FitSugar

Getting Down and Dirty vs. Cleaning Dirty Floors

FitSugar — Tue, 02 Sep 2008 09:00:00 -0700

Yesterday we all celebrated Labor Day, which makes me think of doing some labor intensive housework. Then there is the other kind of labor, childbirth and the activities that lead to pregnancy. I decided to do a little compare and contrast quiz between these drastically different methods of getting domestic. I want to know which burns more calories getting down and dirty or mopping / vacuuming your dirty floors.

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Take the quiz

Clean Green: Mop Your Floors with Vinegar

FitSugar — Sat, 21 Jul 2007 03:00:00 -0700

Weekends are when I get the majority of my house cleaning done. You know, the big jobs like mopping the floors. I like to send my husband to the park with the girls when I do this, not because I use a toxic cleaner that might hurt my loved ones (and my own) lungs. I just don't want them to muck up the floors I just mopped with vinegar.

Well not straight up vinegar, I dilute it of course, about ½ cup distilled white vinegar in a gallon of water. This is a safe way to clean hardwood, laminate or tile floors. It is safe for the floors and for you! Studies have shown that 5% solution of vinegar (straight out of the store-bought bottle) kills 99 percent of bacteria, 82 percent of mold, and 80 percent of germs (viruses). Plus it is not toxic! The smell dissipates much more quickly than Lysol or other cleaners.

Some people add a little dish soap or peppermint into their solution, but I go for the simple mixture and mop to my hearts content. Try it!!!

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Methoxsalen (By mouth)

admin — Thu, 04 Sep 2008 20:05:32 -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

Methoxsalen (meth-OX-a-len)

Treats the symptoms of psoriasis. Used before treatment with ultraviolet radiation (UV light) so your skin will respond better to the treatment.

Brand Name(s)

Oxsoralen-Ultra, 8-Mop

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 methoxsalen (Uvadex®, Oxsoralen®) or any other psoralen medicine, such as trioxsalen (Trisoralen®). You should not use this medicine if your skin is very sensitive to light, or if you have a disease that makes your skin sensitive to light. Do not use this medicine if you have had melanoma skin cancer or squamous cell skin cancer. Do not use this medicine if you have aphakia (no lenses in your eyes).

How to Use This Medicine

Capsule

Your doctor will tell you how much of this medicine to use and how often. Do not use more medicine or use it more often than your doctor tells you to.
Use only the brand of this medicine that your doctor prescribed. Different brands may not work the same way.
Take this medicine about 1½ to 2 hours before you have your UV treatment.
It is best to take this medicine with milk, or low-fat foods such as fresh fruit, crackers, toast or bagels. If this medicine upsets your stomach, ask your doctor or pharmacist if you can take your dose at two different times. You may be able to take half of the dose, and then take the other half about 30 minutes later.

If a dose is missed:

If you do not take your medicine at the correct time, take it as soon as possible. Tell your health caregiver what time you took your medicine.
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.

Tell your doctor if you are using any other medicine that might also make your skin more sensitive to light. These medicines include anthralin (Psoriatec®), coal tar, griseofulvin (Grifulvin®, Gris-Peg®), nalidixic acid (NegGram®), and halogenated salicylanilides (bacteriostatic soaps). They also include thiazide diuretics ("water pills"), such as hydrochlorothiazide (HCTZ), or some staining dyes such as methylene blue, toluidine blue, rose bengal, or methyl orange.
Make sure your doctor knows if you are using a sulfonamide medicine, such as trimethoprim/sulfamethoxazole, Bactrim®, Cotrim®, or Septra®, or if you are using a tetracycline medicine, such as doxycycline (Vibramycin®), or minocycline (Minocin®). Tell your doctor if you are using a phenothiazine medicine, such as prochlorperazine, Compazine®, Mellaril®, Phenergan®, or Thorazine®.
Make sure your doctor knows if you have ever had radiation therapy or arsenic therapy.

Warnings While Using This Medicine

Make sure your doctor knows if you are pregnant or breast feeding, or if you have basal cell carcinoma (a type of skin cancer). Make sure your doctor knows if you have liver disease or any heart problems.
You could get a serious sunburn while using this medicine. Carefully follow all instructions from your doctor. The UV light treatment may also tan your skin or cause freckles.
Do not sunbathe ("lay out") or tan in the 24 hours (1 day) before taking this medicine. Do not sunbathe for 48 hours (2 days) after your UV light treatment.
Stay out of sunlight for at least 8 hours after you have taken this medicine. This includes avoiding sunlight that comes in from a window or when riding in a car. Also be aware that even when the sky is cloudy, the UV light can reach your skin. If you must be in the sun, wear clothing that covers all of your skin. This includes long sleeves, a hat, and gloves. You can also apply sunscreen that has an SPF (sun protection factor) of greater than 15. However, do not put the sunscreen on any areas of your skin where you have psoriasis until after you have had your UV light treatment.
Wear wrap-around sunglasses that will protect your eyes from UV light for at least 24 hours (1 day) after taking this medicine. Show your sunglasses to health caregivers. Caregivers will make sure that your sunglasses protect your eyes from UV light.
Your skin might turn red after your treatment. If your skin turns very red, or starts to blister or peel, call your doctor.
If your skin itches because of this treatment, ask your health caregiver what kind of cream or lotion you can use to stop the itching. If the itching does not stop, call your doctor.
If your symptoms do not improve or if they get worse, call your doctor.
You should have your eyes checked before you start to use this medicine. Schedule eye check-ups every year after you stop using this medicine.

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.
Trouble seeing or any vision changes.

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

Nausea.
Trouble sleeping.
Unusual sadness or nervousness.

Review Date: 8/4/2008

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. © 1997-2009 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

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Source Doc: 45_4983

Lucy Free Sweat Band Giveaway

FitSugar — Tue, 18 Aug 2009 11:00:29 -0700

If you're sweating it out during these dog days of Summer, jog on over to a Lucy store and pick up a free sweat band to mop your workout brow. Just fill out this form (it takes 30 seconds), print it, and take it to your local Lucy store - here is a store locator to find a one near you. While you're there be sure to check out their sale items to save some dough on some cute Lucy gear. No purchase necessary and the offer runs through Aug. 30, while supplies last, of course. Sorry, but the offer is not valid online.

If there is no brick and mortar Lucy store near you, you can still shop its Summer-end sale online.

Vitamins Reduce the Benefits of Your Workout

FitSugar — Wed, 13 May 2009 03:00:00 -0700

Free radicals create oxidative stress on a cellular level and have long been considered a major culprit of the aging process. Since antioxidants clean up those free roaming bits of "reactive oxygen compounds," one would think vitamins loaded with free radicals would help folks live longer. However, last Spring, researchers found that taking high doses of vitamins may decrease life span rather than lengthen it.

Now a new study has found that taking moderate doses of vitamins E and C interferes with the benefits of exercise, specifically the increase of metabolism and diabetes prevention through insulin sensitivity.

It seems the antioxidants found in vitamins C and E are too efficient at mopping up free radicals, and our muscles need a little bit of cellular damage caused by oxidative stress to jump-start their natural defense systems. Researchers wholeheartedly believe more research should be done in this area, and that we should not worry about getting too much of these vitamins in our diet naturally; it is supplements that should possibly be avoided.

Source

Healthy To-Do: Burn Calories While Spring Cleaning

FitSugar — Sun, 05 Apr 2009 04:00:00 -0700

Spring has sprung, so now it's time for some Spring cleaning. Maybe dusting and organizing clutter is not the most exciting way to spend your weekend, but you'll feel so much better you'll feel when it is all done. Go ahead and clean out your closet, dust under your bed and on top of the fridge, vacuum your mattress to get rid of dust mites, and open up the windows to get some fresh air circulating. A huge plus is you'll also be burning some major calories too. To find out how many read more.

These calculations are based on a 130-pound woman.

Activity:	Calories burned per 30 minutes:
Mopping or sweeping the floor	85
Dusting	85
Gardening/weeding	140
Ironing	74
Doing laundry	73
Mowing the lawn	163
Mowing the lawn (push mower)	172
Raking the lawn	125
Rearranging furniture	101
Washing dishes	85
Washing the car	101
Washing windows	85
Cleaning out the garage	101

Source

Psoriasis

FitSugar — Wed, 08 Oct 2008 17:35:27 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Treatment

Psoriasis that develops on the hands or feet is often very difficult to treat. However, an advanced clinical trial showed that a medication called efalizumab (Raptiva) effectively cleared or nearly cleared moderate-to-severe symptoms in adults after 12 weeks.

Several studies have shown that most people with severe psoriasis who are treated with infliximab (Remicade) have significant improvement in symptoms by week 10. The findings were presented at the 2007 annual meeting of the American Academy of Dermatology.

Continuing etanercept (Enbrel) after 12 weeks improves disease severity without an increase in infections or side effects, according to a study published in the Archives of Dermatology.

Disease classification

The National Psoriasis Foundation has proposed a new way to classify psoriasis. Instead of being grouped as mild, moderate, or severe, the group suggests a new two-tiered system that classifies patients as needing either local or body-wide (systemic) treatment.

Coexisting conditions

Studies from Newfoundland and Germany have revealed increased cases of diabetes, obesity, arthritis, and cancer in patients with psoriasis. Previous research has found an increased risk of heart disease in psoriasis patients. Research is underway to determine if there are genetic links between psoriasis and these conditions.

Severe psoriasis has been linked to a significant increase in a patient's risk of death. A study of more than 713,000 patients showed that severe psoriasis increased mortality by 50%. Such patients should receive comprehensive health examinations to reduce the risk, the authors recommended. Study participants were considered to have severe psoriasis if they required systemic treatment.

Smoking and psoriasis

Introduction

Psoriasis is a chronic skin disorder marked by periodic flare-ups of sharply defined red patches, covered by a silvery, flaky surface. The main disease activity leading to psoriasis occurs in the epidermis, the top five layers of the skin.

The process starts in the basal (bottom) layer of the epidermis, where keratinocytes are made. Keratinocytes are immature skin cells that produce keratin, a tough protein that helps form hair, nails, and skin. In normal cell growth, keratinocytes grow and move from the bottom layer to the skin's surface and shed unnoticed. This process takes about a month.

In persons with psoriasis, the keratinocytes multiply very rapidly and travel from the basal layer to the surface in about 4 days. The skin cannot shed these cells quickly enough, so they build up, leading to thick, dry patches, or plaques. Silvery, flaky areas of dead skin build up on the surface of the plaques before being shed. The underlying skin layer (dermis), which contains the nerves and blood and lymphatic vessels, becomes red and swollen.

Types of Psoriasis

Various forms of psoriasis exist. Some can occur alone or at the same time as other types, or one may follow another. The most common type is called plaque psoriasis, also known as psoriasis vulgaris.

Plaque psoriasis leads to skin patches that start off in small areas, about one-eighth of an inch wide. They usually appear in the same areas on opposite sides of the body.

The patches slowly grow larger and develop thick, dry plaque. If the plaque is scratched or scraped, bleeding spots the sizes of pinheads appear underneath. This is known as the Auspitz sign.

Some patches may become ring shaped (annular), with a clear center and scaly raised borders that may appear wavy and snake-like.

As the disease progresses, eventually separate patches may join together to form larger areas. In some cases, the patches can become very large and cover wide areas of the back or chest. This is known as geographic plaques because the skin lesions resemble maps.

Plaque psoriasis may persist for long periods. More often it flares up periodically, triggered by certain factors such as cold weather, infection, or stress.

Patches most often occur on the:

Elbows
Knees
Lower back

The may also be seen on the:

Upper pelvic bone area
Bottom of the feet
Calves and thighs
Genital areas
Palms of hands

Psoriasis of the scalp affects about 50% of patients. In some cases, the psoriasis may cover the scalp with thick plaques that extend down from the hairline to the forehead.

Psoriasis patches rarely affects the face in adulthood. In children, psoriasis is most likely to start in the scalp and spread to other parts of the body. Unlike in adults, it also may occur on the face and ears.

Psoriatic arthritis (PsA) is an inflammatory condition characterized by stiff, tender, and inflamed joints. Estimates on its prevalence among those with psoriasis range from 2 - 42%. AIDS patients and those with severe psoriasis are at higher risk for developing PsA.

About 80% of PsA patients have psoriasis in the nails. Arthritic and skin flare-ups tend to occur at the same time. It is not clear whether psoriatic arthritis is a unique disease or a genuine variation of psoriasis, although evidence suggests they are both caused by the same immune system problem.

Although patients with psoriatic arthritis tend to have mild skin symptoms, the disease affects the entire body. PsA, therefore, is more serious than the more common plaque psoriasis. Infrequently, the course of PsA has been associated with a syndrome known by the acronym SAPHO, which stands for:

Synovitis (inflammation in the joints)
Acne
Pustule eruptions
Hyperostosis (abnormal bony growths)
Osteolysis (bone destruction)

Some experts group PsA into five forms. The forms differ according to the location and severity of the affected joint:

Symmetric PsA: Symptoms occur in the same location on both sides of the body. It usually affects multiple joints. In about half of the cases, the condition will get worse. The condition is very similar to, but less disabling than, rheumatoid arthritis. The psoriasis itself is often severe.
Asymmetric PsA: This form involves periodic joint pain and redness, usually in only one to three joints, which can be the knee, hip, ankle, wrist, or one or more fingers. The pain does not occur in the same location on both sides of the body.
Distal interphalangeal predominant (DIP): DIP involves the joints of the fingers and toes closest to the nail. It occurs in about 5% of PsA cases.
PsA in the spine: Inflammation in the spinal column (spondylitis) is the primary symptom in about 5% of PsA cases. Such patients may have stiffness and burning sensations in the neck, lower back, sacroiliac, or spinal vertebrae. The spine can be involved in many patients with PsA, even though stiffness and burning sensations in these areas are not the primary symptoms. When it affects the spine, psoriatic arthritis most frequently targets the sacrum (the lowest part of the spine). Movement is difficult.
Arthritis mutilans: This is a severe, deforming, and progressive form of arthritis. It affects less than 5% of PsA cases. It mainly affects the small joints of the hands and feet, but it can also be found in the neck and lower back. Arthritic and skin flares and remissions tend to coincide.

