eye. Xanthophylls can be obtained from dark green leafy vegetables (such as spinach), broccoli, and eggs.
Lycopene is an important carotenoid that may also play an important role in eye health as a person ages. Tomatoes are the importance sources of lycopene.
Beta carotene is the most widely studied carotenoid and is a powerful antioxidant. It has been specifically studied for cataract protection. Most studies, however, have found little or no benefits. A 2003 study did suggest that beta carotene may protect against cataracts in smokers, although it is important to note that other studies report a higher risk for lung cancer in smokers who take beta carotene.

Click the icon to see an image of folate sources.

Click the icon to see an image of vitamin B12 sources.

Click the icon to see an image of riboflavin sources.

Phytochemicals. Phytochemicals are substances in plants that have beneficial effects. Dark colored (green, red, purple, and yellow) fruits and vegetables usually have high levels of important plant chemicals and have been associated with a lower risk for cataracts. Tea contains certain plant chemicals called polyphenols that have been associated with protection against cataracts.

Click the icon to see an image of phytochemicals.

Diagnosis

Either an ophthalmologist or an optometrist can examine patients for cataracts, but only ophthalmologists are qualified to treat cataracts.

An ophthalmologist is a doctor who specializes in the medical and surgical care of the eye.
An optometrist is engaged in the practice of eye care, but is not a doctor and cannot prescribe medication or perform surgery.

The eye professional can observe cloudy areas on the lenses with a direct physical examination, even before the cataracts begin to interfere with vision. Cameras can measure the cataract density. Various vision tests are also performed.

Snellen Eye Chart. To determine how clearly a person can actually see, the Snellen eye chart is used, with rows of letters decreasing in size:

From a specified distance, usually 20 feet, a person reads the letters using one eye at a time.
If a person can read down to the small letters on the line marked 20 feet, then vision is 20/20 (normal vision).
If a person can read only down through the line marked 40 feet, vision is 20/40; that is, from 20 feet the patient can read what someone with normal vision can read from 40 feet.
If the large letters on the line marked 200 feet cannot be read with the better eye, even with glasses, the patient is considered legally blind.

The visual acuity test can be performed in many different ways. It is a quick way to detect vision problems and is frequently used in schools or for mass screening. Driver license bureaus often use a small device that can test the eyes individually and then together.

Other Tests. A number of other tests are used to diagnose cataracts or to determine if surgery is needed.

A chart similar to the Snellen chart, which has the same size letters, but in different contrasts with background, is used to test contrast sensitivity,
Glare sensitivity is tested by having the patient read a chart twice, with and without bright lights.
Tests of macular function, which evaluate the eye's acute vision center, can help the ophthalmologist determine the expected improvement from surgery.
The corneal endothelium, a layer of cells lining the cornea, is sensitive to surgical trauma and should be evaluated before any intraocular operation.
Patients with other eye disorders may require a number of other pre-operative tests.

Although eye tests aid in making a diagnosis for cataracts, results do not always reflect the quality of life and how effectively people function at home:

Some people with cataracts perform poorly on the tests yet appear to have no difficulty functioning normally day-to-day.
Others perform well on the tests but insist that their eyesight is bad enough to curtail ordinary activities, such as driving.

Standard eye tests, therefore, may not be useful for determining whether a patient actually needs cataract surgery.

In general, even if cataracts are diagnosed, the decision to remove them should be based on the patient's own perception of vision difficulties and needs and the effect of vision loss on normal activity. The patient should also be aware of all the risks and costs of surgery. In order to determine the quality of life, the patient may be given a questionnaire such as National Eye Institute Visual Function Questionnaire, which asks 39 questions related to vision and daily activities. This test or others may be useful for determining if eye disease is actually impairing the ability to function.

Treatment

Although surgery is the only remedy for cataracts, it is almost never an emergency. Most cataracts cause no problem other than reducing a person's ability to see, so there is no harm in delaying surgery.

Early cataracts may be managed with the following measures:

Stronger eyeglasses or contact lenses
Use of a magnifying glass during reading
Strong lighting
Medication that dilates the pupil. (May help some people with capsular cataracts, although glare might be a problem with this treatment.)

It is important to note, however, that no treatments will prevent cataract formation or progression or make a cataract disappear.

Progression of Cataracts. Patients and their families usually have plenty of time to consider options carefully and discuss them with an ophthalmologist. There is no constant rate at which cataracts progress:

Some develop to a certain point and then stop.
Even if a cataract does progress, it may be years before it interferes with vision.
Only in a very few, very rare circumstances is it necessary that cataract surgery be performed immediately.

Each year about 2.8 million cataract operations are performed, making it the most common operation in the U.S. for people over age 65. Cataract surgery may be the oldest procedure in the world, having been introduced to Europe from India by Alexander the Great's army.

In the past, cataract surgery was not performed until the cataract had become well developed. Newer techniques, however, have made it safer and even more efficient to operate in earlier stages. In fact, modern cataract techniques not only remove cataracts but are also becoming important procedures for correcting astigmatism. Cataract surgery improves vision in up to 95% of cases and prevents millions of Americans from going blind.

Nevertheless, considerable evidence suggests that, because of the ease and relative safety of the procedure, it may be performed more often than needed. Patients having operations now tend to have better preoperative vision than those operated on 10 or 20 years ago. In a study of 800 cataract operations, 25% of the patients said that clouding had had no obvious effect on their lives before the procedure.

Cataract surgery is very successful. It has the following advantages:

Nearly all patients enjoy better vision after surgery. Advanced procedures in lens development are allowing correction of astigmatism as well as cataract removal. (Patients with significant eye disease, such as glaucoma or corneal or retinal disease, may not experience the same degree of improvement.)
Many people experience significant improvement in quality of life after the operation.
Some studies indicate that better vision might even help slow down age-related health problems unrelated to the eyes.

In general, surgery is indicated for people with cataracts under the following circumstances:

The Snellen eye test reports 20/40 or worse, with the cataract being responsible for vision loss and glasses or visual aids no longer being helpful.
Everyday activities have become difficult to perform to the point that independence is threatened. Questionnaires that assess the effects of cataracts on quality of life have been developed.
The patient is at risk for falling in low light.

These guidelines are general, however. Whether surgery is appropriate or not further depends on the cataract patient's specific condition and needs. Some examples include the following:

Even if the criteria for surgery are met, a very sick, very elderly person in a nursing home may have less need for sharp vision than an active younger adult. Among very elderly patients (85 years and older), especially those with serious health problems, there are also higher risks for complications during surgery and poor outcomes afterward. Nevertheless, these cautions should not prevent the very elderly from having this procedure; vision improvement rates are still over 85%.
Even if the criteria for surgery are not met, some people with eye tests of 20/40 or better might want surgery because of problems with glare, double vision, or the need to have an unrestricted driver's license.
Even if the criteria for surgery are not met, if retinal disease is also suspected (usually a complication of diabetes), the doctor may perform cataract surgery in order to have a clear view of the eye.

Because of the risks, albeit small ones, of poorer vision or blindness, no one should be forced to have cataract surgery if they don't want it or are not strong enough to undergo the procedure. If there are any doubts about whether or not to undergo cataract surgery, a second opinion should be considered.

The patient should ask the ophthalmologist the following questions before agreeing to cataract surgery:

Is my cataract surgery an emergency?
Are the cataracts the only cause of my poor vision?
How much experience do you have with this procedure?
Do I have other eye diseases that might complicate surgery or reduce my benefit?
Do I have other health problems that might further complicate eye surgery?
Will you be able to implant an intraocular lens?
What type of procedure will you use?
Will I have to stay in the hospital overnight?
Afterwards, what are my chances of having poorer vision or becoming totally blind in that eye?
How well should I ultimately be able to see out of the operated eye?
How long will it take to heal?
How long will it take to achieve my best eyesight?
Will I have to wear glasses or contact lenses after surgery?
When will I get my final eyeglass prescription?
How soon after surgery will I be able to see well enough to go back to work? Drive a car? Return to full activity?
What will the surgery cost?

Cataract surgery is now usually done as an outpatient procedure under local anesthesia and takes less than an hour. Preoperative preparations may include:

Having a general physical examination is important for patients with medical problems such as diabetes. Diabetes can cause damage to the blood vessels of the eye’s retina, a condition called diabetic retinopathy. Recent research suggests that patients who have diabetic retinopathy and poor blood sugar control should not have their blood sugar rapidly corrected before cataract surgery. Correcting blood sugar too quickly before surgery can cause vision problems after surgery.
The ophthalmologist will use a painless ultrasound test to measure the length of the eye and determine the type of replacement lens that will be needed after the operation.
Topical application of so-called fluoroquinolone antibiotics (such as ofloxacin or ciprofloxacin) may be applied preoperatively to protect against postoperative infection.
Most healthy patients are given either a local injection or topical anesthetic. The patients who report the least pain during the operation are those given a sedative followed by a local injection rather than just the topical drug.
Some patients may require a general anesthetic, such as those who are very anxious, those who are unable to cooperate with the surgeon, and those who are allergic to local anesthetics.

All cataract procedures involve removal of the cataract-affected lens and replacing it with an artificial lens.

Phacoemulsification. Phacoemulsification (phaco means lens, emulsification means to liquefy) is now the most common cataract procedure in the United States and accounts for 85% of cases. Benefits are greater than with standard extracapsular surgery, and it may be particularly helpful for people with diabetes.

The procedure generally involves:

The surgeon makes an incision, which is much smaller than with standard cataract extraction.
Ultrasound is then used to break up the clouded lens into small fragments.
The tiny pieces are sucked out with a vacuum-like device.
A replacement lens is then usually inserted into the capsular bag where the natural lens used to be. In most cases, this is an intraocular lens (IOL), which is foldable and slips in through the tiny incision.
Because the incision is so small, it is often watertight and does not require a suture afterward, particularly if a foldable lens has been used. A suture may be needed if a tear or break occurs during the procedure or the surgeon inserts a rigid lens that requires a wider incision.

Click the icon to see an illustrated series detailing cataract surgery.

Phacoemulsification requires only local anesthesia. Newer methods for administering local anesthesia produce few complications. Most phacoemulsification procedures now take about 15 minutes, and the patient is usually out of the operating room in about an hour. There is little discomfort afterward and visual rehabilitation takes about 1 - 3 weeks.

Phacoemulsification is sometimes combined with viscocanalostomy, a glaucoma surgical procedure, for patients who have both glaucoma and cataracts. Recent research suggests that phacoviscocanalostomy (as this combined procedure is called) is safe and effective for this group of patients.

Surgeons in the U.S. and Europe are currently investigating Microphaco, a new approach to cataract surgery that uses two smaller (micro) incisions. The smaller incisions measure about 1.6 mm compared to the traditional 3 mm. Experts say this procedure is expected to revolutionize refractive and cataract surgery.

Other Lens Removal Techniques. The AquaLase device uses pulses of fluid to wash away the clouded lens. Some experts believe this approach causes less trauma to the eye, and allows for a quicker recovery time for the patient, than the ultrasound used in phacoemulsification.