People who start to smoke after developing psoriasis may delay the onset of psoriatic arthritis, according to research presented at the 2007 annual meeting of the Society for Investigational Dermatology. Researchers found that in nonsmokers, the time between psoriasis diagnosis and psoriatic arthritis development was 13 years, compared to 23 among those who started smoking after the onset of psoriasis. Study participants who smoked before developing psoriasis had psoriatic arthritis occur in about 8 years. However, smoking causes serious health problems and should not be considered as a way to delay this type of psoriasis.


Psoriasis Form	Description of Skin Patches	Comments
Guttate Psoriasis	The patches are teardrop-shaped and appear suddenly, usually over the trunk and often on the arms, legs, or scalp. They often disappear without treatment.	Guttate psoriasis can occur as the initial outbreak of psoriasis, often in children and young adults 1 - 3 weeks after a viral or bacterial (usually streptococcal) respiratory or throat infection. A family history of psoriasis and stressful life events are also highly linked with the start of guttate psoriasis. Guttate psoriasis can also develop in patients who have already had other forms of psoriasis, most often in people treated with widely-applied topical (rub-on) products containing corticosteroids.
Inverse Psoriasis	Patches usually appear as smooth inflamed patches without a scaly surface. They occur in the folds of the skin, such as under the armpits or breast, or in the groin.	Inverse psoriasis may be especially difficult to treat.
Seborrheic Psoriasis	Patches appear as red scaly areas on the scalp, behind the ears, above the shoulder blades, in the armpits or groin, or in the center of the face.	Seborrheic psoriasis may be especially difficult to treat.
Nail Psoriasis	Tiny white pits are scattered in groups across the nail. Toenails and sometimes fingernails may have yellowish spots. Long ridges may also develop across and down the nail. The nail bed often separates from the skin of the finger and collections of dead skin can build up underneath the nail.	Over half of patients with psoriasis have abnormal changes in their nails, which may appear before other skin symptoms. In some cases, nail psoriasis is the only symptom.
Generalized Erythrodermic Psoriasis (also called psoriatic exfoliative erythroderma)	This is a rare and severe form of psoriasis, in which the skin surface becomes scaly and red. The disease covers all or nearly all of the body.	About 20% of such cases evolve from psoriasis itself. The condition may also be triggered by certain psoriasis treatments, and other medications such as corticosteroids or synthetic antimalarial drugs.
Pustular Psoriasis	Patches become pus-filled and blister-like. The blisters eventually turn brown and form a scaly crust or peel off. Pustules usually appear on the hands and feet. When they form on the palms and soles, the condition is called palmar-plantar pustulosis.	Pustular psoriasis may erupt as the first occurrence of psoriasis, or it may evolve from plaque psoriasis. A number of conditions may trigger pustular psoriasis, including infection, pregnancy, certain drugs, and metal allergies. It can also accompany other forms of psoriasis and be very severe.

Causes

The precise causes of psoriasis are unknown. It is generally believed to be due to damage in factors in the immune system, enzymes, and other materials that control skin cell division. This prompts an abnormal immune response, which causes rapid production of immature skin cells and inflammation.

The Normal Immune System Response. The inflammatory process is the result of the body's immune response, 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 invaders, such as bacteria or viruses.
The masses of blood cells that gather at the injured or infected site produce factors to repair wounds, clot the blood, and fight infections.
In the process, the surrounding area becomes inflamed (red and swollen), and some healthy tissue is injured.

The Infection Fighters. The primary infection-fighting units are two types of white blood cells: lymphocytes and leukocytes.

Lymphocytes include two subtypes known as T cells and B cells. Both types of cells are designed to recognize foreign substances (antigens) and launch an offensive or defensive action against them:

B cells produce antibodies, which are designed to attack the antigens. Antibodies can either ride along with a B cell or travel on their own.
T cells have special receptors attached to their surface that recognize the specific antigen.

T cells are further categorized as killer T cells or helper T cells (TH cells).

Killer T cells directly attack antigens found on bacteria or other cells.
Helper T stimulate B cells and other white cells to attack the antigen.

The actions of the helper T cells are of special interest. Researchers have found high numbers of helper T cells in psoriatic plaques. Helper T cells normally stimulate B cells to produce antibodies. In psoriasis, however, they appear to direct the B cells to produce autoantibodies ("self" antibodies), which attack skin cells. In psoriatic arthritis, cells in the joints also come under attack.

Helper T cells also release or stimulate the production of powerful immune factors called cytokines. In small amounts, cytokines are very important for healing. If overproduced, however, they can cause serious damage, including inflammation and injury during the psoriasis disease process. In psoriasis, researchers are particularly interested in cytokines known as GRO-alpha, tumor necrosis factor, and certain interleukins.

Cytokines attract large numbers of other large white blood cells known as neutrophils. Neutrophils stimulate the production of arachidonic acid, producing two key players in the inflammatory process:

Leukotrienes: These chemicals attract even more white blood cells to the inflamed area.
Prostaglandins: These chemicals widen blood vessels and increase blood flow.

A combination of genes is involved with increasing a person's susceptibility to the conditions leading to psoriasis.

HLA Molecules. The processes leading to all autoimmune diseases involve the human leukocyte antigen (HLA) system. HLA molecules pick off parts of antigens and present them on the surface of a cell so that the various infection-fighting factors in the immune system can recognize and destroy them. Most immune disorders, including psoriatic arthritis, are due to problems with this system. For example, psoriasis patients with an HLA genetic factor called HLA-CW6 tend to develop psoriasis at an earlier than average age. However, only 10% of people who have this gene develop psoriasis. Other genetic and environmental factors are required to actually trigger the disease.

PSORs. Researchers have now identified four key genes (named PSOR 1 - 4) that are involved with psoriasis. Of particular interest are the genes located in regions on specific chromosomes that are linked to HLA and tumor necrosis factor, another immune factor strongly associated with psoriasis.

Weather, stress, injury, infection, and medications, while not direct causes, are often important in triggering the disease process leading to the start and worsening of psoriasis.

Weather. Cold, dry weather is a common trigger of psoriasis flare-ups. Hot, damp, sunny weather helps relieve the problem in most patients. However, some people have photosensitive psoriasis, which actually improves in winter and worsens in summer when skin is exposed to sunlight.

Stress and Strong Emotions. Stress, unexpressed anger, and emotional disorders, including depression and anxiety, are strongly associated with psoriasis flare-ups. In one study, nearly 40% of patients remembered a specific stressful event that occurred within a month of a psoriasis flare. Other research has suggested that stress can trigger specific immune factors associated with psoriasis flares.

Infection. Infections caused by viruses or bacteria can trigger some cases of psoriasis. For example:

Streptococcal infections in the upper respiratory tract, such as tonsillitis, sinusitis, and strep throat, are known to trigger guttate psoriasis in children and young adults. The infections may make ordinary plaque psoriasis worse.
Human immunodeficiency virus (HIV) is also associated with psoriasis.
An uncommon form of human papillomaviruses (HPV) called EV-HPV has been associated with psoriasis. Although EV-HPV is probably not a direct cause, it may play a role in the continuation of psoriasis. This HPV form is not the virus associated with cervical cancer and genital warts.

Skin Injuries and the Köbner Response. The Köbner response is a delayed response to skin injuries, in which psoriasis develops later on at the site of the injury. In some cases, even mild abrasions can cause an eruption, which may be a factor in the frequency of psoriasis on the elbows or knees. It should be noted that psoriasis can develop in areas with no history of skin injury.

Medications. Drugs that can trigger the onset of the disease, worsen symptoms, or cause a flare-up include:

Angiotensin-converting enzyme (ACE) inhibitors, drugs used to treat high blood pressure and heart problems
Beta-blockers, drugs used to treat high blood pressure and heart problems
Chloroquine, a medicine used to treat malaria
Lithium for bipolar disorder treatment
Indomethacin, a nonsteroidal anti-inflammatory drug (NSAIDs) -- Note: Other NSAIDs, such as meclofenamate, may actually improve the condition.
Progesterone, used in female hormone therapies

Flare-ups of severe psoriasis may occur in persons who stop taking steroids taken by mouth, or who discontinue use of very strong steroid ointments that cover wide skin areas. The flare-ups may be of various psoriatic forms, including guttate, pustular, and erythrodermic psoriasis. Because these drugs are also used to treat psoriasis, this rebound effect is of particular concern.

Medications that cause rashes, a side effect of many drugs, can trigger psoriasis as part of the Köbner response.

Risk Factors

Between 5.8 and 7.5 million Americans have psoriasis. Risk factors for psoriasis include:

Age under 20. About 40% develop the condition before age 20. Psoriasis (most often plaque psoriasis) can even occur in infants.
Climate. Some studies have found that the disorder develops earlier and more frequently in colder climates. For example, psoriasis occurs more frequently in African-Americans and in Caucasians who live in colder climates than in people of any ethnicity who live in Africa.
Ethnicity. Psoriasis is uncommon in Native Americans of either North or South American descent.
Family history of the disease. About 35% of those with psoriasis have one or more family members with the disorder.
Male gender. Some studies have indicated that more men than women have psoriasis.

Diagnosis

A microscopic examination of tissue taken from the affected skin patch is needed to make a definitive diagnosis of psoriasis and to distinguish it from other skin disorders. Usually in psoriasis, the examination will show a large number of dry skin cells, but without many signs of inflammation or infection. Specific changes in the nails are often strong signs of psoriasis.

Several conditions produce symptoms that resemble those of psoriasis. For example:

Seborrheic psoriasis is hard to distinguish from seborrheic dermatitis (dandruff is one form of this condition). Seborrheic dermatitis patches are usually greasy, yellowish, and crusty. Nail involvement may also help differentiate psoriasis.
Generalized erythrodermic psoriasis may be confused with drug allergic reactions, atopic eczema, and symptoms of lymphomas.
Fungal infections, other skin conditions, or circulation problems may also cause nail changes typical of psoriasis.

Symptoms of psoriatic arthritis may also resemble the following:

Rheumatoid arthritis (RA). As in rheumatoid arthritis, psoriatic arthritis can cause pain or tenderness in one or more joints, and morning stiffness is common. People with psoriatic arthritis, however, lack a particular antibody, called rheumatoid factor, which is found in the blood of many people with rheumatoid arthritis.
Systemic lupus erythematosus (SLE). Symptoms of SLE may include both a psoriasis-like rash and arthritis, which could make the diagnosis difficult.
Reiter's disease. Reiter's disease is a syndrome that includes arthritis and inflammation in the eyes and urinary tract. It also causes skin lesions that are very similar to psoriasis, which are usually raised patches on the lips, penis, palms, and soles.
Gout. Gout causes pain, often in the fingers and toes.

Some evidence now indicates that inflammation in psoriatic arthritis may be distinguished from other arthritic conditions by its occurrence in sites where muscle tissue inserts into the bone (called enthesitis) rather than in the joint, which is a common site in other inflammatory arthritic conditions.

Severity of psoriasis itself ranges from one or two flaky inflamed patches to widespread pustular psoriasis that, in rare cases, can be life threatening. To help determine the best treatment for a patient, doctors usually classify the disease as mild to severe. The classification depends on how much of the skin is affected:

Mild psoriasis affects less than 3% of the body surface. Most cases of psoriasis are limited to less than 2% of the skin.
Moderate psoriasis covers 3 - 10% of the skin.
If more than 10% of the body is affected, the disease is considered severe.

The palm of the hand equals 1% of the body. The severity of the disease is also measured by its effect on a person’s quality of life.

However, the National Psoriasis Foundation has proposed a new classification method. The group suggests a new two-tiered system that classifies patients as needing either local or body-wide (systemic) treatment.

While disease severity impacts treatment success, some forms of psoriasis can be very resistant to treatment even though they are not categorized as severe. They include:

Any psoriasis on the palms and soles (hand and foot psoriasis)
Inverse psoriasis (which occurs in the folds of the skin)
Scalp psoriasis
Psoriatic arthritis

Treatment

Many creams, ointments, lotions, and pills are available for the treatment of psoriasis. Many patients require only over-the-counter treatment, or even none at all during relapses.

About a third of patients with psoriasis, however, do not respond to over-the-counter remedies and lifestyle changes, and require aggressive treatments. In some cases, such treatments need to be lifelong.

In general, there are three treatment options for patients with psoriasis.

Topical medications such as lotions, ointments, creams, and shampoos
Body-wide (systemic) medications, which involve pills or injections that affect the whole body, not just the skin
Phototherapy, which uses light to treat psoriasis lesions

Individual requirements vary widely, and treatment selection must be carefully discussed with the doctor.

Giving treatment in a particular order is a strategy for providing both quick relief of symptoms and long-term maintenance. It involves three main steps:

The quick fix, to clear the psoriatic lesions during an acute outbreak (for example, a high-strength topical steroid in mild-to-moderate psoriasis, or an oral immunosuppressant in more severe cases)
The transitional phase, intended to gradually introduce the maintenance drug
Ongoing maintenance therapy

Choices for transitional or maintenance treatments depend on the severity of the condition. Some examples are described in the following sections.

In severe chronic cases, a doctor may recommend rotational therapy. This approach alternates treatments. The goal is to prevent severe side effects or build-up of resistance from long-term use of a single medicine. An example of a rotational schedule may be the following:

The patient gets phototherapy for about 2 years.
The patient then takes one or two powerful body-wide drugs for 1 - 2 years and stops.
Phototherapy starts again, and the cycle repeats.

Some doctors use the Koo-Menter Psoriasis Instrument (KMPI) to decide which patients should receive a pill or an injection. The KMPI’s questions include:

Does psoriasis cover at least 5% of the patient’s body?
Is the patient disabled by psoriasis?
Does psoriasis affect the patient’s quality of life?

If the answer to these questions is "yes," three additional questions are considered:

Is light therapy inappropriate for the patient?
Is the patient’s psoriasis resistant to light therapy?
Does the patient have psoriatic arthritis?

If the answer to these questions is “yes,” a doctor may decide to prescribe a pill or injected drugs.

Doctors increasingly use combinations of pills, creams, ointments, and phototherapy instead of single medications. Combinations of oral treatments are particularly useful, since the doses of each drug can be reduced. This lowers the risk of severe side effects. Thousands of combinations are possible, and the patient and doctor should discuss the best treatment for individual needs.

Topical Medications

Topical medications are those applied only to the surface of the body. They come in the following forms:

Creams
Foams
Gels
Lotions
Occlusive tapes
Ointments
Shampoos
Solutions
Sprays

In general, topical treatments are the first line for mild-to-moderate psoriasis, but they may also be used, alone or in combination, with more powerful treatments for moderate-to-severe cases. Topical medicines rarely produce complete clearance, however.

Corticosteroid topical treatments are the mainstay of psoriasis treatments in the United States. They work for most patients. Such treatments:

Decrease inflammation
Block cell production
Relieve itching

Corticosteroids are available in a wide range of strengths, and are generally given as follows:

Less potent drugs are used for mild-to-moderate psoriasis.
Stronger drugs are reserved for more severe disease.

In the past, topical steroids have been used twice a day. Studies are reporting, however, that certain drugs may work just as well if taken once a day. Most studies have evaluated high-potency steroids, but one study suggested that those of medium strength, such as triamcinolone (Aureocort, Tri-Adcortyl), may be equally beneficial as a once-daily treatment. However, corticosteroids used alone clear psoriasis in only 4 - 36% of patients.

Combination therapy. Combinations with other drugs are often needed. For example, an effective, topical regimen uses the following combination for maintenance therapy:

A high-potency steroid (such as halobetasol) on the weekend
A vitamin D3 topical medication called calcipotriene, twice daily on weekdays

In one study, more than 75% of patients with mild-to-moderate psoriasis remained in remission for at least 6 months with this regimen.

Side Effects. The more powerful the corticosteroid, the more effective it is. But it also has a higher risk for severe side effects. Side effects may include:

Burning
Irritation
Dryness
Acne
Thinning of the skin; skin may become shiny, fragile, and easily cut
Dilated (widened) blood vessels
Loss of skin color

Loss of Effectiveness. In most cases, the patients become tolerant to the effects of the drugs, and the drugs no longer work as they should. Some experts recommend using intermittent therapy (also called weekend or pulse therapy). This type of treatment involves applying a high-potency topical medication for 3 full days each week.

Note: This list is not all inclusive.
Low potency (some are available over the counter)	Desonide (Tridesilon, DesOwen) Flumethasone pivalate (Locorten) Fluocinolone acetonide (Synalar, Derma-Smoothe) Hydrocortisone (Hytone, Penecort, Synacort, Cort-Dome, Nutracort, Westcort) Triamcinolone acetonide (Aristocort)
Low to medium potency	Alclometasone dipropionate (Aclovate) Hydrocortisone (Locoid, Pandel) Hydrocortisone valerate (Westcort) Prednicarbate (Dermatop)
Medium to upper-mid potency	Clocortolone pivalate (Cloderm) Fluticasone propionate (Cutivate) Mometasone furoate (Elocon) Triamcinolone acetonide (Aureocort, Tri-Adcortyl, Kenalog)
High potency	Betamethasone (Diprosone) Amcinonide (Cyclocort) Desoximetasone (Topicort) Diflorasone diacetate (Florone, Maxiflor) Fluocinonide (Lidex) Halcinonide (Halog)
Very high potency	Halobetasol propionate (Ultravate) Betamethasone (Diprolene, Luxiq) Clobetasol propionate (Temovate, Olux) Diflorasone diacetate (Florone, Maxiflor, Psorcon)

Coal tar preparations have been used to treat psoriasis for about 100 years, although their use has declined with the introduction of topical vitamin D3-related medicines. Crude coal tar stops the action of enzymes that contribute to psoriasis, and helps prevent new cell production. Tar is often used in combination with other drugs and with ultraviolet B (UVB) phototherapy.

Side Effects. Preparations have the following drawbacks:

Stains on clothing
Skin irritation
Sun sensitivity and increased risk of sunburn for up to 24 hours after use

Anthralin (Dritho-Scalp, Drithocreme, Micanol) is related to a medication called chrysarobin, in use since the early 1900s. Anthralin slows skin cell reproduction and can produce remissions that last for months. It is recommended only for chronic or inactive psoriasis, not for acute or inflamed eruptions. Persons with kidney problems should use anthralin with caution.

As with tar, its use has also declined with introduction of the topical vitamin D-related medicines, but newer formulations, such as Micanol, have made its use more tolerable. Micanol (Psoriatec) is an anthralin formulated in microcapsules, which dissolve and allow the drug to be delivered directly to the target skin areas. It is particularly useful for scalp psoriasis, and it is less likely to stain.

Side Effects. Anthralin may cause the following side effects:

Skin irritation and burning
Staining of clothes, hair, fabrics, plastics, and other household products

Patients should not use anthralin on their faces. Fair skinned people should generally avoid it. Triethanolamine (CuraStain) is a chemical that can neutralize anthralin and help reduce irritation from short-contact anthralin treatment. It should be applied 1 or 2 minutes before washing off the anthralin. It is then reapplied after drying the skin.

Washing stained items with hypochlorite (Clorox) detergents can help remove stains. Many people use disposable gloves while applying the treatment to avoid staining hands.

Application. Apply anthralin only to the psoriasis plaques. Rub the cream in well, and wipe off any excess. Wash off only with lukewarm water, not soap. Using hot water will trigger the staining action. A technique called short-contact anthralin therapy (SCAT), also called minute therapy, is useful for local areas of psoriasis. In such cases, anthralin is applied for only 10 minutes to an hour.

A topical form of vitamin D3, calcipotriene (Dovonex) is proving to be both safe and effective. It is now available in a foam preparation, which makes compliance even easier. Several other topical vitamin D3 related drugs showing promise include maxacalcitol (Oxarol), tacalcitol, and calcitriol (Silkis).

Calcipotriene appears to:

Block skin cell reproduction
Enhance the maturity of keratinocytes (the impaired skin cells in psoriasis)
Acts as an anti-inflammatory

It works just as well as moderate topical corticosteroids, short-term anthralin, and coal tar in improving mild-to-moderate plaque psoriasis. Unlike steroids, patients do not develop thinning of the skin or tolerance to the drug.

Using the drug in combination with other topical and systemic treatments may improve effectiveness. Calcipotriene doesn't work as well as the highest potency corticosteroids, but products or regimens that combine both medications are proving to be more effective than either one alone. Taclonex, an ointment containing both calcipotriol and betamethasone, was approved by the U.S. Food and Drug Administration (FDA) in January 2006 for the treatment of adults with psoriasis. Studies show the combination works better than either drug alone.

Combining vitamin D ointments with systemic medicines, notably methotrexate, acitretin, or cyclosporine, increases effectiveness and allows lower doses or either medication, thereby reducing side effects.

Studies also report success in some patients who use vitamin D ointments in combination with phototherapy treatment.

Side Effects. Calcipotriene may cause the following side effects:

A possible lowering of vitamin D levels, which may affect bone growth in some children
A possible increase in blood calcium levels (seen in some people who apply calcipotriene to large areas)
Skin irritation in about 20% of patients, particularly on the face and in skin folds

Calcipotriene appears to cause greater skin irritation than potent corticosteroids. Diluting the drug with petrolatum or applying topical corticosteroids to sensitive areas may prevent this problem.

Retinoids are related to vitamin A. They are used for various skin disorders. Tazarotene (Tazorac) is the first topical retinoid found to be effective for mild-to-moderate psoriasis. It is available in cream or gel form.

Unlike steroids, patients do not develop thinning of the skin or tolerance to the drug. Only a very small amount is needed on each lesion. It can be used on the scalp and nails, but it is not recommended for the genital areas or around the eyes. The gel should be used on only 20% of the body at anytime; the cream on up to 35%. (Note: The palm of the hand is about 1% of the body surface.)

Combining topical retinoids with other psoriasis treatments, such as with topical steroids, works better than using the drug by itself.

Side Effects. Tazarotene may cause dryness and irritation of healthy skin. Applying zinc oxide and moisturizer around the treated area can protect the healthy skin.

At levels high enough to be effective for psoriasis, tazarotene can cause severe skin irritation on treated areas. This medicine, then, is usually used in combination with other treatments, therefore allowing a lower dose. Mixing the drug in equal amounts with petroleum jelly (Vaseline) initially and then gradually increasing the amount of tazarotene may help the skin areas become less sensitive. It should be noted that the skin can become very red while it is actually improving.

Vitamin A derivatives (drugs related to vitamin A) have been associated with birth defects and should not be used by women who are pregnant, who wish to conceive, or who are nursing.

Salicylic acid applied to the skin helps remove scaly plaque and enhance the actions of other medications. It should not be used to cover wide areas of the body, since it can cause nausea and ringing in the ears. Combinations with high potency steroids, such as mometasone furoate (Combisor), clobetasol propionate, and betamethasone, are proving to be very helpful. Only Combisor is available in the United States.

Watertight (occlusive) tapes or wrappings may help heal psoriasis. Occlusive tapes are particularly useful for psoriatic cuts on the palms and soles. In such cases, the tape should be applied across the cuts until they heal.

Occlusive tapes retain sweat, which helps restore moisture to the outer skin layer and prevent scaling. They also protect against abrasion and irritation.

High-Potency Corticosteroid Tapes. Applying a corticosteroid beneath an occlusive tape, or using a tape that already has a potent corticosteroid (Cordran Tape) such as flurandrenolide may be especially beneficial. Studies are showing that high-potency corticosteroid-containing tapes are more effective than using high-potency corticosteroid ointments alone.

However, the tapes are expensive and are associated with a high rate of skin irritation, increased secondary infections, and a greater chance of symptoms relapse after treatment is stopped. Infection risk may be reduced by changing tapes every 12 hours.

The use of corticosteroids under occlusive tapes on large areas of psoriasis also increases the risk for adrenal insufficiency, a sometimes dangerous condition that occurs because the body loses its ability to produce natural steroids. Children are especially vulnerable to this effect.

Other Medications with Occlusive Tapes or Wrappings. The tapes may be used in combination with other medications, such as fluorouracil. Occlusive wrappings are not usually used with tazarotene (Tazorac) and should never be used without a doctor's recommendation.

Numerous topical medications are under investigation. One such medication, tacrolimus (Protopic), is an immunosuppressant that is proving to be useful in allergic skin disorders and is being studied for psoriasis. Studies have been mixed on its benefits, although new delivery methods may make it more effective. It may prove to be safe for sensitive areas, such as the face. Pimecrolimus (Elidel), a similar medication, is also being studied.

Systemic Medications

Systemic treatment uses various medications that affect the whole body, not just the skin. Many systemic drugs used for psoriasis are also used for other severe diseases, including autoimmune diseases (especially rheumatoid arthritis) and cancer.

Systemic treatments for psoriasis may be taken by mouth or injection. The medicines can have significant side effects and are generally reserved for severe psoriasis.

At this time, the only systemic medications specifically approved for psoriasis are:

Cyclosporine
Methotrexate
Retinoids

As with all medications for psoriasis, the patient should use the lowest strength medication first. The primary treatment is called a first-line treatment, the next is known as a second-line treatment, and so on. Combinations of medications are often used.

Methotrexate (Rheumatrex) is a biologic drug that interferes with cell reproduction and has anti-inflammatory properties. It is a first line, or primary, systemic drug used to treat adults with severe psoriasis. The medicine is one of the few systemic drugs proven to help patients with psoriatic arthritis.

The drug is taken weekly, not daily. (Deadly reactions have been reported in people who mistakenly took it once a day.)

Side Effects. Common side effects of methotrexate include:

Anemia
Headache
Mild hair loss
Mouth sores
Nausea
Possible muscle aches
Rash
Vomiting

Many of these side effects are due to folic acid deficiency. Patients should ask their doctor if folic acid supplements (generally recommended at 1 - 5 mg daily) are necessary.

More serious side effects include:

Increased risk for infections, particularly shingles and pneumonia. Methotrexate suppresses the immune system. Patients with active infections should avoid this drug.
Infertility, miscarriage, and birth defects. If used during pregnancy, the drug can cause miscarriages or birth defects in the baby. It may harm fertility in men.
Kidney complications.
Liver damage. In one study, 25% of patients taking methotrexate for 5 years developed scarring of the liver. Those with existing liver problems should not take this medicine, if possible. Regular monitoring for liver toxicity, including blood tests and liver biopsies, is important in patients who take the drug.
Lung disease. This side effect can be sudden and severe, and occurs in up to 5% of people who take methotrexate. Risk factors include diabetes, existing lung inflammation, protein in urine, and use of rheumatoid arthritis drugs called DMARDs.
Lymphomas. A few cases have been reported, which are most likely related to the drug's immune-suppressing (lowering) effects. In most instances, the disease has gone into remission when the drug was stopped. Most studies have found no significant risk for cancers in patients taking methotrexate.
Osteoporosis. Low doses of methotrexate do not appear to have any significant effect on bone loss, but long-term studies are needed to confirm this.
Radiation recall: An uncommon side effect in patients who have previously been burned by radiation cancer treatments or sunburns. In such cases, a flare-up of symptoms occurs in the previously affected skin areas.
Severe anemia. Folic acid supplements can offset this effect.
Toxic effects on bone marrow. This can cause reduced blood cell production.

Despite its side effects, some experts view methotrexate as the best therapy for widespread plaque psoriasis. It may also be effective for some patients with other severe forms of the disease, including psoriatic arthritis, generalized erythrodermic, and pustular psoriasis.

Methotrexate appears to be effective in children, but more safety research is needed.

Drug Interactions. Many drugs interact with methotrexate, occasionally with harmful results. For example, the antibiotic trimethoprim-sulfamethoxazole increases the toxicity of methotrexate.

A serious, harmful reaction can occur if methotrexate is taken with common, nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen, or naproxen. Other NSAIDs, namely ketoprofen, flurbiprofen, and piroxicam, appear to be safe when given with methotrexate and may be used in patients with psoriatic arthritis. Rheumatoid arthritis (RA) patients who take methotrexate often take NSAIDs as well, but methotrexate doses in psoriasis patients are usually much higher than those in RA.

People Who Should Avoid Methotrexate. Pregnant and nursing mothers should never take methotrexate because it increases the risk for severe, even fatal, birth defects and miscarriage. The drug should be discontinued several months before planning a pregnancy. It may also cause temporary impairment of fertility in men.

Persons with the following conditions should also avoid taking methotrexate:

Alcoholism
Anemia or other blood abnormalities
Immunosuppression
Kidney problems
Liver problems (including hepatitis)
Rheumatoid arthritis
Peptic ulcers

Patients at risk for liver complications include those with diabetes and obesity. Anyone with a history of hepatitis should have a liver biopsy before taking methotrexate.