Extracapsular or Intracapsular Cataract Extraction. Extracapsular cataract extraction was the original standard procedure, but is now generally used only in patients who have an extremely hard lens. It typically involves the following steps:

The ophthalmologist works under an operating microscope to make a small incision in the cornea of the eye.
The surgeon then extracts the clouded lens through this incision.
The capsule is left in place, which adds structural strength to the eye and enhances the healing process. (Less commonly, in intracapsular cataract extraction, the surgeon removes the lens and the entire capsule. There are greater risks with this procedure for swelling and retinal detachment.)
A replacement lens is then usually inserted.
A small suture is needed to stitch the incision together.

It takes about 2 - 4 weeks to completely restore vision.

With the clouded lens removed, the eye cannot focus a sharp image on the retina. A replacement lens or eyeglass are therefore needed:

Intraocular Lenses (IOL). In about 90% of cataract operations, an artificial lens, known as an intraocular lens (IOLs), is inserted. Until recently, IOLs used a pair of little spring-loaded loops to hold the lens in place. Most IOLs are now foldable, which makes insertion easier. In fact, a prefolded lens is now available that unrolls to fit the eye as body temperature warms it.

IOLs are available as monofocal or multifocal. Monofocal lenses correct only one type of vision range (such as distance vision). Multifocal lenses are designed for patients who need correction for a range of vision. A 2006 study suggested that the Tecnis IOL works particularly well for patients who require a multifocal IOL.

Although all the lens materials are presumably chemically inert, there are some reports of specific problems, notably a risk for causing a reaction that leads to the development of secondary cataracts, a condition called posterior capsular opacification. IOLs include the following materials:

Acrylic: The majority of IOLs are made from acrylic, which allows a controlled unfolding of the lens. Evidence indicates that this material provides a better visual outcome and fewer complications than other standard IOLs.
Polymethylmethacrylate (PMMA): Has the longest safety record. A PMMA IOL coated with heparin, a blood thinner drug, helps protect against the development of a secondary cataract after surgery.
Silicone: Can be inserted through a smaller incision than other materials. It has the highest rates of secondary cataracts. Newer forms of silicon IOLs may pose a lower risk.

Other materials are under investigation.

IOL brands include:

Crystalens: The FDA approved the Crystalens IOL in 2003. It is made from a form of silicone called Biosil. The Crystalens uses "hinges" that allow the lens to move, mimicking the eye's natural ability to focus automatically and seamlessly at all distances. Studies indicate that when used along with standard cataract removal methods, the Crystalens can restore a full range of functional vision, from distance to reading vision, without total dependence on glasses or contact lenses.
Array: The Array lens also uses silicon. It is one of a number of so-called second-generation IOLs that is available as a multifocal lens to help correct presbyopia (nearsightedness).
Tecnis: The Tecnis foldable IOL was specifically designed to improve functional vision of cataract surgery patients. Tecnis has a patented surface that reduces light scattering (spherical aberration) of the cornea, which can negatively affect vision. In April 2004, The FDA approved new labeling claims for Tecnis, stating the lens may help improve driving safety for senior cataract patients. In clinical trials, simulated night driving and visual acuity (20/20, 20/40) results were significantly better in eyes implanted with the Tecnis IOL. In addition, spherical aberrations were significantly less when compared to the traditional lens with the spherical optic.
AcrySof Natural: Approved in 2003, the yellow-tinted Acrysof Natural IOL was the first foldable lens to filter ultraviolet and blue-light. Eliminating both UV and portions of the high-energy blue light help prevent retinal damage. This lens also conforms to the natural shape of the human lens capsule so it remains centered over the eye.
AcrySof ReSTOR: The AcrySof ReSTOR IOL is approved in the U.S. for patients with and without presbyopia. The lens enhances vision at near, intermediate, and distant ranges. In clinical trials, 80% of patients who received the lens did not require glasses after cataract surgery. The FDA approved the AcrySof ReSTOR in March 2005.

IOLs are designed to improve specific aspects of vision. The choices include:

Lenses that address a single fixed focal point. Such lenses are suitable either for reading or for distance vision, but not both. If a distance lens is implanted, the surgeon prescribes glasses or contact lenses for reading. If a reading lens is implanted, lenses for seeing distances will be prescribed.
Lenses that address multifocal points. Multifocal lenses can focus at different points for both reading and distance vision. One study reported that more than 80% of patients with multifocal lenses were able to see 20/40 or better without correction. However, contrast may be reduced and some patients experience glare and halos, particularly at night.
Lenses are available that will correct astigmatism after cataract surgery.

The patients and the doctor must make these decisions based on specific visual needs.

Contact Lenses or Cataract Glasses. A few patients do not receive a new lens and rely solely on corrective eyeglasses or contact lenses. Such patients may include:

Patients who are extremely near-sighted
Patients with other eye disorders

In such cases, the patient typically returns to the ophthalmologist for a check up the day after surgery, and three additional check-ups are scheduled over a 2-month period. The ophthalmologist can usually give a final prescription for eyeglasses or contact lenses about three months after surgery.

Choosing Contact Lenses. Contact lenses allow clear vision but do not magnify, so those who choose contact lenses after surgery may have to wear reading glasses. Contacts can be prescribed either for use only during the day or for extended-wear. Occasionally contact lenses cause problems, such as infection. Those who wear them should call their eye doctor if they have red or watery eyes, pain, or sensitivity to light.
Cataract Glasses. Until the advent of contact lenses, people who had cataract surgery had no choice but to wear glasses with thick lenses, sometimes called Coke-bottle glasses. These glasses have gotten thinner and lighter in recent years, but they may still be cumbersome. Cataract glasses are different from ordinary glasses and are sometimes difficult to adjust to. Images can seem distorted and may appear suddenly within the peripheral vision. Distances may be hard to judge.

Sometimes a patient has two cataracts and needs to wear glasses between the first and second operation. They are particularly troublesome during this period. The treated eye will see images magnified while the other eye will view them as they actually are, and the brain cannot blend the two images. This is a temporary state that is resolved by the second operation.

Modern cataract surgery is one of the safest of all surgical procedures. Most complications, even if they occur, are not serious. They can include the following:

Swelling and inflammation. Risk is about 1%. This complication is particularly harmful for patients with existing uveitis (chronic inflammation in the eye, which can be due to various conditions).
Glare. Patients may experience glare after surgery from light scattering at the edges of the new lens, particularly with square-edged IOLs, which are typically used with posterior capsular cataracts. In most cases, this is a temporary problem that resolves after a few weeks. Sometimes, the problem persists, and the patient requires another operation. Some research suggests that glare can be significantly reduced by texturizing the edges of the square lens.
Materials used in some lenses trigger an immune response in about half of patients. This causes inflammation and tiny deposits of tissue in the eye that lead to secondary cataracts -- called posterior capsule opacification. Studies suggest that silicone implants pose the highest rates for inflammation and secondary cataracts, particularly in patients with other eye diseases. Newer silicon IOLs pose less risk. In one study, the lowest rates were with IOLs made of acrylic and heparin-coated PMMA.
Retinal detachment. In rare cases, the retina at the rear of the eye can become detached. Risk is very low (0.1%), and phacoemulsification poses less of a risk for this than standard surgery.
Atonia (loss of muscle tone that results in a disturbing glare). (Phacoemulsification poses less of a risk than standard surgery.)
Glaucoma. This is an eye condition in which the pressure of fluids inside the eye rises dangerously. Risk is very low, but patients should be sure to avoid activities after surgery that increase pressure.

Glaucoma is a condition of increased fluid pressure inside the eye. The increased pressure causes compression of the retina and the optic nerve which can eventually lead to nerve damage. Glaucoma can cause partial vision loss, with blindness as a possible eventual outcome.

Infection. This is very rare (0.2%), but is devastating if it does develop.
Blisters on the cornea. There is a higher risk of rupture with phacoemulsification, but the risk is extremely low, particularly for experienced eye surgeons. In 2004, the FDA approved the StabilEyes Capsular Tension Ring (CTR) to help support the eye's capsular bag during cataract surgery, especially in those with weak or broken eye fibers (zonules). A CTR is an open ring made of polymethylmethacrylate (PMMA). The ring goes into the capsular bag itself, stabilizing the eye.
Bleeding can develop inside the eye. Risk is about 1% for minor bleeding and 1 in 10,000 for severe bleeding.
An implanted IOL can become damaged or dislocated. Risk is very low.
The surgery itself can produce vision loss or impairment. The risk for this is 1 in 1,000. (Phacoemulsification poses less of a risk than standard surgery.)
Macular degeneration. Macular degeneration, in which the retina breaks down, is a common cause of vision loss in the elderly. In a 5-year study, people who underwent cataract surgery had twice the risk for progression of age-related macular degeneration. Interestingly, another study reported that cataract surgery significantly helped patients who had existing macular degeneration. More research is needed to refute or confirm this finding.

Click the icon to see an image of macular degeneration.

Phacoemulsification does have some specific complications, although they are rare, particularly with experienced eye surgeons. They include:

Rupture of the lens capsule.
Loss of the lens nucleus into the eye fluid. (This will require removal by a specialist and may result in poorer vision.)
Flying fragments of the lens can damage the cornea or threaten the retina.
Pre- and postoperative changes in blood pressure, which are generally not a problem, should be observed carefully, since in some cases the changes may be extreme.

In about 30% of cases patients develop secondary cataracts within 1 - 5 years after either procedure, which require different treatment choices.

Preventing Infection and Reducing Swelling. The ophthalmologist may prescribe the following medications:

A topical antibiotic (neomycin or, more effectively, gentamicin). This drug protects against infection.
Corticosteroid eyedrops or ointments are often used to reduce swelling. Corticosteroids (commonly called steroids) are potent anti-inflammatory drugs. However, they also pose a risk for pressure in the eye and infection. One study reported less visual sharpness with the use of steroids compared to antibiotics. Some newer steroids such as rimexolone, loteprednol, and fluorometholone may pose a lower risk for abnormal pressure.
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as diclofenac, ketorolac, naproxen, and voltaren, also reduce swelling and do not pose the same risks as steroids. Newer NSAIDS that have been approved to treat pain and swelling after cataract surgery include bromfenac (Xibrom) and nepafenac (Nevanac).

In one study, applying an ice pack for 2 hours immediately after phacoemulsification improved comfort level and reduced inflammation, even days after the operation. This simple procedure has no adverse effects and patients should discuss it with their surgeons before the operation.

Factors That Increase Risk for Complications. The risks of complications are greater for the following people:

Patients who have other eye diseases.
People with diabetes. Intracapsular and extracapsular cataract extraction are known to pose a high risk for the development or worsening of retinopathy, a known eye complication of diabetes. Experts have hoped that phacoemulsification would pose a lower risk, but a 2001 study reported a high percentage of retinopathy progression after this procedure. The amount of experience a surgeon has plays a role in whether or not a patient has this complication.
People who have taken tamsulosin (Flomax) or other alpha-1 blocker drugs. Tamsulosin is a muscle relaxant prescribed for treatment of several urinary conditions including benign prostatic hyperplasia (BPH). In 2005, a leading ophthalmologic association and the FDA warned that tamsulosin may cause intraoperative floppy iris syndrome (IFIS), a loss of muscle tone in the iris that can cause complications during eye surgery. Problems have been reported both for patients who were taking the drug during surgery as well as those who had stopped taking the drug weeks or months before surgery. Men who have taken tamsulosin or similar drugs should inform their eye surgeon. The surgeon may need to use different techniques to minimize the risk of IFIS. A 2006 study indicated that patients can have safe and successful surgeries with these modified techniques.

Returning Home and Follow-up Visits.

Patients usually leave the surgical site within an hour of surgery. Cataract surgery almost never requires an overnight hospital stay.
They need to have someone drive them home and stay with them for a few days until their vision is acclimated.
The patient is usually examined the day after surgery and then during the following month. Additional visits are made as required.
Vision usually remains blurred for a while but gradually clears, usually over a 2 - 6 week period. (It can take longer.)
When the doctor decides the condition has stabilized, the patient will receive a final prescription for glasses or contacts.

Protecting the Eye. Postoperative protection of the eye typically involves:

The ophthalmologist usually tapes a bandage over the eye to protect it during the healing process.
When changing the bandage, the eye can be cleaned gently using a washcloth dipped in warm water without soap. A new bandage can then be positioned and taped.
It is very important not to press or rub the eye during this procedure.
An eye shield may be placed over the bandage at night.

Avoiding Glaucoma. Cataract surgery can cause glaucoma, a condition in which the pressure of fluids inside the eye rises dangerously. It is very important to minimize any activity that increases internal eye pressure. Postoperative cataract patients take the following precautions:

Minimize vigorous exercise.
Put on shoes while sitting and without lifting up the feet.
Kneel instead of bending over to pick something up.
Avoid lifting.
Limit reading since it requires eye movement (watching television is all right).
Sleep on the back or on the unoperated side.

Cataracts and Glaucoma. For patients with both glaucoma and cataracts, experts recommend:

In patients with cataracts and poorly controlled glaucoma, a two-step procedure for both eye conditions is needed. The patient first receives a trabeculectomy for glaucoma, followed by cataract surgery. Fluid leakage and the presence of blood in the back chamber of the eye are potential complications of this combined procedure. Phacoemulsification has improved success rates and reduced high complication rates of the double procedure compared with extracapsular cataract extraction. New advances that replace trabeculectomy with nonpenetrating glaucoma surgery may prove to be beneficial.
In patients who have cataracts plus either closed-angle glaucoma or open angle glaucoma that is stabilized with medication, the cataract may be able to be extracted and medication continued for the glaucoma.
A major 2002 analysis suggested that the combined approach generally offers better control over eye pressure for patients with both cataracts and glaucoma. The best surgical procedure, however, is still uncertain.

Cataracts and Corneal Disease. Patients who have both cataracts and corneal disease may undergo one of the following:

Combination Procedure. A single operation that combines three procedures. The combined procedure has been used since the late 1970s and employs extracapsular cataract extraction and intraocular lens insertion with corneal transplantation (called penetrating keratoplasty).
Sequential Procedure. An operation that uses two procedures sequentially. The sequential option performs the cataract procedures and the corneal transplantation separately.

Recovery of vision is usually much more rapid after the combined procedure than after the sequential procedures. Performing the procedures sequentially may also carry a higher rejection rate of the implant, although a 2003 study found no differences in failure rates between the two approaches after a year.

In any case, many experts recommend that for most patients the sequential procedures may be the better option because it appears to have fewer of the following complications than with the combined procedure:

Posterior capsule rupture
Eye fluid loss
Postoperative refractive errors, which result in abnormal distribution of light patterns

The rate of these errors still depends on the skill of the surgeon and the power of the implanted lens no matter what approach is used.

About 30% of patients who undergo extracapsular cataract surgery develop a secondary "after-cataract" called posterior capsular opacification. Posterior capsular opacification generally occurs because of the following events:

After surgery, there are still some natural lens cells left behind that proliferate on the back of the capsule.
The capsule gradually becomes cloudy and interferes with clear vision the same way the original cataract did.

According to a 2001 study, the probability of developing a secondary cataract was 6% at 1 year, 15% at 2 years, 23% at 3 years, and 38% at 9 years. The risk is lower with phacoemulsification. Secondary cataracts are more likely to occur in younger patients, in those with diabetes, or when cataract surgery is combined with vitrectomy (clearance of debris from the fluid in the eye).

Preventing Posterior Capsular Opacification. Studies suggest that acrylic lenses pose the lowest risk for posterior capsular opacification. A number of substances to prevent posterior capsular opacification are under investigation, including tranilast eyedrops, new lens materials, special capsular rings inserted during phacoemulsification, and new coatings on the implanted lens.

Treatment Decisions for Cataracts in the Second Eye. If a person has a cataract in a second eye, the issues for decision making are the same as for the first eye. The time of the procedure in the case of two cataracts is unclear. Doctors have long recommended that surgery on the second eye should be postponed until the first eye has healed and the results known (about a year).

One study has called this recommendation into question. It was conducted in England, where for budgetary reasons, there are long waits for second-eye cataract surgeries. In the study, patients who waited 7 - 12 months for the second-eye surgery reported significant difficulty in reading and performing ordinary tasks during the waiting period. Only 1% of patients who had the second surgery within 6 weeks reported having trouble seeing. In addition, 70% of those who waited experienced problems in depth perception, which can cause difficulty in walking and driving; only 12% who didn't wait reported this problem. Patients with double cataracts should discuss all options with their surgeon.

Treatment for Posterior Capsular Opacification. The standard treatment is laser surgery known as a YAG capsulotomy. (Capsulotomy means cutting into the capsule, and YAG is an abbreviation of yttrium aluminum garnet, the laser most often used for this procedure.)

This is an outpatient procedure and involves no incision.
Using the laser beam, the ophthalmologist makes an opening in the clouded capsule to let light through.
After the procedure the patient should remain in the doctor's office for an hour to be sure that pressure in the eye is not elevated.
An eye examination for any complications should follow within 2 weeks.

Complications. Laser surgery has become so commonplace that some ophthalmologists use it after cataract surgery to prevent later clouding. However, laser surgery carries its own risks and possible complications, similar to those of cataract surgery itself, and can also lead to poorer vision or blindness. About 1% of laser surgery patients develop a detached retina, which is much higher than the risk from the original cataract surgery.

Click the icon to see an image of a detached retina.

In some people, particularly those with glaucoma or who are severely nearsighted, the pressure in the eye may spike after laser surgery. Certain drugs used for treating glaucoma, such as dorzolamide (Trusopt) or apraclonidine (Iopidine), may helpful for preventing this occurrence. It is strongly recommended, however, that this surgery not be performed to prevent a secondary cataract, but only if the lens capsule clouds up again.

Infants. Treatment of infants first depends on whether one or both eyes are affected:

For infants born with cataracts in one eye, the American Academy of Ophthalmology recommends surgery as soon as possible, by 4 months or ideally even earlier. The procedure is followed by contact lens correction and patching of the unaffected eye. Although this approach is successful in many cases, some children still become blind in the affected eye. There is also a high risk for glaucoma after surgery.
In infants with cataracts in both eyes, surgery is not always an option. In some cases, it may be performed sequentially, with the second eye operated on a few days after the first. Phacoemulsification appears to pose a much higher risk for secondary cataracts than standard lens removal.

Toddlers and Older Children. Intraocular lens replacement is now becoming standard treatment for children 2 years and older.

Resources

www.ascrs.org -- The American Society of Cataract and Refractive Surgery
www.aao.org -- American Academy of Ophthalmology
www.nei.nih.gov -- National Eye Institute
www.eyesurgeryeducation.com -- Eye Surgery Education Council
www.lighthouse.org -- Lighthouse International
www.aao.org/aao/find_eyemd.cfm -- Find an ophthalmologist

References

Eke T, Thompson JR. Serious complications of local anaesthesia for cataract surgery: a one-year national survey in the United Kingdom. Br J Ophthalmol. 2006 Nov 23; [Epub ahead of print]

Hutz WW, Eckhardt HB, Rohrig B, Grolmus R. Reading ability with 3 multifocal intraocular lens models. J Cataract Refract Surg. 2006 Dec;32(12):2015-21.

Klein BE, Klein R, Lee KE, Grady LM. Statin use and incident nuclear cataract. JAMA. 2006 Jun 21;295(23):2752-8.

Rein DB, Zhang P, Wirth KE, Lee PP, Hoerger TJ, McCall N, et al. The economic burden of major adult visual disorders in the United States. Arch Ophthalmol. 2006 Dec;124(12):1754-60.

Wishart MS, Dagres E. Seven-year follow-up of combined cataract extraction and viscocanalostomy. J Cataract Refract Surg. 2006 Dec;32(12):2043-9.

Review Date:
3/1/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital

A.D.A.M. Copyright

adam.com

Rheumatoid arthritis

FitSugar — Wed, 08 Oct 2008 17:35:00 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Symptoms
Complications
Diagnosis
Treatment
Medications
Surgery
Lifestyle Changes
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Treatment Approaches

Patients with rheumatoid arthritis who do not respond to single-drug therapy often do better when a combination of drugs is used, indicates a review of 23 clinical trials published in 2007 in the Annals of Internal Medicine. However, the researchers were unable to determine which combinations of drugs work best or which individual drugs are more effective than others.
Combination drug treatment is now becoming a standard approach to treating rheumatoid arthritis while it is still in its early stages. Another 2007 Annals of Internal Medicine study indicated that initial combination therapies slow progression of joint damage more rapidly than single-drug therapy but, after several years, all treatment strategies produce benefits.

Fish Oil for Joint Pain

The omega-3 fatty acids found in fish oil may have anti-inflammatory properties that can help relieve joint pain, indicates a 2007 review in Pain. The researchers found that taking omega-3 fatty acids for 3 - 4 months helped reduce joint pain intensity, minutes of morning stiffness, the number of painful or tender joints, and consumption of non-steroidal anti-inflammatory drugs (NSAIDs). Salmon, mackerel, and herring are types of fish that are particularly high in these fatty acids. Fish oil can also be taken through dietary supplements, but these can interact with some types of prescription medications and may not be safe or appropriate for all patients. (Check with your doctor before taking these or any other supplements.)

Introduction

Rheumatoid arthritis (RA) is a chronic disease in which various joints in the body are inflamed, leading to swelling, pain, stiffness, and the possible loss of function.

Rheumatoid arthritis is an autoimmune disease in which the body's immune system attacks itself. The pattern of joints affected is usually symmetrical, involves the hands and other joints, and is worse in the morning. Rheumatoid arthritis is a systemic (body-wide) disease, involving other body organs, whereas osteoarthritis is limited to the joints. Both forms of arthritis can be crippling.