Oral retinoids are vitamin A-related medications taken by mouth. This group of medicines is also a first-line treatment for adults with severe psoriasis. Oral retinoids used for psoriasis include acitretin (Soriatane) and isotretinoin (Accutane).

Acitretin is the retinoid of choice and may be dramatically effective for severe psoriasis, particularly pustular or erythrodermic variants. When used alone, it is much less effective against more common forms, such as plaque or guttate psoriasis. However, combinations with PUVA phototherapy can markedly improve the response even in these patients.

Accutane, more commonly used to treat acne, is far less potent than acitretin, but may still be effective against pustular psoriasis and also be effective with phototherapy.

Oral retinoids help control cell reproduction and have anti-inflammatory properties. They may even improve arthritis that accompanies psoriasis.

Combination therapy. Acitretin may work the best when combined with other treatments, usually topical drugs and especially phototherapy. Combination therapy allows lower doses of oral retinoids to be used, which diminishes many skin and mucous membrane side effects. Acitretin combined with phototherapy has some of the highest clearance rates of any treatment.

Side Effects. All retinoids have the same potentially serious toxicities as do high doses of vitamin A. Side effects include:

Bone and joint pain
Bruising
Depression and possible suicide risk (with isotretinoin)
Eye problems, including blurred vision, cataracts, conjunctivitis, and a sudden deterioration in night vision
Fatigue
Headache
Increased bone growth, particularly in the ankles, pelvic area, and knees
Increased triglyceride levels
Liver damage
Nail problems
Skin and mucous membrane problems, including dry nose, nosebleeds, dry eyes, chapped lips, thinning hair, dry or "sticky" feeling skin, and peeling of the palms and soles

In rare cases, retinoids, particularly isotretinoin, may cause a condition called benign intracranial hypertension (pseudotumor cerebri), which occurs in the brain. Symptoms include headache, nausea, vomiting, and blurred vision. Patients experiencing these symptoms should call a doctor immediately and stop taking the drug.

Oral retinoids should not be taken during pregnancy.

Despite these side effects, oral retinoids remain among the safest systemic therapies for psoriasis. A low-fat diet, aerobic exercise, and fish oil supplements may help reduce the side effects. Certain cholesterol-lowering drugs, including gemfibrozil (Lopid) or certain statins, such as atorvastatin (Lipitor), may help control triglyceride levels.

Maintenance doses should be as low as possible and should be taken every second or third day.

Taking retinoids during pregnancy significantly increases the risk for severe birth defects in the unborn child. Pregnant or nursing women or those planning to become pregnant should not use these drugs. Women of childbearing age who take retinoids should have regular pregnancy tests.

Doctors recommend that acitretin should not be given to any woman who may become pregnant within 3 years of taking it. Drinking alcohol changes acitretin to a retinoid that is stored in fat cells for 3 years. It may have the potential for causing birth defects during that time. It's important to note that cooking products and over-the-counter preparations, such as cough syrup, may contain alcohol and be inadvertently consumed.
Women who are pregnant or plan to become pregnant should not use isotretinoin. As of December 31, 2005, everyone who takes, prescribes, or dispenses the drug must enroll in a national registry called iPLEDGE.

Cyclosporine (Neoral, Sandimmune, SangCya) blocks certain immune factors and may be effective for all forms of psoriasis. It is also a first line, or primary, systemic drug used to treat adults with severe psoriasis. Neoral is the preparation used most often for psoriasis and clears psoriasis in many patients within 8 - 12 weeks.

Side Effects. Cyclosporine has significant side effects if used for a long time, notably kidney problems and non-melanoma skin cancers. It should be reserved for patients who do not respond to phototherapy or less potent systemic medications (for example, methotrexate or acitretin).

Common and temporary side effects include:

Fatigue
Gingivitis
Gout
Hair growth
Headaches
Joint pain
Tremor

More serious complications may include:

Kidney damage
High blood pressure (Some doctors advise treating high blood pressure with calcium channel blockers, since other standard blood pressure drugs may worsen psoriasis. Calcium channel blockers also help prevent kidney problems.)
High cholesterol and lipid levels
High levels of calcium and low levels of magnesium
Increased risk for infections
Liver problems
Lymphomas
Skin cancers (Patients who have taken cyclosporine after PUVA therapy have a higher incidence of squamous cell skin cancer. According to a 2003 study, the risk is six times that of the general population. The risks are highest with long use and previous use of PUVA, methotrexate, or other immunosuppressants.)

To reduce complications of cyclosporine, the dosage is decreased after improvement occurs. Maintenance therapy is usually limited to a year, although some experts believe that a microemulsion form of Neoral (Neoral-Neo) may be safe for up to 2 years. Patients should be monitored regularly for high blood pressure and signs of kidney or liver problems and skin cancers.

Patients Who Should not Use Cyclosporine. Because the drug suppresses the immune system, people with active infections or cancer should avoid it. Patients with uncontrolled high blood pressure and impaired kidney function should also not use this medication. Cyclosporine therapy for children with psoriasis has not been well studied.

Drug and Food Interactions. Cyclosporine interacts with numerous drugs -- both prescription and over-the-counter preparations -- and also grapefruit and grapefruit juice.

Biological response modifiers, sometimes called "biologics," belong to a new class of drugs that are considered the most exciting development in psoriasis treatment. Biologics are genetically engineered drugs that interfere with specific components of the autoimmune response. Because of their precise targets, these drugs do not damage the entire immune system the way that general immunosuppressants do.

Biologics are considered second- or third-line treatments, and may be used alone or sometimes in combination with first-line systemic drugs.

There are different types of biologics used to treat psoriasis:

T cell blockers block immune cells linked to inflammation.
Tumor necrosis factor (TNF) blockers target the chemical messenger TNF-alpha, which is released during the inflammatory response.

Types of T-cell blockers:

Alefacept (Amevive). This drug is approved for the treatment of moderate-to-severe plaque psoriasis. Studies suggest that the drug produces 50 - 75% improvement in symptoms. Alefacept is given in a doctor's office or clinic. Patients receive weekly injections for 12 weeks. Patients need weekly blood tests to make sure T cell levels do not drop too low. Side effects are generally mild and include sore throat, dizziness, and cough. There have been a few reports of serious infection and cancer.
Efalizumab (Raptiva). This drug is approved for the treatment of moderate-to-severe plaque psoriasis. Many patients experience 50 - 75% improvement in symptoms within 4 - 6 weeks of starting the drug. Patients give themselves shots of this drug for 12 weeks. Some clinical trials suggest that a longer course of treatment (24 weeks) may also be safe and effective for patients with chronic plaque psoriasis. Some patients have flare-ups of psoriatic lesions after stopping efalizumab. Very serious, but rare, side effects include hemolytic anemia and antibiotic-resistant infections.

Types of TNF blockers:

Etanercept (Enbrel) is approved for the treatment of psoriatic arthritis and moderate-to-severe plaque psoriasis. The drug is given either alone or in combination with methotrexate. Side effects include infections and lymphoma, a type of cancer. Patients inject themselves under the skin, once or twice a week for 12 weeks. However, a 2007 study published in the Archives of Dermatology found that continuing etanercept after 12 weeks lowers the severity of disease without increasing infections or side effects. Study participants randomly received 50 milligrams of the drug or a placebo biweekly up to 84 weeks. Strongest improvements were noted at 48 weeks among those who received the drug.
Infliximab (Remicade) is approved for the treatment of psoriatic arthritis. Patients receive three intravenous infusions during the first 6 weeks of treatment. After the initial treatment period, patients receive an infusion every 8 weeks. Therapy takes 2 hours and is given in a doctor’s office or clinic. Patients with a history of infection or heart failure should not take this drug. Several studies have shown that symptoms improve significiantly by week 10 in the majority of patients with severe psoriasis who are treated with infliximab.
Adalimumab (Humira) is being tested in clinical trials for treatment of psoriasis and psoriatic arthritis. Results from a Phase III (late-stage) study show that the drug works better than methotrexate in the treatment of moderate-to-severe psoriasis.
Efalizumab (Raptiva) appears to effectively clear or nearly clear moderate-to-severe hand and foot psoriasis after 12 weeks. This type of psoriasis is often very difficult to control and treat.

Interleukins (IL) being investigated as sources or targets of therapy include IL-4, IL-2, IL-8, IL-11, and IL-12. For example, in a 2003 study, 75% of patients with severe psoriasis who were treated with interleukin-4 (rhuIL-4) experienced improvement rates of more than 68%.

A study of 180 patients with moderate-to-severe plaque psoriasis has shown that an investigational medicine called ABT-874 greatly reduced symptoms in most patients. ABT-874 targets proteins that are responsible for psoriasis-related inflammation.

Leflunomide. Leflunomide (Arava) is a disease-modifying antirheumatic drug (DMARD), which blocks autoimmune antibodies and is a powerful anti-inflammatory medication. It is proving to be active against psoriatic arthritis. 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.

Sulfasalazine. Sulfasalazine (Azulfidine) is sometimes used for psoriasis. In one major analysis, sulfasalazine and methotrexate were the only medications proven to help patients with psoriatic arthritis. Many people, however, stop taking the drug because of common side effects that include headaches, gastrointestinal complaints, and rash. Benefits, if any, should be apparent in 4 - 6 weeks.

Immunosuppressants. Some immunosuppressants being studied for psoriasis include tacrolimus (Prograf), pimecrolium, and sirolimus. In one study, for example, tacrolimus showed an 83% reduction in symptoms in patients with psoriasis who used the drug. Studies have been limited, however. Side effects of these medications are similar to those of cyclosporine. Pimecrolimus may specifically target the skin and so have fewer side effects. (Some are also being studied as topical treatments.)

Phototherapy

Phototherapy means to treat with light.

When sunlight penetrates the top layers of the skin, this ultraviolet radiation bombards the DNA inside skin cells and injures it. This can cause wrinkles, aging skin, and skin cancers. However, these same damaging effects can destroy the skin cells that form psoriasis patches.

Phototherapy for psoriasis can be given as ultraviolet A (UVA) light in combination with medications, or as variations of ultraviolet B (UVB) light with or without medications. Not everyone is a candidate. For example, it may not be appropriate for patients who should avoid sunlight or those with very severe psoriasis.

Ultraviolet A (UVA) is a main part of sunlight. UVA phototherapy uses a photosensitizing medication (usually psoralen) in combination with UVA radiation to be effective. A photosensitizing medication makes a person more sensitive to light. Treatment with psoralen and UVA is referred to as PUVA. This approach is very powerful and effective in more than 85% of patients who use it. However, it poses a higher risk for skin cancers than UVB.

PUVA treatments cause inflammation and redness in the skin to develop within 2 - 3 days after treatment. Such damage inhibits skin cell proliferation and reduces psoriasis plaque formation.

Forms of psoralen include methoxsalen, 8-methoxypsoralen (8-MOP), or bergapten (5-MOP). The effectiveness of the treatment is based on a chemical reaction in the skin between the psoralen and light, which creates redness and inflammation that prevents the psoriasis disease process.

People should avoid this treatment if they are taking drugs or have conditions that cause them to be light sensitive. They should also take protective measures before, during, and after each treatment.

Initial PUVA Treatment Phase. The initial phase typically follows these steps:

Psoralen is typically taken by mouth in the form of 8-methoxypsoralen (for example, Oxsoralen) 75 minutes to 2 hours before the treatment starts. Psoralen reaches the skin through the bloodstream, where it increases the skin's sensitivity to UVA radiation.
Topical preparations of psoralen are alternatives to pills. They can be "painted on" or applied to the affected areas by soaking or bathing in a psoralen solution. PUVA-bath therapy may be especially useful for persistent psoriasis on the palms and soles or for patients with liver disease or who get severe nausea from taking the pill form. UVA should be given within 15 minutes of using topical psoralen.
The patient enters and stands in a light box, a unit lined with ultraviolet lamps. The initial UVA exposure time is very short (seconds to several minutes), and then increases to 20 minutes or longer. The amount of time a person is exposed to UVA rays depends on the skin type, with the shortest times recommended for fair-skinned patients.
Treatments may be repeated two or three times a week. They should never be performed more frequently than once every other day, since the full effects of the treatments are not evident for 48 hours.

It takes an average of about 25 PUVA treatments for full effect, but during that period, treatment intensity may vary.

If there is no response after 10 treatments, the doctor may increase the UVA energy.
If there is still no response after 15 treatments, the psoralen dosage may be increased.
If a patient's skin does not improve at all or worsens after these changes, the treatment is temporarily stopped. PUVA may be causing a toxic response in such cases, and, often, the condition gradually improves over the following 2 weeks.
If the skin does not improve over the following 2 weeks, PUVA treatment has failed. If skin improves during this resting period, treatment resumes.

Maintenance Phase. Once the psoriasis has improved by about 95%, the patient may be put on a maintenance schedule. Often only one or two treatments a month are needed, but some people may need more frequent treatments. As maintenance continues and the interval between treatments lengthens, the patients may become more susceptible to tanning and sunburn. They should reduce exposure to natural sunlight during this time.

Success Rates. Nearly 90% of patients achieve marked improvement or clearing within 20 - 30 treatment sessions.

Combinations. Combining acitretin, calcipotriene, methotrexate, or tazarotene gel with PUVA may enhance effectiveness or increase response. In addition, combinations may allow for lower doses of radiation or medications to be used, minimizing side effects. Retinoids may also help protect against skin cancers, while methotrexate may increase the risk. In some cases, patients resistant to PUVA or UVB may respond when the phototherapies are combined.

Side Effects and Complications of PUVA.

The psoralen methoxsalen causes a general ill-feeling and nausea in 20% of patients. Dividing up the dose and taking it in 15-minute intervals with food, or taking ginger 20 minutes before taking the drug, may be helpful.
Skin reactions, including itching, sunburn, and blistering, are common. These can generally be avoided with careful administration of PUVA therapy and protective measures. Antihistamines, baths with special oatmeal preparations (Aveeno), and capsaicin ointment (Zostrix) may be helpful.
After treatment, white spots commonly develop where psoriasis plaques had been, particularly in people with naturally darker skin. If they are troublesome, tanning products may help darken them. Small, dark raised spots called PUVA lentigines may also develop in affected areas with long-term treatment
Prolonged standing may trigger fainting in people with certain heart or blood pressure problems.
People with liver disease should discuss using topical psoralens, since oral forms may have adverse effects on the liver.
UVA penetrates the skin more deeply than UVB, so there is a greater danger of deep skin damage, accelerated skin aging, and skin cancers. Anyone who needs to avoid sunlight should not get this treatment.
The procedure increases the risk for cataracts if eyes are not protected for up to 24 hours after treatment.