The process probably develops in the following way:

The disease process leading to rheumatoid arthritis begins in the synovium, the membrane that surrounds a joint and creates a protective sac.
This sac is filled with lubricating liquid called the synovial fluid. In addition to cushioning joints, this fluid supplies nutrients and oxygen to cartilage, a slippery tissue that coats the ends of bones.
Cartilage is composed primarily of collagen, the structural protein in the body, which forms a mesh to give support and flexibility to joints.
In rheumatoid arthritis, an abnormal immune system produces destructive molecules that cause continuous inflammation of the synovium. Collagen is gradually destroyed, narrowing the joint space and eventually damaging bone.
If the disease develops into a form called progressive rheumatoid arthritis, destruction to the cartilage accelerates. Fluid and immune system cells accumulate in the synovium to produce a pannus, a growth composed of thickened synovial tissue.
The pannus produces more enzymes that destroy nearby cartilage, aggravating the area and attracting more inflammatory white cells, thereby perpetuating the process.

This inflammatory process not only affects cartilage and bones but can also harm organs in other parts of the body.

Click the icon to see an image of rheumatoid arthritis.

Causes

Although much has been learned about the process leading to rheumatoid arthritis, researchers have yet to uncover all the factors that lead to this devastating disease. One prevalent theory is that a combination of factors triggers rheumatoid arthritis, including an abnormal autoimmune response, genetic susceptibility, and some environmental or biologic trigger, such as a viral infection or hormonal changes.

The Normal Immune System Response. The inflammatory process is a byproduct of the activity of the body's immune system, which fights infection and heals wounds and injuries:

When an injury or an infection occurs, white blood cells are mobilized to rid the body of any foreign proteins, such as a virus.
The masses of blood cells that gather at the injured or infected site produce factors to repair wounds, clot the blood, and fight any infections.
In the process the surrounding area becomes inflamed and some healthy tissue is injured. The immune system is then called upon to repair wounds by clotting off any bleeding blood vessel and initiating fiber-like patches to the tissue.
Under normal conditions, the immune system has other special factors that control and limit this inflammatory process.

The Infection Fighters. Two important components of the immune system that play a role in the inflammation associated with rheumatoid arthritis are B cells and T cells, both of which belong to a family of immune cells called lymphocytes.

When macrophages recognize foreign particles entering the bloodstream, they are programmed to ingest them, split them into pieces, and bring specific sections of them (antigens) into contact with the surface of the T cell. These antigens are placed within specialized proteins on the surface of the T cell that signal to a T cell and begin a process of immune system inspection. This process involves the interaction of several proteins on B cells and T cells, which seem to signal back and forth.

If the T cell recognizes an antigen as "non-self," it will produce chemicals (cytokines) that cause B cells to multiply and release many immune proteins (antibodies). These antibodies circulate widely in the bloodstream, recognizing the foreign particles and triggering inflammation in order to rid the body of the invasion. T cells can be further categorized as killer T cells or helper T cells. Killer T cells directly attack antigens, such as viruses and tumor cells. Helper T cells recognize antigens that are presented to them by macrophages (or other specialized cells), and can stimulate B cells to mount various kinds of attacks on the antigen. They also produce chemicals (cytokines) that can have a more direct role in the inflammatory process.

For reasons that are still not completely understood, both the T cells and the B cells become overactive in patients with RA. In an immune response it is normal for the antibody response to change over time, particularly if the first antibodies that are made do not eliminate the invading particles. Little by little, the types of antibodies being made undergo changes in an attempt to achieve better recognition and a stronger inflammatory response against a recalcitrant invader. In RA, a complex interaction between activated immune cells and an impaired antigen-elimination process leads to a greater than normal repertoire of what the antibodies recognize. Eventually, antibodies are made that recognize more of the body's own tissues in a stronger or more persistent manner than is healthy, and inflammatory responses are mounted in these tissues.

An antigen is a substance that can provoke an immune response. Typically antigens are substances not usually found in the body.

Cytokines. Cytokines are very important in the destructive process of rheumatoid arthritis, particularly those known as interleukins (ILs) -- notably IL1 and IL6 -- and tumor necrosis factor (TNF). TNF is now known to be the major cause of joint damage and various systemic manifestations of RA, including weight loss.

Leukocytes. The leukocytes, the other major white blood cells in the body, are also spurred into action by the over-zealous T cells. Leukocytes stimulate the production of key players in the inflammatory process, including leukotrienes, prostaglandins, and nitric oxide.

The Hypothalamic-Pituitary-Adrenal Axis and Stress Hormones. Some research suggests that abnormalities in the hypothalamic-pituitary-adrenal axis (HPA axis) may contribute to RA. The HPA system includes two parts of the brain (the hypothalamus and the pituitary) and the adrenal gland.

Click the icon to see an image of the adrenal glands.

The HPA axis regulates a person's response to stress, which includes the release of cortisol (an important stress hormones) and DHEA (a weak male hormone). The cytokines interleukin-6 and TNF-alpha normally stimulate a surge in these hormones, which then block further release of the cytokines. Research suggests, however, that in RA, a defective HPA axis responds to the cytokines with a lower-than-normal release of cortisol and DHEA. Without a strong stress response, the cytokine levels remain high and become destructive, causing inflammation.

Genetic factors play some role in RA, but are clearly not the only important factor. The presence of certain genetic mutations, however, may worsen the disease process. It should be pointed out that defective genes not only can be inherited but they may be changed and mutated by environmental or other factors. More research is needed to determine the specific genetic contributions to this disease.

HLA. HLA (human leukocyte antigen) is a genetically regulated molecule that traps part of antigens and presents them on the surface of cells for destruction by antibodies and T cells. It is designed to recognize self- from non-self cells. A number of HLA genetic forms called HLA-DRB1 alleles are referred to as the RA-shared epitope because of their association with rheumatoid arthritis. These genetic factors do not cause RA, but they may make the disease more severe once it has developed. Genetic variations in the HLA region may also predict drug treatment response to etanercept and the disease-modifying anti-rheumatic drug methotrexate.

Lack of Corticotropin-Releasing Hormone. Some people with RA may have a genetic deficiency of a hormone known as corticotropin-releasing hormone (CRH), which produces corticosteroids, hormones that suppress the inflammatory process.

Infections. Although many bacteria and viruses have been studied, no single organism has been proven to be the primary trigger for the autoimmune response and subsequent damaging inflammation. Higher than average levels of antibodies that react with the common intestinal bacteria E. coli have appeared in the synovial fluid of people with RA. Some experts think they may stimulate the immune system to prolong RA once the disease has been triggered by some other initial infection. Other potential triggers include Mycoplasma, parvovirus B19, retroviruses, mycobacteria, and Epstein-Barr virus.

Chemicals. A number of chemicals are being investigated as triggers of rheumatoid arthritis, but it is very difficult to determine causal effects of any specific trigger.

Risk Factors

Rheumatoid arthritis (RA) is an ancient disease. The condition has been identified in skeletons thousands of years old. According to the Arthritis Foundation, RA affects an estimated 2.1 million Americans.

Although the disease can occur at any age from childhood to old age, it usually starts in young adulthood, with onset peaking between the ages of 20 - 45. Still, about 50,000 children may be afflicted with juvenile rheumatoid arthritis.

Women are more likely to have RA than men. (The risk for women is slightly lower if they have been pregnant.) Women are also at higher risk for the severe type 2 rheumatoid arthritis.

Some people may inherit genes that make them susceptible to RA, but a family history of RA does not appear to increase an individual's risk.

Other factors may place certain susceptible individuals at higher risk for developing RA:

Heavy long-term smoking is a very strong risk factor for RA, particularly in patients without a family history of the disease.
Women who have a shorter fertility time (and so lower levels of reproductive hormones) may be at higher risk.
History of blood transfusions.

Most studies have not found any association between silicone breast implants and rheumatoid arthritis or other autoimmune disease (except possibly Sjögren syndrome).

Reports from a Dutch study suggest that hay fever sufferers have a reduced risk of developing rheumatoid arthritis, and, conversely, arthritis patients are less likely to have hay fever.

Symptoms

The hallmark symptom of rheumatoid arthritis is morning stiffness that lasts for at least an hour. (Stiffness from osteoarthritis, for instance, usually clears up within half an hour.) Even after remaining motionless for a few moments, the body can stiffen. Movement becomes easier again after loosening up.

Swelling and pain in the joints must occur for at least 6 weeks before a diagnosis of rheumatoid arthritis is considered. The inflamed joints are usually swollen and often feel warm and "boggy" when touched. The pain often occurs symmetrically but may be more severe on one side of the body, depending on which hand the person uses more often.

Although rheumatoid arthritis almost always develops in the wrists and knuckles, the knees and joints of the ball of the foot are often affected as well. Indeed, many joints may be involved, including those in the cervical spine, shoulders, elbows, tips, temporomandibular joint (jaw), and even joints between very small bones in the inner ear. Rheumatoid arthritis does not usually show up in the fingertips, where osteoarthritis is common, but joints at the base of the fingers are often painful.

In about 20% of people with RA, inflammation of small blood vessels can cause nodules, or lumps, under the skin. They are about the size of a pea or slightly larger, and are often located near the elbow, although they can show up anywhere. Nodules can occur throughout the course of the disease. Rarely, nodules may become sore and infected, particularly if they are in locations where stress occurs, such as the ankles. On rare occasions, nodules can reflect the presence of rheumatoid vasculitis, a condition that can affect blood vessels in the lungs, kidneys, or other organs.

Fluid may accumulate, particularly in the ankles. In rare cases, the joint sac behind the knee accumulates fluid and forms what is known as a Baker cyst. This cyst feels like a tumor and sometimes extends down the back of the calf causing pain.

Symptoms such as fatigue, weight loss, and fever may accompany early rheumatoid arthritis. Some people describe them as being similar to those of a cold or flu except, of course, RA symptoms can last for years.

In children, juvenile rheumatoid arthritis, also known as Still's disease, is usually preceded by high fever and shaking chills along with pain and swelling in many joints. A pink skin rash may be present.

Complications

Rheumatoid arthritis is not fatal, but complications of the disease may shorten survival by a few years in some individuals. Although type 2 rheumatoid arthritis is progressive and there is no cure, over time the disease becomes less aggressive, and symptoms may even improve.

Treatments for RA are increasingly effective in slowing this debilitating disease, and some may even prevent initial destruction by aggressively reducing inflammation. If bone and ligament destruction and any deformities have occurred, however, the effects are permanent. It is essential, therefore, to seek a doctor's help as soon as symptoms develop. Side effects of the treatments often contribute to the severity of the disease.

Affected joints can become deformed, and the performance of even ordinary tasks may be very difficult or impossible. According to one survey, 70% of patients with rheumatoid arthritis feel the disease prevents them from living a fully productive life. A 2000 study found that about one-third of people with RA stop working within 5 years of onset of the disease.