Special Warning on PUVA and Skin Cancers. It has been known for some time that PUVA can change DNA and cause genetic mutations. PUVA is known to increase the risk for squamous cell skin cancer and slightly increase the risk for basal cell skin cancer, both of which are nearly always curable. One study reported an increased risk of melanoma. The risk for skin cancers is higher in persons who have:

A family or personal history of skin cancer
Light skin and fair or red hair
Received radiation or x-ray treatments or taken immunosuppressant drugs
Received over 200 PUVA treatments

Discussions are under way about discontinuing PUVA for psoriasis. The arguments generally are as follows:

Opponents of PUVA argue that studies suggest a long-term risk for melanoma, starting about 15 years after treatment, particularly in people who receive more than 250 treatments. In one long-term study, only 9 out of 1,380 patients developed melanoma. However, 7 of these cases occurred in the last 5 years of the study, indicating that the danger persists and more patients in this study are likely to develop this serious skin cancer as time goes on.
Supporters of PUVA argue that it is not yet known if the people who developed melanoma experienced sunburn during the procedures or if they already had risk factors for skin cancers. If so, then properly given treatments could still be considered safe for patients without risk factors. They also argue that PUVA is still the most effective treatment for severe psoriasis, and the alternatives are usually very powerful and relatively new drugs that may have even more serious side effects. Furthermore, the addition of retinoids may protect against skin cancers while proving to be a very effective combination.

Side effects of UVA radiation can be severe. Protective measures are needed during, before, and after treatment. Patients should avoid prolonged exposure to the sun for 24 hours before the oral treatment starts.

Protective Measures During Treatment:

Patients should wear specially designed goggles to protect the eyes from UVA radiation.
Sensitive areas, such as genitals, abdominal skin, and breasts, should be covered until tanning occurs in the exposed areas, after about a third of the treatment period. Note that PUVA is associated with a high risk for genital skin cancers, so male genitals must be covered throughout the process.

The following safety features should be available in the PUVA chamber:

Lamps with protective shields
A viewing window for a health professional to check the patient periodically
A door that can be opened by the patient easily and with little pressure
A timer that terminates the session automatically
An accessible alarm device

Protective Measures After Treatment. The drugs used in PUVA increase susceptibility for a natural sunburn for hours after treatment. The patient should take the following precautions:

Patients should wear UVA absorbing wrap-around sunglasses that are designed to completely block out stray radiation. They should begin wearing them as soon as they take the drug, and for at least 12 hours after the treatment. This is important to prevent a PUVA reaction around the eyes that can cause cataracts. There is no need to wear these glasses after sundown.
For about 8 hours after taking the drug, patients must also avoid exposure to daylight, even if the day is cloudy or exposure occurs through windows.
Patients who must go out should wear heavy opaque clothing (clothes that do not let light through), including hats and gloves.
Patients should apply sunblock over all exposed areas, including the lips. The sunblock should have an SPF (sun protection factor) of more than 15 and include ingredients that block both UVB and UVA radiation.
No patient should spend a long time in sunlight for at least 2 days after the combined treatment.

Ultraviolet B is another main part of sunlight, and is the main cause of sunburn. It generally affects the outer skin layers. UVB radiation reduces the abnormally rapid skin cell growth that occurs with psoriasis.

Types of UVB therapy:

Broadband UVB
Narrowband UVB (NB-UVB)
Laser treatments

Broad spectrum or broad band UVB is radiation in the wavelength of 290 - 350 nanometers, and is the standard UVB phototherapy treatment in the United States. It is not as potent as the treatments that use narrow-band UVB or PUVA, and is not useful for chronic psoriasis.

Broadband UVB may be given with or without medications. When used without medication (known as selective ultraviolet phototherapy), UVB treatment generally is given as follows:

Treatment starts in the doctor's office or another medical setting. Once the disease has stabilized, the patient can obtain a prescription for equipment that can be used at home. Even at home, treatment must always be supervised.
In preparation, the patient fully undresses, although unaffected areas may be covered to avoid overexposure.
The initial session may last as little as a few seconds, depending on whether the patient has a lighter or darker skin, with the lightest skin exposed to the briefest session. The duration increases with each treatment until the skin clears or the patient experiences itching or irritation. It should be noted that the condition may worsen initially.
UVB therapy usually requires about 20 - 40 treatments (about three per week). Full results take about 3 weeks.

Use of Medication. UVB was commonly used with coal tar (the Goeckerman regimen) in past decades, and then with anthralin (the Ingram regimen). Other medications are being studied with some success, and may prove to be tolerated better.

The Goeckerman regimen requires daily treatments for up to 4 weeks. The coal tar or anthralin are applied once or twice each day and then washed off before the procedure. Studies indicate that a low-dose (1%) coal tar preparation is as effective as high dose (6%). Such regimens are unpleasant, but still useful for some patients with severe psoriasis, since they can achieve long-term remission (up to 6 - 12 months).

Some evidence suggests that using a simple emollient (such as Vaseline or mineral oil) that enhances UVB light penetration can be effective. This addition to the treatment increases the risk for sunburns, however, and patients must be careful to avoid sun exposure. Researchers are tring combinations of other topical and oral medications. For example, combining UVB with methotrexate, or retinoids such as a tazarotene gel or oral acitretin, is producing positive results. Combinations with any of these drugs, however, must be supervised carefully to avoid serious reactions.

Side Effects of UVB. The treatment can cause itching and redness. UVB radiation from sunlight is known to increase the risk for skin cancers. There is no strong evidence, however, that UVB treatments pose any risk for skin cancers except on male genitalia. This risk, however, can be significant (4.5%) at high doses.

Narrow band radiation may be safer than other approaches, and some experts now believe it should be the first option for patients with chronic plaque psoriasis.

NB-UVB is used without medications and is very strong. Whether it has any affect, however, on the disease process itself is unclear. The light wavelength is between 310 - 312 nanometers, which, theoretically, is the most beneficial part of sunlight.

Exposure times are shorter but of higher intensity than with broadband UVB. This therapy is probably less likely than PUVA to cause skin cancers.

Clearance of 75% typically occurs after 10 - 12 treatments. NB-UVB treatments performed three times a week achieve results that are equal to twice-weekly PUVA treatments. Weekly NB-UVB treatments are not effective. Studies so far are mixed on whether NB-UVB remission rates are equal to those of PUVA.

Patients prefer NB-UVB over other PUVA treatments because they do not have to wear protective eyewear, take medications, or experience unpleasant side effects, notably nausea. It is also safe for pregnant women and children.

Combinations with topical medications, such as tazarotene or psoralens, may help NB-UVB therapy work better.

Laser UVB Treatment. A recent variation of a device called an excimer laser (Xtrac) delivers a precise UVB wavelength of 308 nanometers. The laser is more effective than narrow-band UVB for localized psoriasis, since it allows very specific areas of skin to be targeted. (Note: The therapy is not suitable for the scalp.) Generally, 8 - 10 treatments given twice a week will clear psoriasis. Remission rates are similar to NB-UVB, but the excimer laser can clear the psoriasis faster and at lower doses. It also spares the healthy skin around it. Blistering is a common side effect. More comparison studies are needed to determine risk and benefits compared to NB-UVB, particularly any long-term risk for skin cancer.

Pulsed-Dye Lasers. Pulsed-dye lasers give off high-intensity yellow light, which destroys the tiny blood vessels that make up psoriatic plaques. This treatment has been used for years to remove birthmarks, such as port wine stains and unsightly blood vessels on the skin. Some studies have reported significant (but not complete) improvement, and remissions that have lasted up to 13 months. Treatment sessions last up to 30 minutes and can feel uncomfortable (similar to being repeatedly snapped with a rubber band). It typically takes up to six sessions to clear the target areas. Bruising is common, and there is a small risk for scarring.

Home tanning devices and tanning salons are not usually recommended, but they may be helpful for patients without access to a medical unit. In a 2003 study, many patients achieved a significant reduction in symptoms when taking acitretin and exposed to a UVB commercial tanning unit (specifically, a Wolff tanning bed).

However, UV outputs can vary widely among tanning beds and salons. Some units emit UVA radiation, which poses a higher risk for skin cancers. Adverse effects of tanning salons that use UVA or UVB radiation are the same as with any UV phototherapies, including a risk for skin cancer.

Managing Psoriasis

Although sunburn carries a risk for skin cancer and can make psoriasis worse, regular exposure to the sun helps clear psoriasis in people with mild-to-moderate conditions. People should cover non-affected areas with clothing or sunscreen and sun bath only until the skin starts to tan.

Vacations in sunny areas, such as Hawaii or the Caribbean, can offer relief. For those who can afford it, a prolonged stay of several weeks at the Dead Sea in Israel has proven to significantly improve or clear 88% of those with psoriasis who go there. The region offers a unique combination of intense but naturally filtered UVA radiation combined with minerals and salts from the sea.

Because of the association between negative emotions and psoriatic flare-ups, relaxation and anti-stress techniques may be helpful. A small 1999 study found that hypnosis aimed at reducing stress may relieve symptoms.

Another study found that some patients with psoriasis had a traumatic or stressful event coincide with the appearance of psoriasis. Talking to a psychiatrist about the issue resulted in significant symptom improvement in 62% of study patients who recalled such an event.

If skin becomes dry and itchy, the patient may try the following:

Soak in a warm bath for about 15 minutes.
Afterward, apply salicylic acid first, which removes scaly skin and may promote the penetration of both moisturizers and topical prescription medications.
Then, apply a thick moisturizer or emollient, such as Vaseline, Cetaphil cream, or Eucerin cream. Lotions are not good enough moisturizers.
Special gloves made of Gore-Tex (DermaPore) may be worn at night over a thick moisturizer cream. These gloves are protective but also allow moisture to escape.

Some experts suggest that many common moisturizers may actually increase water loss in psoriasis, but studies still have to confirm this. In the meantime, if moisturizers help relieve the condition, patients should use them.

Capsaicin (Zostrix) is an ointment prepared from the active ingredient in hot chili peppers. It is used to relieve arthritic pain and may help relieve psoriatic itching. Capsaicin should be handled using a glove and applied to affected areas three or four times daily. The patient will usually have a burning sensation when the drug is first applied, but this sensation lessens with use.

Folic Acid. Patients should be sure they get enough of the B vitamin folate (folic acid). Folate-rich foods include liver, asparagus, fruits, green leafy vegetables, dried beans and peas, orange juice, and yeast. Many types of bread and other commercial grain products now have added folic acid.

Omega-3 Fatty Acids. Omega-3 fatty acids, particularly those found in some fish oil, have anti-inflammatory properties that may benefit some patients with psoriasis and other autoimmune conditions.

Patients with persistent psoriasis may be tempted to try alternative or untested treatments, including herbs and other nontraditional therapies. Researchers at the Medical College of Georgia say green tea slowed the growth of skin cells in animal studies and may one day prove to be useful in treating psoriasis. More research is needed.

Several traditional remedies for psoriasis include various other herbal supplements, but to date no clinical studies have been reported on these substances. No one should use any unproven therapy without consulting a doctor to be sure such treatment is not harmful, and does not interfere with any standard medications they take.

Herbal remedies and dietary supplements are not regulated by the FDA. This means that manufacturers and distributors do not need FDA approval to sell their products. In addition, any substance that affects the body's chemistry can, like any drug, produce side effects that may be harmful. There have been many reported cases of serious and even deadly side effects from herbal products.

The following are special concerns for people taking natural remedies for psoriasis:

Zinc pyrithione is sometimes used, but its effectiveness is doubtful. A number of so-called natural psoriasis products (Skin-Cap, Blue Cap, Miralex) that contain this compound also contain prescription-strength corticosteroids. Such steroids have the same side effects as those in standard psoriasis agents. These products have been banned in the U.S. and Canada, but similar untested medications are available over the Internet.
Gotu Kola (Centella asiatica) is sometimes applied in a cream for psoriasis. The oral form of the herb has serious side effects, however, including increasing the risk for miscarriage in pregnant women.

Outlook

Psoriasis is lifelong and not curable. Although it is also marked by rapid cell growth, psoriasis is neither cancerous nor contagious.

In general, studies report the following features of its course:

The condition almost always relapses. In a few cases, large areas of plaque can persist for years.
Psoriasis nearly always goes into remission, however, often clearing on its own. In one study, 30% of patients reported untreated psoriasis going into remissions that lasted 1 - 54 years.
Psoriasis can improve during pregnancy, especially during the second and third months. Increased levels of estrogen may be responsible for this improvement. Relapse may occur after giving birth.

The emotional and social consequences of psoriasis should not be underestimated.

Many patients suffer severe humiliation and depression if plaques are visible. Some even withdraw from society and become isolated.
Some patients are forced to leave their jobs and go on disability if the condition becomes incapacitating.

Researchers have reported the following:

Surveys of patients with psoriasis report a negative mental and physical impact that is nearly equivalent to that of other major chronic conditions, including cancer, high blood pressure, diabetes, heart disease, and depression.
In one study, 75% of patients reported that psoriasis hurt their confidence.
Another study reported that 8% of people with psoriasis felt their life was not worth living.

Some patients, particularly men, use alcohol and smoking as self-medication to reduce the emotional consequences of psoriasis. In fact, studies have found that people with psoriasis have higher mortality rates, mostly from heavy drinking. Smoking has also been cited as a major risk, particularly for pustular psoriasis. Some experts believe that drinking and smoking may actually cause biological damage that contributes to psoriasis itself.

However, smoking may delay the onset of psoriatic arthritis in some patients, depending on when they started the habit. Psoriatic arthritis tends to occur about a decade after psoriasis develops. The review of 281 psoriasis patients showed that the condition appeared after about 13 years in nonsmokers, compared to 23 years in those who began smoking after the first onset of psoriasis. Psoriatic arthritis appeared after 8 years in people who smoked before developing psoriasis.

Folate Deficiency in Severe Psoriasis. Severe psoriasis can also cause folate deficiency. Folate is a B vitamin that is important for nerve function, preventing birth defects. It also prevents elevations of homocysteine, a factor that may play a critical role in heart disease.