Rheumatoid arthritis can affect other parts of the body as well as the joints. Some patients with severe disease may then be at higher risk for complications, such as the following:

Peripheral Neuropathy. This condition affects the nerves, most often those in the hands and feet. It can result in tingling, numbness, or burning.
Muscle problems. Many patients have weakness of the muscles.
Anemia. People with RA may develop anemia, which involves a decrease in the production of red blood cells.
Scleritis and Episcleritis. This is an inflammation of the blood vessels in the eye that can result in corneal damage. Symptoms include redness of the eye and a gritty sensation.
Infections. Patients with RA have a higher risk for infections, particularly from some of the immune-suppressing drugs (corticosteroids, anti-tumor necrosis factors, disease modifying drugs) that they take.
Skin Problems. Skin problems are common, particularly on the fingers and under the nails. Some patients develop severe skin complications that include rash, ulcers, blisters (which may bleed in some cases), lumps under the skin, and other problems. Severe skin disease can reflects a more serious case of RA in general.
Osteoporosis. Osteoporosis, a disorder in which bone density decreases, is more common than average in postmenopausal women with RA. The hipbone is particularly affected. The risk for osteoporosis also appears to be higher than average in men with RA who are over 60 years old.
Lung Disease. Patients with RA are susceptible to chronic lung diseases, including interstitial fibrosis, pulmonary hypertension, and other problems. Both rheumatoid arthritis itself and some treatments may cause this damage.
Kidney. Although rheumatoid arthritis only rarely involves the kidney, many of the drugs used to treat it can damage kidneys.
Vasculitis. Vasculitis involves autoimmune inflammatory abnormalities in very small vessels and can affect many organs in the body. Manifestations of vasculitis include mouth ulcers, nerve disorders, rapid worsening of the lungs, inflammation of coronary arteries, and inflammation of the arteries supplying blood to the intestines.
Heart Disease. Inflammation of the heart muscle itself in the sac around the heart can cause many problems. Mounting evidence suggests that RA can increase the risk for heart disease, possibly because of the inflammatory response in RA, which may also injure arteries and heart muscle tissue. Some studies have reported that people with RA are 30 - 50% more likely to suffer heart vessel blockages and 60 - 70% more likely to die as result than people without RA.
Lymphoma and Other Cancers. Research suggests that patients with RA are four times more likely than healthy patients to develop non-Hodgkin’s lymphoma. There has also been concern that some RA treatments may increase the risk for lymphoma. Studies from 2006 indicate that RA’s chronic inflammatory process may play a role in the development of lymphoma. Researchers found that patients with very severe and long-term RA had a substantially increased risk of developing lymphoma. Other 2006 research suggests that RA drugs, such as biologic response modifiers, do not increase lymphoma risk, although they do increase skin cancer risk.
Periodontal Disease. People with RA may be twice as likely as non-arthritic individuals to have periodontal disease. Chronic inflammation and immune dysfunction are central to both diseases.
Pregnancy. Women with RA have an increased risk for premature delivery. They are also three times more likely than healthy women to develop hypertension during the last trimester of pregnancy.

Juvenile rheumatoid arthritis often resolves before adulthood. Patients who experience arthritis in only a few joints do better than those with more widespread (systemic) disease, which is very difficult to treat. Although it can be very serious, very few people die from this condition.

MAS. Macrophage activation syndrome (MAS) is a life-threatening complication of this disorder and requires immediate treatment with high-dose steroids and cyclosporin A. Parents should be aware of symptoms, which include persistent fever, weakness, drowsiness, and lethargy.

Diagnosis

Rheumatoid arthritis can be difficult to diagnose. Many other conditions resemble it and its symptoms can develop insidiously. Blood tests and x-rays may show normal results for months after the onset of joint pain. Even after rheumatoid arthritis has been diagnosed, it is extremely important to determine whether the course of the disease is benign (type 1) or aggressive (type 2) in order to treat the problem appropriately.

Specific findings or presentation more likely to suggest the diagnosis of rheumatoid arthritis include morning stiffness, involvement of three joints at the same time, involvement of both sides of the body, subcutaneous nodules, positive rheumatoid factor, changes in x-rays.

Various blood tests may be used to help diagnose RA, determine its severity, and detect complications of the disease.

Rheumatoid Factor. In RA, antibodies that collect in the synovium of the joint are known as rheumatoid factor. In about 80% of cases of RA, blood tests reveal rheumatoid factor. It can also show up in blood tests of people with other diseases. However, when it appears in patients with arthritic pain on both sides of the body, it is a strong indicator of type 2 RA. The presence of rheumatoid factor plus evidence of bone damage on x-rays also suggests a significant chance for progressive joint damage.

Erythrocyte Sedimentation Rate Test. An erythrocyte sedimentation rate (ESR or sed rate) measures how fast red blood cells (erythrocytes) fall to the bottom of a fine glass tube that is filled with the patient's blood. The higher the sed rate the greater the inflammation. In addition to rheumatoid arthritis, the sed rate can be high in many conditions ranging from infection to inflammation to tumors. The test is used, then, not for diagnosis, but to help determine how serious the condition is.

C-Reactive Protein. High levels of C-reactive protein (CRP) are also indicators of active inflammation. However, because obesity also increases CRP levels, the doctor should consider a patient’s body mass index when evaluating CRP levels during RA diagnosis.

Anti-CCP Antibody Test. The presence of antibodies to cyclic citrullinated peptides (CCP) can identify RA years before symptoms develop. In combination with the test for rheumatoid factor, the CCP antibody test is the best predictor of which patients will go on to develop severe RA. Used in Europe, the test is now beginning to be used somewhat more commonly in the U.S. U.S. laboratories have not yet developed consistent standards for interpreting the test, however.

Tests for Anemia. Anemia is a common complication. Blood tests are needed often to determine the amount of red blood cells (hemoglobin and hematocrit) and iron (soluble transferrin receptor and serum ferritin) in the blood.

Analyzing the synovial fluid might prove to be helpful in detecting markers of joint destruction, but this is not commonly performed. Some investigational examples include the following:

An enzyme called MMP-3 (matrix metalloproteinase 3) is involved with the degradation of cartilage. Its presence in synovial fluid is strongly associated with progressive joint destruction in patients with chronic RA.
High levels urocortin, a member of the peptide family involved in the stress response, may also be a major player in the RA inflammation.

X-Rays. X-rays generally have not been helpful to detect the presence of early rheumatoid arthritis because they cannot show images of soft tissue. The use of a technique known as dual energy x-ray absorptiometry, however, may be useful in detecting early bone loss in rheumatoid arthritis (2 - 27 months after onset). Evidence of damage on x-rays along with elevated rheumatoid factor is a significant predictor for progressive joint destruction.

Ultrasound. Special ultrasound techniques called power Doppler ultrasonography (PDUS) or quantitative ultrasound (QUS) may be helpful in RA. PDUS may be reliable for monitoring inflammatory activity in the joint. QUS, which is used for osteoporosis, can detect bone loss in fingers, which may prove to be a good indicator of early RA.

Magnetic Resonance Imaging. Specially designed magnetic resonance imaging (MRI) equipment called extremity MRI may be able detect bone erosions in the hands of RA patients where x-rays cannot. Further evaluation is necessary.

Symptoms of rheumatoid arthritis can be mimicked by things as benign as a bad mattress or as serious as cancer. A number of rare genetic diseases attack the joints. Physical injuries, infections, and poor circulation are among the many problems that can cause aches and pains. It would be impossible to discuss in this report the dozens of all conditions with symptoms of joint aches and pains.

Osteoarthritis. Osteoarthritis requires some special mention because it is the most common form of arthritis. It differs from RA in several important respects.

Osteoarthritis usually occurs in older people.
It is located in only one or a few joints. (In fact, osteoarthritis is probably most often confused with rheumatoid arthritis if it affects multiple joints in the body.)
The joints are less inflamed.
Progression of pain is almost always gradual.

Gout. Gout also causes swelling and severe pain in a joint, although most commonly starting in one joint. It is particularly difficult to distinguish chronic gout in older people from rheumatoid arthritis, however, since gout in this population can occur in a number of joints. A proper diagnosis can be made with a detailed medical history, laboratory tests, and detection in the affected joint of a salt called monosodium urate (MSU), which identifies gout.


Disease	Specific Subtypes
Osteoarthritis
Infectious Arthritis	Lyme disease, septic arthritis, bacterial endocarditis, mycobacterial and fungal arthritis, viral arthritis
Postinfectious or Reactive Arthritis	Reiter syndrome (a disorder characterized by arthritis and inflammation in the eye and urinary tract), rheumatic fever, inflammatory bowel disease
Crystal Induced Arthritis	Gout and pseudogout
Other Rheumatic Autoimmune Diseases	Systemic vasculitis, systemic lupus erythematosus, scleroderma, Still's Disease (also called juvenile rheumatoid arthritis), Behcet's disease
Other Diseases	Chronic fatigue syndrome, hepatitis C, familial Mediterranean fever, cancers, AIDS, leukemia, bunions, Whipple's disease, dermatomyositis, Henoch-Schonlein purpura, Kawasaki's disease, erythema nodosum, erythema multiforme, pyoderma gangrenosum, pustular psoriasis

Treatment

The treatment of rheumatoid arthritis involves medications and lifestyle changes.

Many drugs are used for managing the pain and slowing the progression of rheumatoid arthritis, but none completely cure the disease. Some experts believe that no single drug will ever cure rheumatoid arthritis because of the many factors that affect the disease at various times. The goals of drug treatment for rheumatoid arthritis include:

Reduce inflammation
Prevent damage to the bones and ligaments of the joint
Preserve movement
To be as inexpensive and as free from side effects as possible over the long-term

The drug categories used for RA include:

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) are the least potent drugs used for RA. These drugs relieve pain by reducing inflammation, but do not affect the course of the disease.
Disease-Modifying Anti-Rheumatic Drugs (DMARDs) are the main drugs used for treating rheumatoid arthritis. They slow the progression of the disease. They are much more effective than NSAIDs but also have more side effects. Methotrexate (Rheumatrex, Trexall) is the most widely used of these drugs.
Biologic Response Modifiers (also known as Biologic DMARDs) are often prescribed to patients who have failed to respond to DMARDs. They may be used alone or in combination with DMARDs such as methotrexate. They modify or block destructive immune factors such as tumor-necrosis factor (TNF). Current anti-TNF drugs include infliximab (Remicade), etanercept (Enbrel), and adalimumab (Humira). Other biologic response modifiers include the interleukin-1 antagonist anakinra (Kineret), the T cell co-stimulation modulator abatacept (Orencia), and rituximab (Rituxan), which targets CD20-positive B cells.
Corticosteroids, or steroids, are powerful anti-inflammatory drugs that are used to quickly reduce inflammation. These drugs include prednisone and prednisolone.

The question of how early and how aggressively to treat RA has been the subject of great debate. Among patients with RA, some will go into remission and remain in remission for the length of their lives even in the absence of treatment, while others will go on to develop active, sometimes severe RA.

Current practice has moved towards treating the disease aggressively while it is in its early stages to help prevent it from reaching a more severe and chronic state. Studies have found less joint damage in patients with early, aggressive treatment, particularly with the use of DMARDs and TNF modifiers in combination with methotrexate. Intensive early dosing of methotrexate may help slow progression of rheumatoid arthritis. Early combination therapy with DMARDs and corticosteroids is also showing good results.

During the first year of treatment, combination therapy appears to reduce the progression of joint deterioration more rapidly and effectively than single drug treatment. In addition, patients who have not been helped by one drug often benefit from a combination of drugs. However, over a longer period of time, it is not clear whether a drug combination approach offers many advantages over single drugs. It is also not certain which combination of drugs works best. Depending on your particular health condition, and how you respond to the drugs prescribed, your doctor may try various treatment strategies.