Skin Cancers. In one study, patients with severe psoriasis (who receive medications that affect the whole body) were at higher than normal risk for developing cancers, primarily skin cancers and lymphomas. The risk was not any higher for patients with milder psoriasis. There is some indication, however, that patients with psoriasis have a higher risk for non-melanoma skin cancers regardless of treatments.

Heart Attacks. A study released in October 2006 shows an increased risk of heart attacks in people with psoriasis. The risk was highest in young patients with severe psoriasis.

Other Coexisting Conditions: Studies done in Newfoundland and Germany have also revealed increased cases of diabetes, obesity, arthritis, and cancer in patients with psoriasis. Research is underway to determine if there are genetic links between psoriasis and these conditions.

Increased Risk of Death. Severe psoriasis has been linked to a significant increase in a patient's risk of death. A study of more than 713,000 patients showed that severe psoriasis increased mortality by 50%. Study authors encourage patients to receive comprehensive health examinations to reduce the risk. Study participants were considered to have severe psoriasis if they required systemic treatment.

Impaired Temperature Regulation. Erythrodermic psoriasis, in which psoriasis covers the entire skin, can cause abnormalities in the body's ability to regulate temperature.

Zumbusch Psoriasis. A combination of erythrodermic and pustular psoriasis causes a serious condition called Zumbusch psoriasis:

The condition can develop abruptly.
Symptoms may include fever, chills, weight loss, and muscle weakness.
Patients may develop excessive fluid build-up, protein loss, and electrolyte imbalances. In such cases, hospitalization is required. Fluid and chemical balances must be restored and temperature stabilized as soon as possible.

Zumbusch psoriasis can be life threatening, particularly in the elderly. The condition is very rare in children and, if it occurs, tends to improve more quickly than in adults, possibly even without medication.

Most cases of psoriatic arthritis (PsA) are mild, but complications can occur:

Severe joint deformity and destruction (called arthritis mutilans) may develop, generally in the small joints of the hands and feet. Studies report this happens in about 5 - 16% of patients. Psoriasis patients with other arthritic conditions (osteoarthritis or rheumatoid arthritis) in the joints of the fingers tend to have a higher risk.
People with PsA may have a higher risk for respiratory illnesses.

Some earlier studies indicated that patients with psoriatic arthritis had a shorter lifespan than the general population, but more recent studies found no significant difference.

Resources

www.psoriasis.org -- National Psoriasis Foundation
www.aad.org -- American Academy of Dermatology
www.niams.nih.gov -- National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.clinicaltrials.gov -- Find clinical trials

References

Gelfand JM, Neimann AL, Shin DB, et al. Risk of myocardial infarction in patients with psoriasis. JAMA. 2006 Oct 11;296(14):1735-41.

U.S. Food and Drug Administration. CDER Drug and Biologic Approvals for Calendar Year 2006 -- Updated through August 31, 2006. Last accessed on 15 October, 2006.

FDA Announces Strengthened Risk Management Program to Enhance Safe Use of Isotretinoin (Accutane) for Treating Severe Acne. US Food and Drug Administration. Rockville, MD: National Press Office; August 12, 2005.

Anstey AV and Kragballe K. Retrospective assessment of PASI 50 and PASI 75 attainment with a calcipotriol/betamethasone dipropionate ointment. Int J Dermatol. 2006 Aug;45(:970-5.

National Psoriasis Foundation. About Psoriasis: Statistics. Last Accessed 9 October, 2006.

Antoni CE, Kavanaugh A, Kirkham B, Tutuncu Z, Burmester GR, Schneider U. Sustained benefits of infliximab therapy for dermatologic and articular manifestations of psoriatic arthritis: results from the infliximab multinational psoriatic arthritis controlled trial (IMPACT). Arthritis Rheum. 2005;52(4):1227-1236.

Bowcock AM, Cookson WO. The genetics of psoriasis, psoriatic arthritis and atopic dermatitis. Human Mol Genet. 2004;13 Spec No 1:R43-55.

Feldman SR, Koo JY, Menter A, Bagel J. Decision points for the initiation of systemic treatment for psoriasis. J Am Acad Dermatol. 2005;53(1):101-107.

Murase JE, Chan KK, Garite TJ, Cooper DM, Weinstein GD. Hormonal effect on psoriasis in pregnancy and post partum. Arch Dermatol. 2005;141(5):601-6.

Review Date:
9/19/2007
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Scleroderma

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

In This Report

Highlights
Introduction
Symptoms and Complications...
Causes
Risk Factors
Prognosis
Diagnosis
Treatment
Medications
Other Treatments
Treatment for Raynaud's Phe...
Treatment for Skin Thickeni...
Treatment for Lung Complica...
Treatment for Gastrointesti...
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Symptoms

Because significant depression can affect more than 50% of people with scleroderma, researchers say it may be beneficial for scleroderma patients to get routine screening for depression.

Causes

Researchers have discovered a gene called connective-tissue growth factor (CTGF), which they say is more common in people with systemic scleroderma than in those without the disease.

Prognosis

The prognosis for patients with systemic scleroderma has improved since the 1970s. Ten-year survival rates are up, and deaths from kidney crises have dropped. However, deaths from pulmonary fibrosis have increased during this time period.

Treatment

High-dose immunosuppressant therapy with cyclophosphamide significantly improved skin and overall function in patients with scleroderma.
Evidence shows that intravenous iloprost given in progressively increasing doses can reduce the duration and frequency of Raynaud's phenomenon attacks.
A potential new therapy using PVAC, a substance derived from the bacterium, Mycobacterium vaccae, can improve skin symptoms without causing significant side effects.

Introduction

The name scleroderma comes from the Greek words skleros, which means hard, and derma, which means skin. The disease is categorized as a rheumatologic disorder because it affects the connective tissues in the body.

Scleroderma is a rare disease marked by the following:

Damage to the cells lining the walls of small arteries
An abnormal buildup of tough scar-like tissue in the skin

Patients with scleroderma may develop either a localized or a systemic (body-wide) form of the disease.

Localized scleroderma usually affects only the skin on the hands and face. Its course is very slow, and it rarely, if ever, goes throughout the body (becomes systemic) or causes serious complications. There are two main forms of localized scleroderma: morphea and linear scleroderma.

Morphea Scleroderma. In morphea scleroderma, patches of hard skin form and can last for years. Eventually, however, they may improve or even disappear. There is less than a 1% chance that this disorder will progress to systemic scleroderma.

Linear Scleroderma. Linear scleroderma causes bands of hard skin across the face or on a single arm or leg. Linear scleroderma may also involve muscle or bone. Rarely, if this type of scleroderma affects children or young adults, it may interfere with growth and cause severe deformities in the arms and legs.

Systemic scleroderma is also called systemic sclerosis. This form of the disease may affect the organs of the body, large areas of the skin, or both. This form of scleroderma has two main types: limited and diffuse scleroderma. Both forms are progressive, although most often the course of the disease in both types is slow.

Limited Scleroderma (also called CREST Syndrome). Limited scleroderma is a progressive disorder. It is classified as a systemic disease because its effects can be widespread throughout the body. It generally differs from diffuse scleroderma in the following ways:

Most often the internal organs are not affected.
Patients with scleroderma have a less serious course, unless they develop pulmonary hypertension (a particular danger with the CREST syndrome). Pulmonary hypertension is high blood pressure in the lungs (see the Lung Complications section).

Limited scleroderma is commonly referred to by the acronym CREST, whose letters are the first initials of characteristics that are usually found in this syndrome:

Calcinosis. With this condition, mineral crystal deposits form under the skin, usually around the joints. Skin ulcers filled with a thick white substance may form over the deposits.
Raynaud's phenomenon. In this syndrome, the fingers of both hands are very sensitive to cold, and they remain cold and blue-colored after exposure to low temperatures. This occurs in nearly all cases of scleroderma, both limited and diffuse. It is caused by abnormal changes in small blood vessels. These changes cause the vessels to narrow, and blood flow is temporarily interrupted, usually in the fingers.
Esophageal motility dysfunction. The esophagus carries food from the mouth to the stomach. In esophageal motility dysfunction, the muscles in the esophagus become scarred by scleroderma and do not contract normally. This can cause severe heartburn and other symptoms of gastroesophageal reflux disorder (GERD).
Sclerodactylia (also called acrosclerosis). This is the stiffness and tightening of the skin of the fingers, a classic symptom of scleroderma. Bone loss may occur in the fingers and toes.
Telangiectasia. In this situation, widening of small blood vessels causes numerous flat red marks to form on the hands, face, and tongue.

Click the icon to see an image of symptoms that are known as CREST.

In general, people with limited scleroderma develop Raynaud's phenomenon long before they develop any of the other symptoms. One or more of the CREST conditions can also occur in other forms of scleroderma.

Diffuse Scleroderma. Diffuse scleroderma, the other systemic sclerosis, has the following characteristics:

It can affect wide areas of the skin, connective tissue, and other organs.
It can have a very slow course, but it also may start quickly and be accompanied by swelling of the whole hand. If it gets worse quickly early on, the condition can affect internal organs and become very severe -- even life threatening.
Diffuse scleroderma can overlap with other autoimmune diseases, including systemic lupus erythematosus and polymyositis. In such cases, the disorder is referred to as mixed connective disease.

Click the icon to see an image of systemic lupus erythematosus.

Symptoms and Complications

Raynaud's phenomenon is often the first sign of the scleroderma disease process. With this condition, small blood vessels narrow in the fingers, toes, ears, and even the nose.

Attacks of Raynaud's phenomenon can occur several times a day, and are often brought on or worsened by cold. Warmth relieves these attacks. In severe cases, attacks can develop regardless of the temperature. Severe cases may also cause open sores or damage to the skin and bones, if the circulation is cut off for too long. Stress also can trigger the syndrome.

Typically, the fingers go through three color changes:

First, they become very pale.
As the blood flow is cut off, they turn a bluish color, usually in the top two sections of the second and third fingers.
Finally, when blood flow returns, the fingers become red.

Tingling and pain can occur in the affected regions.

Click the icon to see an image of Raynaud's phenomenon.

Raynaud's is very common and occurs in 3 - 5% of the general population. It's important to note that more than 80% of patients with Raynaud's phenomenon do not have scleroderma, lupus, rheumatoid arthritis, or other more serious illnesses. Raynaud's is more likely to be a symptom of scleroderma or some other connective tissue disease if it develops after age 30, if it is severe, and if it is accompanied by other symptoms (such as skin changes and arthritis).

Course of Typical Skin Changes. The primary symptoms of scleroderma occur in the skin. They often take the following course:

Typically, pitted scars appear first on the hands. The skin begins to thicken and harden on the hands, feet, and face. The fingers may swell. This condition is called sclerodactylia or acrosclerosis. Patients with diffuse scleroderma may have swelling of the whole hand before the skin significantly thickens.
Thickened or hardened patches may also develop on other areas of the body. (Their appearance on the trunk and near the elbows or knees tends to be a sign of a more severe condition.)
For the first 2 or 3 years, the skin continues to thicken and feel puffy.
This process then stops, and can even get better. The skin may soften.
As the disease progresses further, however, the skin loses its ability to stretch, and becomes shiny as it tightens across the underlying bone, particularly in the fingers, toes, and around the mouth.
Eventually, in severe cases, the fingers may lose the ability to move, and can be difficult to bend. The hands and feet may curl from the tightness of the skin. It may be difficult to open the mouth widely.

Click the icon to see an image of sclerodactylia.

Other Skin Changes. The following skin symptoms may also occur:

Flat red marks, known as telangiectasis, may appear in various locations, usually the face, palms, lips, or the inside of the mouth.

Click the icon to see an image of telangiectasia.

In calcinosis, small white lumps form beneath the skin, sometimes oozing a white substance that looks like toothpaste. Calcinosis can lead to infections.
Small blood vessels at the base of the fingernails may be lost in some places, and may widen in other places. This is an indication that internal organs might be involved.
The entire surface of the skin may get darker over time, and contain patches of abnormally pale skin.
Hair loss may occur.
About 1% of patients have Sjogren syndrome, a group of symptoms that include dry eyes and dry mucus membranes (such as those in the mouth).
Inside the mouth, scleroderma can also cause changes that impair gum healing.

Changes in bones, joints, and muscles can cause the following symptoms:

Mild arthritis. The condition is usually distributed equally on both sides of the body.
Bone loss in the fingers. The destruction is not as severe as it is in rheumatoid arthritis, although the fingers may shorten over time.
Trouble bending the fingers, if the disease has affected the tendons and joints.
Muscle weakness may occur, especially near the shoulder and hip.

Complications in the Upper Digestive Tract.

Esophageal motility disorder develops when scarring in the muscles of the esophagus causes them to lose the ability to contract normally, resulting in trouble swallowing, heartburn, and gastroesophageal reflux (also known as GERD). Some experts believe that patients with severe GERD may breathe in microscopic amounts of stomach acid, which in turn may be a major cause of lung scarring.
About 80% of patients also experience impaired stomach activity. A delay in stomach emptying is very common.
Some patients develop "watermelon stomach" (medically referred to as CAVE syndrome), in which the stomach develops red-streaked areas from widened blood vessels. This causes a slow bleeding that can lead to anemia (low red blood cell counts) over time.
There may be a higher risk for stomach cancer.
Problems with movement of the food through the intestines (motility) also develop. Patients may experience an increase in bacteria and have trouble absorbing nutrients from foods through the intestines.

Complications in the Lower Digestive Tract. Complications in the lower tract are uncommon. If they do occur, they can include the following:

Scarring can cause blockages and constipation. In rare cases, constipation can become so severe that the bowel develops holes or tears, which can be life threatening.
Scarring can also damage the absorption of fats in the intestines. This can lead to an increase in the number of bacteria, which causes watery diarrhea.
Fecal incontinence (the inability to control bowel movements) may be more common than studies indicate, because patients are reluctant to report it.

Many patients, however, have few or even no lower gastrointestinal symptoms.

In severe cases, the lungs may be affected, causing shortness of breath or difficulty in taking deep breaths. Shortness of breath may be a symptom of pulmonary hypertension, an uncommon but life-threatening complication of systemic scleroderma.

Click the icon to see an image of the respiratory system.

Lung problems are usually the most serious complications of systemic scleroderma. They are now the leading cause of death in scleroderma patients. Two major lung conditions associated with scleroderma, pulmonary fibrosis and pulmonary hypertension, can occur either together or independently.