Medications

Two-thirds of people with RA rank pain as their primary reason for seeking professional help. The most common pain relievers for RA are nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs block prostaglandins, the substances that dilate blood vessels and cause inflammation and pain. There are dozens of NSAIDs:

Over-the-counter NSAIDs include aspirin, ibuprofen (Motrin IB, Advil, Nuprin, Rufen), naproxen (Aleve), ketoprofen (Actron, Orudis KT).
Prescription NSAIDs include ibuprofen (Motrin), naproxen (Naprosyn, Anaprox), flurbiprofen (Ansaid), diclofenac (Voltaren), tolmetin (Tolectin), ketoprofen (Orudis, Oruvail), dexibuprofen (Seractil). In 2004, a new NSAID, meloxicam (Mobic) was approved in the U.S. for the management and treatment of rheumatoid arthritis.

Studies suggest that the best times for taking an NSAID may be after the evening meal and then again on awakening. RA symptoms increase gradually during the night, reaching their greatest severity at the time of awakening. Taking NSAIDs with food can reduce stomach discomfort, although it may slow down the pain-relieving effect.

In April 2005, the Food and Drug Administration (FDA) asked drug manufacturers of prescription NSAIDs to include with their products the same warning label used for the COX-2 inhibitor celecoxib (Celebrex). This "black box" warning, the FDA's strongest warning, emphasizes the increased risks for cardiovascular events and gastrointestinal bleeding associated with these drugs’ use. The FDA also requested manufacturers of OTC NSAIDs to revise their labels to include more specific language concerning potential cardiovascular and gastrointestinal risks. Due to its proven heart benefits, aspirin was excluded from these labeling revisions. In December 2006, the FDA proposed even stronger labeling changes to highlight these drugs’ risk for liver damage as well as alcohol and drug interactions.

Long-term, regular use of NSAIDs can increase the risk for heart attack, especially for people who have a heart condition. Long-term use of NSAIDs is also the second most common cause of ulcers and gastrointestinal bleeding. To reduce the risks associated with NSAIDs, take the lowest dose possible for pain relief.

Other possible side effects of NSAIDs may include:

Upset stomach
Dyspepsia (burning, bloated feeling in pit of stomach)
Drowsiness
Skin bruising
High blood pressure
Fluid retention
Headache
Rash
Reduced kidney function

Long-term use of NSAIDs is the second most common cause of ulcers. Ulcers caused by NSAIDs are more likely to bleed than those caused by the bacteria Helicobacter pylori.

NSAID-related bleeding and stomach problems may be responsible for 107,000 hospital admissions and 16,500 deaths each year. Those at high risk for bleeding include people over age 60, anyone with a history of ulcers of gastrointestinal bleeding, patients with serious heart conditions, people who abuse alcohol, and those who take medications such as anticoagulants (blood thinners) and corticosteroids.

Proton-pump inhibitor (PPI) drugs may help prevent and heal ulcers caused by NSAIDs. PPIs include omeprazole (Prilosec), esomeprazole (Nexium), and lansoprazole (Prevacid).

COX-2 Inhibitors (Coxibs). Coxibs inhibit an inflammation-promoting enzyme called COX-2. This drug class was initially thought to provide benefits equal to NSAIDs but cause less gastrointestinal distress. However, following numerous reports of heart problems, skin rashes, and other adverse effects, the FDA re-evaluated the risks and benefits of this drug class. This lead to the removal of rofecoxib (Vioxx) and valdecoxib (Bextra) from the United States market. Celecoxib (Celebrex) is still available, but patients should ask their doctor whether the drug is appropriate and safe for them. In December 2006, the FDA approved celecoxib for the relief of symptoms of juvenile rheumatoid arthritis in patients ages 2 years and older.

Disease-modifying anti-rheumatic drugs (DMARDs) are the standard treatments for RA. They are used either alone or in combination with newer biologic DMARDs.

DMARDs do not have any common properties other than their ability to slow down the progression of rheumatoid arthritis. Many were used for other diseases and were found accidentally to help RA. DMARDs include:

Methotrexate (considered to be the current standard of care)
Leflunomide
Hydroxychloroquine
Sulfasalazine
Gold
Minocycline
Azathioprine
Cyclosporine

Unfortunately, all DMARDs tend to lose effectiveness over time, even methotrexate. Patients rarely use one drug for more than 2 years. Combining DMARDs with each other or with drugs in other categories offers the best approach for many patients. The addition of a corticosteroid to any combination may also be helpful.

All DMARDs may produce stomach and intestinal side effects, and, over the long-term, each poses some risk for rare but serious reactions. (In some cases, however, they may be less harmful than long-term NSAID treatment.)

Methotrexate. Methotrexate (Rheumatrex, Trexall) acts as an anti-inflammatory drug and is now the most frequently used DMARD, particularly for severe disease. It has a faster mode of action than other DMARDs, (it starts working within 3 - 6 weeks), and its effectiveness as a well proven in studies.

Even this drug loses effectiveness, however, when used alone. It may be more effective when used in combination with other DMARDs or other drugs. Recent studies have focused on combining methotrexate with various biological response modifier drugs, especially for treatment of patients with early aggressive arthritis. The combination appears to work better than single drug therapy.

About 20% of patients withdraw from methotrexate because of its side effects. They include nausea and vomiting, rash, mild hair loss, headache, mouth sores, and muscle aches. Methotrexate reduces levels of folic acid (folate) in the body, which can lead to some of these side effects. Doctors may prescribe folic acid supplements to prevent side effects. However, some research suggests that folic acid may interfere with methotrexate’s effectiveness.

Methotrexate is usually given as pills. Patients who need higher doses can take it as an injection. Methotrexate has fewer serious toxic effects than many DMARDs. Although these severe reactions are rare, they may include:

Kidney and liver damage. People at particular risk for liver damage from methotrexate include those with diabetes, obesity, and alcoholism.
Increased risk for infections
Lung disease occurs in up to 5% of people. People who have poor lung function are most at risk.
The drug increases the risk for birth defects and should not be taken by pregnant women. However, methotrexate will not harm a woman’s chance for future healthy pregnancy.

Leflunomide. Leflunomide (Arava) blocks autoimmune antibodies and reduces inflammation. It also may inhibit metalloproteinases (MMP), which are involved in cartilage destruction. It has the following benefits:

It slows disease progression as early as 6 months into treatment.
Comparison studies with methotrexate report a better quality of life with leflunomide, including more energy, greater vitality, and fewer emotional side effects. (Studies comparing their risk for serious adverse effects are mixed. One, for example, showed fewer problems with leflunomide, while another reported identical rates.)

The combination of methotrexate and leflunomide (which has different effects on the immune system) is very effective compared to either drug alone. (This combination poses a risk for liver toxicity and requires monitoring.)

Reports of adverse effects are comparable to those with methotrexate. Common problems include nausea, diarrhea, hair loss, and rash. Potentially serious side effects include infections and liver injury. Everyone taking leflunomide should be monitored regularly, including blood tests for liver function, and anyone with liver problems should not take this drug. Monitoring of serum concentrations of the most active metabolite of leflunomide may help predict treatment response.

Hydroxychloroquine. Hydroxychloroquine (Plaquenil) was originally used for preventing malaria and is now also used for mild, slowly progressive arthritis. It can help relieve pain and improve mobility. It has one of the least toxic profiles of the DMARDs. The downside is that this drug can take up to 6 months to achieve full benefit. It also does not appear to slow disease progression. One study concluded that joint erosion after 2 years was worse than with no DMARD at all.

As with all DMARDs, gastrointestinal complaints are fairly common. This drug used to be associated with eye and vision problems, but with current lower doses this side effect is rare. If vision problems occur, it is usually with people taking very high doses, those with kidney disease, or those over 60 years of age. Still, you should have regular eye exams while taking this drug and notify your doctor if you experience any sudden changes in vision.

Sulfasalazine. Sulfasalazine (Azulfidine) was developed in the 1930s for treating rheumatoid arthritis, but fell into disfavor when gold treatment emerged. It has regained popularity, however, and is now used for both adult and juvenile RA. It works best when the disease is confined to the joints. Symptom relief occurs within 1 - 3 months.

Side effects are common, particularly stomach and intestinal distress, which usually occur early in the course of treatment. (However, serious gastrointestinal side effects, such as stomach ulcers, occur less frequently with sulfasalazine than with NSAIDs.) A coated-tablet form may help reduce side effects. Other side effects include skin rash and headache. Sulfasalazine increases sensitivity to sunlight. Be sure to wear sunscreen (SPF 15 or higher) while taking this drug. People with intestinal or urinary obstructions or who have allergies to sulfa drugs or salicylates should not take sulfasalazine.

Gold. Gold has been a long-standing DMARD for rheumatoid arthritis, although its use has decreased with the development of disease modifying and biologic drugs. Gold is usually administered in an injected form because the oral form, auranofin (Ridaura), is much less effective. There are two injectable forms of gold: Gold sodium thiomalate (Myochrysine) and aurothioglucose (Solganal). It can take 3 - 6 months before injections have an effect on RA symptoms.

Gold injections cause mouth sores in about a third of patients. Skin side effects include itching and rash, which can be severe in some patients. . The most serious side effects of gold injections, while rare, are kidney damage and decreased white blood cell count. Gold injections are not usually given to pregnant women. It is not definite that gold causes birth defects but doctors generally recommend that women use birth control while receiving this drug.

Minocycline. Minocycline (Minocin) is a tetracycline antibiotic that is usually prescribed for patients with mild RA. It can take 2 - 3 months before symptoms begin to improve and up to a year for full benefit. Side effects include upset stomach, dizziness, and skin rash. Long-term use of minocycline can cause changes in skin color, but this side effect usually disappears once the medication is stopped. Minocycline can cause yeast infections in women. Minocycline increases sensitivity to sunlight and patients should be sure to wear sunscreen. In rare cases, minocycline can affect the kidneys and liver.

Azathioprine. Azathioprine (Imuran) suppresses immune system activity. It takes 6 - 8 weeks for early symptom improvement and up to 12 weeks for full benefit. Azathioprine can cause serious problems with the gastrointestinal tract. About 10 - 15% of patients experience nausea and vomiting, often accompanied by stomach pain and diarrhea. (Taking the medication twice daily, instead of once daily, or taking it after eating may help avoid this problem.) Azathioprine can also cause problems with liver function and pancreas gland inflammation, and can reduce white blood cell count.

Cyclosporine. Like azathioprine, cyclosporine (Sandimmune, Neoral) is an immunosuppressant. It is used for people with RA who have not responded to other drugs. It can take a week before symptoms improve and up to 3 months for full benefit. The most serious and common side effects of cyclosporine are high blood pressure and kidney function problems. While kidney function usually improves once the drug is stopped, mild-to-moderate high blood pressure may continue. Cyclosporine can also cause gout or worsen gout in people who have this condition.