Interstitial Pulmonary Fibrosis. Scleroderma involving the lung causes scarring (pulmonary fibrosis). Pulmonary fibrosis occurs in about 70% of scleroderma patients, although the progression is very slow and patients have a wide range of symptoms:

Some patients may not experience any symptoms.
When pulmonary fibrosis progresses, patients develop a dry cough, shortness of breath, and reduced ability to exercise.
Severe pulmonary fibrosis occurs in about 16% of patients with diffuse scleroderma. About half of these patients experience the most profound changes within the first 3 years. In such cases, lung function worsens rapidly over that period, and then the progression slows down.

This condition also places the patient at higher risk for lung cancer. One study suggested that interstitial lung disease may be due to severe dysfunction in the esophagus, which causes patients to breathe in tiny amounts of stomach acid.

The most important indication of future worsening in the lungs appears to be inflammation in the small airways (alveolitis). Doctors detect alveolitis by using a lung test called bronchoalveolar lavage.

Pulmonary hypertension is the narrowing of the pulmonary arteries in the lung. The narrowing of the arteries creates resistance and increases the workload of the heart. The heart becomes enlarged from pumping blood against the resistance. Some symptoms include chest pain, weakness, shortness of breath, and fatigue. The goal of treatment is to control the symptoms, although the disease usually develops into congestive heart failure.

Pulmonary Hypertension. The primary symptom of pulmonary hypertension is shortness of breath, which becomes severe over time.

Pulmonary hypertension can develop in one of two ways:

As a complication of pulmonary fibrosis
As a direct outcome of the scleroderma process itself. In this case, it is most likely to develop in patients with limited scleroderma after many years.

Click the icon to see an image of cor pulmonale.

Signs of kidney problems, such as increased levels of protein in the urine and mild high blood pressure (hypertension), are common in scleroderma. As with pulmonary hypertension, the degree of severity depends on whether the kidney problems are acute or chronic.

Slow Progression. The typical course of kidney involvement in scleroderma is a slow progression that may produce some damage but does not often lead to kidney failure.

Renal Crisis. The most serious kidney complication in scleroderma is renal crisis. It is a rare event that occurs in a small number of patients with diffuse scleroderma, most often early in the course of the disease. This syndrome includes a life-threatening condition called malignant hypertension, a sudden increase in blood pressure that can cause rapid kidney failure. This condition may be fatal. However, if the condition is successfully treated, it rarely recurs.

Until recently, renal crisis was the most common cause of death in scleroderma. Aggressive treatment with drugs that lower blood pressure, particularly those known as ACE inhibitors, is proving to be successful in reducing this risk.

Many patients with even limited scleroderma have some sort of functional heart problem, although severe complications are uncommon and occur in only about 15% of patients with diffuse scleroderma. As with other serious organ complications, they are more likely to occur within 3 years after the disease begins.

Fibrosis of the Heart. The most direct effect of scleroderma on the heart is fibrosis (scarring). It may be very mild or it can cause pain, low blood pressure, or other complications. By damaging muscle tissue, the scarring increases the risk for heart rhythm problems, problems in electrical conduction, and heart failure. The membrane around the heart can become inflamed, causing a condition called pericarditis.

Click the icon to see an image of pericarditis.

Pulmonary hypertension and hypertension associated with kidney problems in scleroderma can also affect the heart.

Other complications of scleroderma may include the following:

Patients with CREST may be at increased risk for biliary cirrhosis, an inflammatory autoimmune disorder of the liver.
Nerve damage may occur in the extremities (legs and feet, arms and fingers), causing numbness and pain. This damage can progressively worsen and lead to severe open sores (ulcerations), particularly in the hands. The feet are less often affected, but when they are, the disease tends to affect the joints and cause pain.
Bone loss (osteoporosis) can occur because of impaired blood flow.
About half of patients develop underactive thyroid gland (hypothyroidism).

Click the icon to see an image of hypothyroidism.

Impotence, usually due to scarring of the penis, may be one of the first complications of the disease in men.
Some studies using imaging techniques have found changes in brain tissue, but because the brain has little connective tissue, scleroderma appears to have little effect on mental functioning, except possibly in the late stages of severe disease.
Systemic scleroderma does not generally affect fertility in women. Pregnant women with scleroderma, however, have a slightly increased risk of premature birth and low-birth-weight babies. Although they can carry a baby to term, because complications such as kidney crisis can occur with the disease, pregnant women with scleroderma need to be monitored closely in a high-risk obstetric facility.
More than half of scleroderma patients are likely to experience significant depression. Researchers say it may be beneficial for scleroderma patients to be routinely screened for depression.

Causes

Most likely this disease is caused by a number of inherited (genetic) abnormalities, which are triggered by environmental factors.

Researchers have found a gene, called connective-tissue growth factor (CTGF), which they say regulates the production of a protein that may be a key to systemic scleroderma. This gene is more common in scleroderma patients than in people without the condition. However, researchers say the gene is just one factor that affects the development of the disease.

Research published in 2005 also showed that the growth of new blood vessels is abnormal in people with scleroderma, particularly those whose disease affects the blood vessels in the lungs. Researchers now know that cells in the blood vessels and skin of scleroderma patients make too much of certain chemicals, and not enough of others. Studies revealed that the cause is an alteration in the hereditary material, DNA. These changes "turn off" some genes and "turn up" others. It is hoped that certain drugs, some of which are already used in cancer treatments, can some day be used to stop these DNA changes.

The disease process leading to scleroderma appears to occur as an autoimmune response, in which an abnormal immune system attacks the body itself. In scleroderma, this response produces swelling (inflammation) and too much production of collagen. Collagen is the tough protein that helps build connective tissues such as tendons, bones, and ligaments. Collagen also helps scar tissue form. When normal tissue from skin, lungs, the esophagus, blood vessels, and other organs is replaced by this type of abnormal tissue, none of these body parts work as well, and many of the symptoms previously described occur.

Antigens are large molecules (usually proteins) on the surface of many cells -- both human cells, and cells of viruses, fungi, bacteria, and some non-living substances such as toxins, chemicals, drugs, and foreign particles. When the immune system recognizes an antigen as being foreign (not part of the human body), it starts offensive and defensive actions against them by producing antibodies and other chemicals such as cytokines that destroy any cells in the area.

Much of this activity is directed by T cells, which are categorized as killer T cells or helper T cells (TH cells).

The actions of the helper T cells are of special interest in scleroderma. For some unknown reason, the T cells become overactive in scleroderma and mistake the body's own collagen as a foreign antigen. This triggers a series of immune responses to destroy the collagen. When the body creates antibodies against itself in this way, it is called an autoimmune response.

Cytokines and the Inflammatory Response. Helper T cells also release powerful immune factors called cytokines. In small amounts, cytokines are necessary for healing. If overproduced, however, they can cause serious damage, including inflammation and injury.

Neutrophils. Cytokines attract to the scene large numbers of other white blood cells known as neutrophils. Neutrophils help activate chemicals known as leukotrienes. Scleroderma patients have high levels of specific leukotrienes that may contribute specifically to lung disease in scleroderma.

A process called microchimerism has been proposed as a cause of scleroderma. The theory arose from the fact that scleroderma occurs mostly in women, and its symptoms resemble those of graft-versus-host disease (GVHD). GVHD occurs in bone marrow transplant patients who have received cells from another person. It happens when the transplanted donor immune cells launch an attack against the patient's cells.

Chimerism occurs when cells from two different individuals exist in the same body. When there is a low number of cells of one body in another, the condition is referred to as microchimerism.

However, if microchimerism plays a role, it most likely does so only in a subset of patients.

It is still not clear why the immune system responds abnormally in people with scleroderma. Some experts believe that environmental factors, such as a virus or a chemical, may trigger the response in individuals with a genetic vulnerability.

Oxygen-Free Radicals and Abnormal Metal Accumulation. One focus for researchers investigating scleroderma involves an observation that, as blood vessels narrow and become inflamed, destructive particles known as oxygen-free radicals are produced. Oxygen-free radicals are made by natural processes in the body. They cause harm by setting off a chemical chain reaction, which can damage any type of cell in the body. Environmental toxins, infections, and other factors may cause very high amounts of these oxygen-free radicals to build up in the body.

Chemicals. Occupational exposure to certain chemicals can cause blood vessel constriction and attacks of Raynaud's phenomenon. Despite the fact that women are at higher overall risk for scleroderma, among people who are exposed to solvents at work, men face a higher risk for the disease. However, no specific work-related factors have been proven to cause the disorder.

It is nearly impossible to determine whether specific chemicals may actually cause systemic scleroderma, primarily because few people develop the disease, even though many people are exposed to such chemicals. In addition, research has been unable to consistently repeat studies that have reported links with chemicals.

Studies have found, however, that certain industrial toxins are significantly associated with severe lung problems in people with scleroderma. The toxins most likely to be associated with severe disease include epoxy resins, white spirit, solvents, and silica mixed with welding fumes.

Repetitive Stress Injuries. Raynaud's phenomenon and symptoms of scleroderma have been associated with jobs that require intense repetitive hand and arm movements, such as working jackhammers or other vibrating tools. However, many workers are involved in such occupations, yet scleroderma is still very rare, even in this group. If there is a link, the disease would most likely develop in individuals with genetic factors that make them susceptible to the disease in the first place.

Radiation. Radiation therapy has been reported to cause local patches of scleroderma (morphea) or worsen preexisting scleroderma in a few patients. In some cases, scleroderma may occur years after radiation treatments.

Researchers think that infections may play a role in triggering the process leading to some cases of scleroderma. There is no real evidence of any single type of bacteria or other organism that might be responsible, although some are of particular interest.

Some studies reported an association between Borrelia burgdorferi, the cause of Lyme disease, and some cases of morphea (localized scleroderma). However, the evidence is weak. If there is a connection, it is possibly limited to a specific type of the bacteria in Europe and Asia. There is no connection between systemic scleroderma and Lyme disease.

Other infections associated with scleroderma include parvovirus and hepatitis C. However, there is no evidence of a cause-and-effect relationship.

Risk Factors

Scleroderma is uncommon. It afflicts about 300,000 Americans, but only about 49,000 have the systemic form of the disease. The cause of scleroderma has not been determined, and there are few specific risk factors. The incidence tends to be higher in certain groups, however.

Age. Systemic scleroderma usually develops between the ages of 35 and 55. Localized scleroderma is more common in children than adults, but is extremely rare even in the young age group. It occurs in between 0.2 and 0.4 per 100,000 people. Systemic scleroderma in children is even more rare.

Gender. The incidence of scleroderma is three to eight times higher in women than in men. This may reflect a different cause of the disease in these two genders. (It should be noted that pregnancy itself is not a risk factor for scleroderma.)

Family History. A family history is the strongest risk factor for scleroderma, but even among family members, the risk is very low (less than 1%).

Genetics. Genetic factors appear to play a role in triggering the disease, but most cases are unlikely to be inherited. Preliminary research suggests that patients with certain gene variations may be more susceptible to scleroderma than those who do not carry these variations.

Ethnicity. Limited data on risk by ethnic group in the United States suggests that the risk from highest to lowest is the following: Choctaw Native Americans (highest), African-Americans, Hispanics, Caucasians, Japanese Americans.

African-Americans have a higher rate of diffuse scleroderma, lung involvement, and a worse prognosis than Caucasians. Other studies also found lower survival rates among Japanese Americans.

Genetic factors affect population groups differently. Studies are finding that ethnic groups differ in the number of specific scleroderma-related antibodies they produce. Caucasians, for instance, have a higher rate of anti-centromere antibodies, which are associated with limited disease, while African-American patients have higher rates of autoantibodies and genetic factors that are associated with a more severe condition.

Geography. There appears to be certain geographic clusters of scleroderma, or specific types of scleroderma related to location. This may suggest an infectious or genetic factor at work, but the reasons are largely unknown. The following are some examples:

Studies reported significantly higher-than-average scleroderma mortality rates in male patients (both African-American and Caucasian) who live in two specific regions of the Southeast: one cluster around Coffee, Tennessee, and two others near Northampton, North Carolina.
A cluster of scleroderma cases has been observed in South Boston, Massachusetts.

Prognosis

At this time there is no cure for scleroderma and no treatment to change its course, but outlook varies widely. Many patients, even those with systemic scleroderma, can expect a normal lifespan.

General Outlook of Localized Scleroderma. Localized scleroderma nearly always carries a good prognosis and a normal life span. Even localized scleroderma, however, can cause some severe effects in children, including impaired growth, limb imbalance, and problems in flexing and bending muscles.

General Outlook of Systemic Scleroderma. The outlook for patients with systemic scleroderma has generally improved over the years. Ten-year survival rates rose from 54% in 1972 to 66% in 2001.

The causes of death related to systemic scleroderma also have changed. The proportion of deaths from kidney crises dropped significantly, from 42% to just 6% in that time period; however, the proportion of deaths from pulmonary fibrosis increased from 6% to 33%. Today, lung complications account for 60% of scleroderma-related deaths.

Limited Scleroderma. Patients with limited CREST scleroderma can usually expect a favorable outlook and normal lifespan if the disease affects only the hands and face. The course of this type of scleroderma still tends to be slowly progressive and, in some cases, may affect internal organs.
Diffuse Scleroderma. The severity of diffuse scleroderma varies widely, and it is very difficult to predict its course. It generally follows one of two paths: If it is acute or rapidly progressing, it may be a life-threatening condition that affects internal organs. The most critical period for rapid progression is usually within the first 2 - 5 years of the start of the disease. In the absence of rapid progression, or if the patient survives the initial acute progression, the disease tends to progress very slowly. The more severe the condition of the skin is at the start of the disease, the poorer the survival rates.

Many patients with systemic scleroderma experience a plateau in which the condition stabilizes. This plateau is followed by a period of improvement and skin softening. No one knows why this occurs, and it can happen regardless of treatment. In one study, patients with systemic scleroderma who experienced such improvements also had better survival rates (80% at 10 years) than those whose skin did not improve (60% 10-year survival rate).

The many complications of scleroderma can have a major impact on a person's sense of well-being. Patients are greatly concerned about changes in their appearance, particularly those changes caused by tightening of the facial skin. A 2002 study on scleroderma patients reported that 63% experienced at least mild pain, and half of them had some degree of depression. Depression had the greatest impact, even more than pain, in reducing patients' ability to function socially.