Other common side effects include headache, nausea, vomiting, stomach pain and upset, and swelling of hands and feet. About 10% of patients who take cyclosporine develop tremors, increased hair growth, muscle cramps, and numbing or tingling in hands and feet (neuropathy). Swelling of the gums is also common. Patients should practice good dental hygiene, including regular brushing and flossing.

Biologic response modifiers are drugs made from living cells. These drugs target specific components of the immune system that contribute to the joint inflammation and damage that are part of the rheumatoid arthritis disease process.

Currently approved biologic response modifiers include:

Etanercept (Enbrel). Etanercept is an anti-tumor necrosis factor (anti-TNF) drug. Approved in 1998, etanercept was the first biologic response modifier drug for treatment of rheumatoid arthritis. It is also approved for juvenile RA and psoriatic arthritis.
Infliximab (Remicade). Approved in 1999, infliximab is also an anti-TNF drug. It is used in combination with methotrexate.
Adalimumab (Humira). Adalimumab is another anti-TNF drug. First approved in 2002 as a second-line treatment for RA, adalimumab received additional approvals in 2005 as a first-line treatment for RA and psoriatic arthritis. It is used alone or in combination with methotrexate or other DMARDs. It is also showing promising results in clinical trials for juvenile rheumatoid arthritis.
Anakinra (Kineret). Approved in 2001, anakinra targets interleukin-1 (IL-1), another type of immune factor.
Abatacept (Orencia). Approved in 2005 for adults with moderate-to-severe RA who have not responded to DMARD or anti-TNF drugs. Abatacept is known as a T cell co-stimulation modulator. It blocks T cell activation. It is used alone or in combination with other DMARDs aside from anti-TNF drugs.
Rituximab (Rituxan). Approved in 2006, rituximab targets CD20-positive B cells and blocks their activation. It is used in combination with methotrexate for patients with moderate-to-severe RA who have not responded to anti-TNF therapies.

Some of these drugs are used as first-line treatments for RA. Others are used for patients who have not responded to DMARDs or other types of treatment. Depending on the specific drug, they may be used alone or in combination with the DMARD methotrexate. However, biologic response modifiers are not used in combination with each other, as they can lead to serious infections.

As with other rheumatoid arthritis drugs, these drugs do not cure the disease but can help slow progression and joint damage. In recent clinical trials, some patients have achieved remission using methotrexate in combination with infliximab, adalimumab, or rituximab.

Side Effects and Complications. Etanercept, adalimumab, and anakinra are given by injection and may cause pain at the injection site. To prevent injection reactions, patients are sometimes pretreated with betamethasone, a corticosteroid drug, but some research suggests that the steroid does little good. Infliximab, abatacept and rituximab are given by intravenous infusion. Common infusion reactions include headache, nausea, and flu-like symptoms. Because biologic response modifiers affect the immune system, patients who take these drugs have an increased risk for infections.

Other risks associated with these drugs include:

Anti-TNF drugs (etanercept, infliximab, adalimumab) have been associated with sepsis, pneumonia, and tuberculosis; non-melanoma skin cancer, lymphoma, and other malignancies; lupus; heart failure; blood disorders (including aplastic anemia); palmoplantar psoriasis; lung disease; and liver damage.
Anakinra may cause a sudden drop in white blood cells (leukopenia) that increases the risk for infections.
Abatacept should be used cautiously in patients with chronic obstructive pulmonary disorder (COPD) as it may increase the risk for respiratory complications.
Rituximab has been associated with cases of a rare and deadly brain infection called progressive multifocal leukoencephalopathy (PML). It also may cause hepatitis B reactivation, viral infections, and heart rhythm disturbances and other heart problems.

Corticosteroids work rapidly to control inflammation and pain. Long-time use, however, can have severe adverse effects. Still, they are often used under the following conditions:

Oral corticosteroids, such as prednisolone and prednisone (Deltasone, Orasone), are most often used in combination with DMARDs, which significantly enhances the benefits of DMARDs.
Oral corticosteroids are sometimes used in early stage-RA for patients who cannot tolerate NSAIDs. Studies, in fact, suggest that low-dose corticosteroids may significantly slow joint pain when it is the first drug administered and then used for 2 years. (Even low-dose oral steroids have adverse effects on bone density, blood sugar, and weight.)
Higher doses of corticosteroids are used for flareups of vasculitis and severe reactions to medications.
Corticosteroids may also be used during pregnancy to avoid exposure to more toxic drugs.
Daily, low-dose corticosteroids are also needed in some patients to control their rheumatoid arthritis symptoms.
Corticosteroids are sometimes injected directly into joints for relief of flare-ups when only one or a few joints are affected. Experts suggest no more than three or four injections into a specific joint a year. Steroid injections in the joints may be a safe and effective treatment for juvenile rheumatoid arthritis and reduce the need for oral medication.
Corticosteroid pulse therapy (intravenous administration) may work as well as DMARDs.

Side Effects of Oral Corticosteroids. Serious side effects are associated with long-term use of oral steroids. (Low doses may reduce these risks, but they do not eliminate them.) Osteoporosis is a common and particularly severe long-term side effect of prolonged steroid use. Medications that can prevent osteoporosis include calcium supplements, parathyroid hormone, or bisphosphonates (alendronate etidronate, risedronate). Other adverse effects include cataracts, glaucoma, diabetes, fluid retention, susceptibility to infections, weight gain, hypertension, capillary fragility, acne, excess hair growth, wasting of the muscles, menstrual irregularities, irritability, insomnia, and, rarely, psychosis. Recent research suggests that prednisone can increase the risk of developing non-melanoma skin cancer.

Withdrawal from Long-Term Use of Oral Corticosteroids. Long-term use of oral steroid medications suppresses secretion of natural steroid hormones by the adrenal glands. After withdrawal from these drugs, this so-called adrenal suppression persists and it can take the body a while (sometimes up to a year) to regain its ability to produce natural steroids again. There have been a few cases of severe adrenal insufficiency that occurred when switching from oral to inhaled steroids, which, in rare cases, has resulted in death.

No one should stop taking any steroids without consulting a doctor first, and if steroids are withdrawn, regular follow-up monitoring is necessary. Patients should discuss with their doctor measures for preventing adrenal insufficiency during withdrawal, particularly during stressful times, when the risk increases.

Biologic Drugs. For many years, therapeutic treatment of rheumatoid arthritis focused on T cell mediation. New research is now examining the role of B cells, which become overactive in autoimmune disease, and how B cell depletion may help to reduce disease activity. Other areas of intense research include interleukin receptor antagonists, which target cytokines involved in the inflammatory process.

Many of the current investigational drugs are monoclonal antibodies (MAbs), biologic drugs that are designed to target specific receptors. Promising candidates in late-stage research include tocilizumab (Actemra), golimumab, denosumab, ocrelizumab, ofatumumab, and certolizumab.

Statins. Some research suggests that compounds derived from statins, the highly regarded cholesterol-lowering drugs, may suppress the inflammation responsible for RA damage.

Stem cell transplantation. Stem cells are the early versions of mature, specialized blood cells. Investigators are reporting that transplantation of donated hemopoietic stem cells, which mature into various blood cells, has induced remission in a few children with severe juvenile rheumatoid arthritis. The procedure is promising in select cases, but it can be highly toxic. More studies are needed to determine risks and benefits for RA patients.

Plasmapheresis. A device called the Prosorba column is used to remove inflammatory antibodies from the patient's blood. Small, short-term studies have shown that this therapy may slow or even halt the progression of the disease in a third to a half of patients. Side effects from the Prosorba column may include anemia, fatigue, itching, fever, a drop in blood pressure, and nausea. Nearly all patients experience an immediate flare-up of joint pain that lasts a few days. Some patients develop infection from the catheter used to remove blood. Long-term studies are needed.

Surgery

Certain surgical techniques may be helpful for people with severe deformities or disabilities.

Arthroscopy. Arthroscopy is performed to clean out bone and cartilage fragments that cause pain and inflammation. It is usually performed on the knee, but it also may be done on the hip:

The surgeon makes a small incision and injects a sterile solution to make the joint swell for easier viewing.
A lighted tube, called an arthroscope (which enables the surgeon to view the joint), is then inserted through another small incision.
Through a third incision, the surgeon trims, shaves, or stitches the damaged tissue. (Arthroscopy is most successful when the removal of cartilage only, and not bone, is involved.)

In many cases, the procedure can be done using local anesthetic, and the patient can go home within a day. In the case of knee operations, patients can resume mild activity in a couple of days, but full recovery can take up to 3 months.

Osteotomy. If only a certain section (the medial compartment) of the knee is damaged and deformed, the surgeon may choose to perform osteotomy:

The knee is opened.
A debridement (removal of damaged tissue) is performed in the joint to eliminate the loose or torn fragments that are causing pain and inflammation.
The bone is then reshaped to remove the deformity.

The procedure is best used in heavier adults who are under 60 years old.

Unicompartmental Knee Arthroplasty. Unicompartmental knee arthroplasty (also called unicondylar knee arthroplasty) may be a useful procedure in some cases of limited damage in the knee. It is intended to relieve pain and preserve function as long as possible before a total knee replacement is necessary. The procedure involves a small incision and insertion of small implants. It retains important knee ligaments, which should preserve more movement than a total knee replacement. The procedure is not widely available and is somewhat controversial, since the implants may not be as reliable as those in total knee replacement.

Synovectomy. Synovectomy is a procedure whereby the diseased joint lining is removed. It is used when more conservative measures fail, particularly in the wrist. Studies are suggesting, however, that with the use of lasers for the procedure, eventually synovectomy may prove to be an alternative to DMARD treatments in reducing symptoms and achieving long-term remission.

Joint Replacement Surgery. Eventually, even after these procedures, rheumatoid arthritis may progress to the point that normal functioning is impossible. In such cases, artificial (prosthetic) replacement joint implants may be considered for knees, hips, or other joints. The prosthesis is usually made of a chromium alloy and plastic and may be attached to the adjoining bones using a cement, polymethyl methacrylate, or the prosthesis may be composed of a porous material that allows bone to grow into and eventually adhere to the device.

Although this procedure has usually been performed in people over 60, implants are now lasting 20 years and more and younger patients with severe disability are finding them useful. Uncemented arthroplasty using porous material is showing particularly good results. Studies on hip replacement, for example, now report that after 10 years, 5% of patients require reoperation and 12% of patients report some pain.

Lifestyle Changes

It is important to maintain a balance between rest (which will reduce inflammation) and exercise (which will relieve stiffness and weakness). Studies have suggested that even as little as 3 hours of physical therapy over 6 weeks will help people with RA, and that these benefits are sustained.

The goal of exercise is to:

Maintain a wide range of motion
Increase strength, endurance, and mobility
Improve general health
Promote well-being

In general, doctors recommend the following approaches:

Start with the easiest exercises, stretching and tensing of the joints without movement.
Next attempt mild strength training. (One study found that people with RA who exercised with machines that use compressed air for gentle resistance experienced less pain and increased muscle tone.)
The next step is to try aerobic exercises. These include walking, dancing, or swimming, particularly in heated pools. Avoid heavy impact exercises, such as running, downhill skiing, and jumping.
Tai chi, which uses graceful slow sweeping movements, is an excellent method for combining stretching and range-of-motion exercises with relaxation techniques. It is of particularly value for elderly RA patients who report significantly less pain after practicing this technique.

While traditional guidelines have restricted RA patients to only gentle exercise, recent research suggests that more intense exercise may not only be safe, but may actually produce greater muscle strength and overall functioning. Common sense is the best guide:

If exercise is causing sharp pain, stop immediately.
If lesser aches and pains continue for more than 2 hours afterwards, try a lighter exercise program for a while.
Using large joints instead of small ones for ordinary tasks can help relieve pressure, for instance, closing a door with the hip or pushing buttons with the palm of the hand.

Many patients with RA try dietary approaches, such as fasting, vegan diets, or eliminating specific foods, that seem to worsen RA symptoms. There is little scientific evidence to support these approaches but some patients report anecdotally that they are helpful.

In recent years, a number of studies have suggested that the omega-3 fatty acids contained in fish oil may have anti-inflammatory properties useful for RA joint pain relief. The best source of fish oil is through increased consumption of fatty fish such as salmon, mackerel, and herring. Fish oil supplements are another option, but they may interact with certain medications. If you are thinking of trying fish oil supplements, talk to your doctor first.

Various ointments, including Ben Gay and capsaicin (a cream that use the active ingredient in chilli peppers), may help soothe painful joints.

Orthotic devices are specialized braces and splints that support and help align joints. Many such devices made from a variety of light materials are available and can be very helpful when worn properly.

A number of specially designed appliances and devices are available to ease daily activities.

Although the influence of stress or emotions on the progression of RA is not fully known, having a history of major depression that persists or reoccurs seems to increase the pain, disability, and fatigue. Stress management alone cannot reduce pain, but it may be very helpful in helping people deal with their condition.

One study found that people with RA reported significant clinical improvement after writing about their pain, stress, or other traumatic experiences. Writing for 20 minutes, just a few days a week, resulted in improvement that lasted for months. One study found that spirituality (defined as "a belief in a power outside oneself and one's own existence," as opposed to the practice of any specific religion) is associated with better health, happiness and well-being among RA patients. (Spiritual healing does not appear to offer any advantages.)

People often turn to alternative therapies or nontraditional remedies to relieve the pain of rheumatoid arthritis. Some alternative procedures, such as acupuncture, massage, relaxation techniques, biofeedback, and hypnosis, are not harmful and may be a useful adjunct to standard treatments.

In a small study, acupuncture reduced pain by a third in 73% of patients, and more than half reported at least a 50% improvement in pain. Patients also reduced their use of pain medications. Research presented at the 2006 American College of Rheumatology annual meeting suggested that both electroacupuncture and traditional acupuncture may help reduce joint tenderness.
Balneotherapy, also known as hydrotherapy or spa therapy, is an ancient form of therapy that involves mineral baths to soothe pain, and some patients have reported relief using such baths.
The NIH is conducting clinical trials to examine whether relaxation response, tai chi, stress management, and cognitive-behavioral therapy can help patients with RA feel better.

Herbal remedies used for RA include boswellia, equisetum arvense (horsetail), devil's claw, borage seed oil, and many others. To date, no evidence supports their efficacy.

Researchers are currently conducting studies in animals to determine if supplements extracted from the turmeric spice can help prevent joint inflammation. The U.S. National Institutes of Health is also conducting a clinical trial to compare the clinical effects of the Chinese herb Tripterygium wilfordii Hook F (TwHF) with the pharmaceutical drug sulfasalazine. TwHF is traditionally used in Chinese medicine for its anti-inflammatory properties.

Generally, manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been a number of reported cases of serious and even lethal side effects from herbal products. Always check with your doctor before using any herbal remedies or dietary supplements.

Resources

www.niams.nih.gov -- The National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.rheumatology.org -- American College of Rheumatology
www.arthritis.org -- The Arthritis Foundation
www.fda.gov/cder/drug/infopage/cox2 -- FDA information on COX-2 inhibitors and NSAIDs
www.clinicaltrials.gov -- Find a clinical trial

References

Chen YF, Jobanputra P, Barton P, Jowett S, Bryan S, Clark W, et al. A systematic review of the effectiveness of adalimumab, etanercept and infliximab for the treatment of rheumatoid arthritis in adults and an economic evaluation of their cost-effectiveness. Health Technol Assess. 2006 Nov;10(42):iii-iv, xi-xiii, 1-229.

Donahue KE, Gartlehner G, Jonas DE, Lux LJ, Thieda P, Jonas BL, et al. Systematic Review: Comparative Effectiveness and Harms of Disease-Modifying Medications for Rheumatoid Arthritis. Ann Intern Med. 2007 Nov 19 [Epub ahead of print]

Firestein GS. In: Harris ED Jr, ed. Kelley's Textbook of Rheumatology. 7th ed. Saunders; 2005.

Furst DE, Breedveld FC, Kalden JR, Smolen JS, Burmester GR, Sieper J, et al. Updated consensus statement on biological agents for the treatment of rheumatic diseases, 2007. Ann Rheum Dis. 2007 Nov;66 Suppl 3:iii2-22.

Goekoop-Ruiterman YP, de Vries-Bouwstra JK, Allaart CF, van Zeben D, Kerstens PJ, Hazes JM,, et al. Comparison of treatment strategies in early rheumatoid arthritis: a randomized trial. Ann Intern Med. 2007 Mar 20;146(6):406-15.

Goldberg RJ, Katz J. A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain. Pain. 2007 May;129(1-2):210-23. Epub 2007 Mar 1.

Harris ED Jr. In: Harris ED Jr, ed. Kelley's Textbook of Rheumatology. 7th ed. Saunders; 2005. O’Dell JR. In: Goldman, ed. Cecil Medicine. 23rd ed. Saunders; 2007.

Smolen JS, Aletaha D, Koeller M, Weisman MH, Emery P. New therapies for treatment of rheumatoid arthritis. Lancet. 2007 Dec 1;370(9602):1861-74.

Smolen JS, Keystone EC, Emery P, Breedveld FC, Betteridge N, Burmester GR,. et al. Consensus statement on the use of rituximab in patients with rheumatoid arthritis. Ann Rheum Dis. 2007 Feb; 66(2): 143-50.

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Captopril/hydrochlorothiazide (By mouth)

admin — Thu, 04 Sep 2008 20:04:43 -0700

Overview

Introduction
Brand Name(s)
When This Medicine Should Not Be Used
How to Use This Medicine
How to Store and Dispose of This Medicine
Drugs and Foods to Avoid
Warnings While Using This Medicine
Possible Side Effects While Using This Medicine

HEALTH GUIDE REFERENCE FROM A.D.A.M

Introduction

Captopril (KAP-toe-pril), Hydrochlorothiazide (hye-droe-klor-oh-THYE-a-zide)

Treats high blood pressure (hypertension). This medicine is a combination of an ACE inhibitor and a thiazide diuretic.

Brand Name(s)

Capozide 25/15, Capozide 50/25, Capozide 50/15, Capozide 25/25

There may be other brand names for this medicine.

When This Medicine Should Not Be Used

You should not use this medicine if you have had an allergic reaction to captopril or hydrochlorothiazide. Do not use this medicine if you are allergic to sulfa drugs, or other blood pressure medicines such as enalapril, lisinopril, Accupril®, Altace®, Lotensin®, Lotrel®, Monopril®, Prinivil®, Vasotec®, or Zestril®. Do not use this medicine if you are pregnant, or if you have problems urinating.

How to Use This Medicine

Tablet

Your doctor will tell you how much of this medicine to use and how often. Your dose may need to be changed several times in order to find out what works best for you. Do not use more medicine or use it more often than your doctor tells you to.
It is best to take this medicine on an empty stomach, 1 hour before you eat a meal.
Be sure to drink plenty of fluids if you exercise, sweat more than usual, or have diarrhea or vomiting. Most adults should drink at least 6 to 8 (eight-ounce) cups of water each day.

If a dose is missed:

If you miss a dose or forget to use your medicine, use it as soon as you can. If it is almost time for your next dose, wait until then to use the medicine and skip the missed dose. Do not use extra medicine to make up for a missed dose.

How to Store and Dispose of This Medicine

Store the medicine in a closed container at room temperature, away from heat, moisture, and direct light.
Ask your pharmacist, doctor, or health caregiver about the best way to dispose of any outdated medicine or medicine no longer needed.
Keep all medicine away from children and never share your medicine with anyone.

Drugs and Foods to Avoid

Ask your doctor or pharmacist before using any other medicine, including over-the-counter medicines, vitamins, and herbal products.

There are many other drugs that can interact with captopril/hydrochlorothiazide. Make sure your doctor knows about all other medicines you are using, especially any other blood pressure medicines or diuretics ("water pills"). Examples of diuretics include furosemide, hydrochlorothiazide, spironolactone, triamterene, Aldactone®, Dyrenium®, Dyazide®, Hyzaar®, Lasix®, Maxzide®, Midamor®, and Moduretic®.
You should not use lithium together with captopril/hydrochlorothiazide, unless your doctor tells you to.
Do not use potassium supplements or salt substitutes that contain potassium without asking your doctor.
Avoid using narcotic pain relievers, phenobarbital, or other sedatives.
Do not drink alcohol while you are using this medicine.

Warnings While Using This Medicine

Using this medicine while you are pregnant can harm your unborn baby. Use an effective form of birth control to keep from getting pregnant. If you think you have become pregnant while using the medicine, tell your doctor right away.
Make sure your doctor knows if you are breast feeding, or if you have lupus, scleroderma, polychondritis, or Behcet's syndrome. Tell your doctor if you have asthma, allergies, congestive heart failure, gout, diabetes, liver disease, or kidney disease, or if you are on dialysis.
Your doctor will need to check your blood or urine at regular visits while you are using this medicine. Be sure to keep all appointments.
Make sure any doctor or dentist who treats you knows that you are using this medicine. You may need to stop using this medicine several days before having surgery or medical tests.
Do not stop using this medicine suddenly without asking your doctor. You may need to slowly decrease your dose before stopping it completely.

Possible Side Effects While Using This Medicine

Call your doctor right away if you notice any of these side effects:

Allergic reaction: Itching or hives, swelling in your face or hands, swelling or tingling in your mouth or throat, chest tightness, trouble breathing.
Chest pain, fast or pounding heartbeat.
Confusion, weakness, irregular heartbeat, shortness of breath, or numbness or tingling in your hands, feet, or lips.
Dark-colored urine or pale stools, loss of appetite, pain in your upper stomach.
Dry mouth, increased thirst, muscle cramps, nausea or vomiting.
Fever, chills, cough, sore throat, and body aches.
Increase in how much or how often you urinate.
Lightheadedness or fainting.
Yellowing of your skin or the whites of your eyes.
Rapid weight gain, swelling in your hands, ankles, or feet.
Unusual bleeding, bruising, or weakness.

If you notice these less serious side effects, talk with your doctor:

Cough.
Hot, dry skin.
Increased sweating.
Mild skin rash.

Review Date: 8/4/2008

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