Diagnosis

There are no specific tests for scleroderma. The doctor may suspect scleroderma after taking a history of the symptoms and performing a physical examination. As part of this examination, the doctor does the following:

Checks the skin for thickened and hardened areas. The major signs of scleroderma are hardening and thickening of the skin in any areas on the fingers and toes.
Presses affected tendons and joints to detect crackling or grating sensations, which can indicate changes related to scleroderma beneath the skin.
Examines the fingernails underneath a microscope. The doctor may find changes in capillaries that are characteristic of scleroderma and mixed connective tissue disease.

Scientists recently found that antibodies that are often found in patients with scleroderma and systemic lupus erythematosus (SLE) bind to different parts of a single protein. Scientists hope this finding will one day lead to a specific diagnostic test for scleroderma.

Tests may be done to detect immune factors called antinuclear antibodies (ANAs). Detecting specific types of ANAs may help diagnose scleroderma. ANA subtypes include the following:

Rheumatoid factor, anti-single-stranded DNA, and antihistone antibodies are autoantibodies associated with scleroderma, but they are also common in other autoimmune disorders, such as rheumatoid arthritis and systemic lupus erythematosus. Some ANAs attack RNA or DNA, the genetic material in cells.
Anti-RNA polymerase III, anti-topoisomerase I (also called anti-DNA topo 1) and anti-centromere antibodies (ACA) are three other autoantibodies. Most patients with systemic scleroderma (but not localized scleroderma) have one or more of these autoantibodies. They do not appear at the same time, and seem to relate to different phases of the disease process. For example, anti-DNA topo 1 often occurs with diffuse skin scleroderma and lung complications. Anti-centromere antibodies usually occur with a less severe form of the disease.
Higher-than-normal levels of autoantibodies to fibrillin 1, a protein found in muscle and other connective tissues, is more common in patients with both systemic and localized scleroderma. This autoantibody in localized scleroderma is more common in some ethnic groups (such as Japanese and Native Americans) than in others (Caucasians). It is not found in other autoimmune diseases.

These antibodies are also found in other rheumatologic disorders, so detecting them does not necessarily prove that a patient has scleroderma. At the same time, studies have found that specific antibodies are associated with specific aspects of the disease. Therefore, identifying their presence could help diagnose, treat, and monitor people with scleroderma. Here are a few examples:

Anti-U1-RNP and anti U3-RNP are associated with muscle inflammation.
ACA is commonly associated with pulmonary hypertension and vascular disease.
TOPO is associated with pulmonary fibrosis.
RNA Polymerase III (Pol 3) is rarely linked to severe interstitial fibrosis, although this autoantibody is strongly present in patients with kidney crisis.
Patients with diffuse scleroderma who have Pol 3 have the best survival rate.

Diagnosing Lung Complications. Changes in the lungs may occur early in scleroderma lung disease, and prompt treatment is very important to prevent complications. For this reason, once a diagnosis is made, the doctor will check for lung changes in the following ways:

Listen to the lungs through a stethoscope. Rales, a crackling sound at the base of the lungs as the patient breathes in, is a sign of pulmonary fibrosis, even if breath function is normal.
Perform respiratory function tests to determine lung capacity.
Take a chest x-ray (however, x-rays do not always find lung disease, especially in children).
Have patients inhale nitric oxide to test the ability of blood vessels to open.
Perform more extensive tests, such as high-resolution computed tomography (CT) scans and bronchoalveolar lavage, if the doctor suspects severe lung scarring.

Newer tests showing promise in diagnosing lung complications include:

The induced sputum test, which looks at cells taken from coughed-up phlegm
Another test that uses the inhaled chemical, technetium-labeled diethylenetriamine pentaacetate (99mTC-DTPA), to detect lung damage

Diagnosing Heart Complications. Patients with suspected heart complications should have the following tests:

Electrocardiography (ECG): A test of the heart's electrical activity
Echocardiography: A look at the beating heart through the use of sound waves
Radionucleotide ventriculography: An evaluation of the working heart using a radioactive dye

Advanced imaging techniques, which provide a more detailed picture of the heart, may also be useful to determine the extent of heart complications in scleroderma patients.

Diagnosing Pulmonary Hypertension. Echocardiography is a noninvasive imaging technique for detecting pulmonary hypertension, a common and life-threatening complication of scleroderma. (Neither materials nor equipment are put into the body.) To confirm the diagnosis, doctors sometimes use an invasive procedure called right-heart catheterization. Right-heart catheterization involves the passage of a catheter (a thin flexible tube) into the right side of the heart to get diagnostic information about the heart.

Diagnosing Gastrointestinal (Digestive) Complications. Endoscopy may detect gastrointestinal problems. Endoscopy is an invasive procedure in which a tube is inserted down the esophagus. The tube contains a small camera and other instruments. Another diagnostic test is manometry, which measures the pressure that the muscles in the esophagus apply.

Electrogastrography (EGG) measures the electrical activity in muscles in the stomach, and may be an effective method for detecting stomach problems.

Diagnosing problems in growth of blood vessels. Capillaroscopy is the microscopic examination of blood vessels under the skin. It is now considered a useful tool for identifying problems with the growth of blood vessels, because more than 95% of patients will have some capillary abnormalities. Such problems can show the severity and progression of scleroderma. In a technique called nailfold capillaroscopy, the doctor places a drop of oil on the nailfolds (the skin at the base of the fingernails), and then looks at the nailfold under a microscope for signs of changes in the capillaries that may indicate a connective tissue disease such as scleroderma.

Click the icon to see an image about endoscopy.

Other Autoimmune and Connective Tissue Disorders. Several other autoimmune conditions that affect connective tissue can strongly resemble, or occur together with, scleroderma. They include the following:

Rheumatoid arthritis
Systemic lupus erythematosus
Polymyositis

Symptoms of such diseases may also include fever, arthritis, muscle aches, rash, and lung and heart problems.

Eosinophilic Fasciitis. Eosinophilic fasciitis is a muscle disorder that is known to occur after intense hard work. It can cause symptoms similar to scleroderma, including pain, swelling, and tenderness in the hands and feet, as well as skin thickening. The disorder can be ruled out with blood tests.

Although Raynaud's phenomenon occurs in most scleroderma patients, over 80% of the cases of Raynaud's phenomenon are harmless. In one study, only 12% of Raynaud's cases were associated with some other condition, and few of those were scleroderma. The following are other problems that might accompany or cause Raynaud's phenomenon:

Other autoimmune connective tissue diseases
Diabetes (patients with diabetes may develop Raynaud's phenomenon and other scleroderma-like symptoms)
Certain drugs, including bleomycin, ergot derivatives (used for migraines), and methysergide
Hereditary hemorrhagic telangiectasia (a very rare condition that is very similar to CREST syndrome)

Click the icon to see an image of a keloid.

Repetitive stress injuries (particularly from vibrating tools)
Hypothyroidism

Treatment

Scleroderma treatments vary depending on these variables:

Is it local or systemic, and if systemic, is it limited or diffuse?
If the disease is systemic, what organs, if any, are involved?

Although there is still no treatment for the underlying process of scleroderma, specific drugs and treatments help combat the various mechanisms and consequences of the disease.

Some medications keep blood vessels open (prostacylins, endothelin receptor antagonists, ACE inhibitors, phosphodiesterase 5 inhibitors, and others) and are used to treat Raynaud's phenomenon, heart and kidney problems, and pulmonary hypertension.
Other drugs reduce inflammation and block damaging immune factors. These treatments, which include cyclophosphamide, penicillamine, bone marrow transplantation, and others may be helpful for improving skin thickness and reducing scarring, even in the lungs.
Doctors use other treatments for specific complications, such as proton pump inhibitors and pro-kinetic agents for gastrointestinal problems, or light treatments for skin thickening.
Various investigative approaches exist, including stem-cell transplants.

Patients should receive treatments for specific complications as early as possible in the course of the disease, to reduce progression before irreversible hardening of tissues occurs.

There is no cure for scleroderma. Many drugs that are useful for other autoimmune inflammatory disorders have not proven to be very effective for scleroderma. Experimental work is ongoing to develop procedures or to find drugs that can treat the underlying processes that cause damage. Developing effective treatments for scleroderma is very problematic, however, for the following reasons:

The course of scleroderma is hard to predict, making it one of the most difficult rheumatic diseases to treat. It also makes drug development complicated.
The disease, when advanced, affects many organs. Designing treatment strategies that will improve symptoms in some organs without affecting other organs is very difficult.
The disease is so uncommon that there are few patients available for clinical trials. Studies, then, are very small, sometimes having only four or five patients. It is very difficult to design studies of this size that can provide strong evidence on treatment effects. Drugs that seem promising on small groups of patients often fail to show effectiveness on larger groups.

The disease can evolve slowly over time with few symptoms, or progress rapidly and become very severe. The patient, then, must live with considerable uncertainty and emotional stress. Support associations, non-medical aids to help relieve symptoms, and other lifestyle measures can be extremely important and helpful.

Medications

Calcium-channel blockers are the standard drugs to open the blood vessels, and may be used for pulmonary artery hypertension and Raynaud's phenomenon. Short- or sustained-release nifedipine (Adalat, Procardia) is the gold standard. Other drugs used include diltiazem (Cardizem, Dilacor), and the newer dihydropyridines (felodipine, amlodipine, and isradipine). Side effects vary among different medications, and may include fluid buildup in the feet, constipation, fatigue, gingivitis, impotence, flushing, and allergic symptoms. Calcium channel blockers should not be taken with grapefruit juice, as it appears to boost the effects of these drugs. [The medications listed below are also discussed under many of the sections covering treatment complications.]

Nitrates

Nitrates relax smooth muscles and open arteries, and are therefore sometimes used for the short-term management of Raynaud's phenomenon. They are available in topical and oral (by mouth) forms. Side effects of nitrates include headaches, dizziness, nausea, blurred vision, fast heartbeat, and sweating. Lying down with the legs elevated can relieve low blood pressure and dizziness. Alcohol, beta blockers, calcium-channel blockers, and certain antidepressants can significantly worsen these side effects. Withdrawal from nitrates should be gradual. Some severe reactions have occurred when people have stopped taking these drugs too quickly.

Prostacyclins (also called Prostaglandins)

Prostacyclins open blood vessels and also have anti-blood-clotting properties. One or all of these drugs is used to treat pulmonary artery hypertension and Raynaud's phenomenon. Several prostacyclins are being used for scleroderma, although none have been approved specifically for the condition. Promising prostacyclins or similar drugs include iloprost (Ventavis), alprostadil (prostaglandin E1), epoprostenol (Flolan), and treprostinil (Remodulin).

Endothelin Receptor Antagonists

Bosentan (Tracleer) is a drug taken by mouth. It is called an endothelin receptor antagonist. It controls endothelin, a powerful molecule that causes blood vessels to narrow. It improves blood flow and is becoming important for treating patients with scleroderma, especially for preventing finger ulcers and improving hand function. This drug is also a treatment option for pulmonary hypertension.

The most effective approach at this time for preventing kidney (renal) crises is to start aggressive blood pressure-lowering treatment before blood tests show kidney damage has occurred.

Angiotensin Converting Enzyme (ACE) Inhibitors. Many medications are available for controlling blood pressure, but ACE inhibitors appear to be the most effective for scleroderma patients, because of their protective actions in the kidney. These drugs are also used to treat patients with evidence of kidney damage, whether or not they have high blood pressure. ACE inhibitors include captopril (Capoten), enalapril (Vasotec), quinapril (Accupril), benazepril, and lisinopril (Prinivil, Zestril). Side effects are uncommon, but may include an irritating cough, large drops in blood pressure, and allergic reactions. The drug picotamide can help reduce the frequency of coughs.

Angiotensin II Receptor Antagonists. Angiotensin II receptor antagonists (losartan, candesartan cilexetil, and valsartan) have benefits similar to ACE inhibitors and may have fewer or less severe side effects, including coughing. They may also have positive effects on blood vessels. Small studies showing improvement in Raynaud's phenomenon warrant further research.

One major approach to scleroderma is to use treatments that suppress the immune system, and therefore reduce the activity of the harmful processes that lead to scleroderma. Such treatments are used effectively in other autoimmune diseases. Their use in scleroderma varies, depending on the location and severity of the disease process.

Cyclophosphamide (Cytoxan). Cyclophosphamide is the most important immunosuppressant currently used for scleroderma. This drug can be taken through a vein (intravenous) or by mouth. It blocks some of the destructive actions of scleroderma in the lungs. Intravenous cyclophosphamide can be life-saving for patients with pneumonia caused by interstitial lung disease. Side effects of this drug include hair loss, infection, and bleeding into the urinary tract. To date, no other immunosuppressive drugs have shown any significant benefits for scleroderma.

Other drugs used to suppress the immune system may be useful in specific cases. They include D-penicillamine (which may be useful for skin symptoms), methotrexate (Rheumatrex), corticosteroids, cyclosporine (Sandimmune, Neoral), and chlorambucil (Leukeran). All of these drugs have potentially severe side effects.

Other Treatments

Tumor-Necrosis Factor Modifiers. Tumor-necrosis factor (TNF) modifiers are major breakthroughs in the treatment of rheumatoid arthritis. They interfere with specific parts of TNF, a powerful immune factor. Researchers believe they should be tested in other inflammatory conditions, including scleroderma. The current agents include infliximab (Remicade), etanercept (Enbrel), alefacept (Amevive), and adalimumab (Humira).

Blood Exchange (Plasmapheresis or photopheresis). Plasmapheresis is a process in which the liquid part of the blood, called plasma, is separated from blood cells. The procedure involves first withdrawing blood from the patient. The plasma, which contains the active immune factors, is discarded and replaced with other fluids. The blood is then returned to the patient.

Autologous Stem-Cell Transplantation. Researchers are investigating a possible benefit of transplanting the patient's own stem cells (an autologous transplant). (Patients with autoimmune diseases cannot be given cells from donors.) The transplant procedures introduce normal white blood cells that replace the abnormal autoimmune cells. The procedure has improved or stabilized systemic scleroderma in some patients, with remissions lasting up to 5 years or more, and improvements in skin and overall function. Initial results of ASTIS, a major study evaluating stem-cell transplants and high-dose immunosuppressive therapy in severe scleroderma, indicate that this combination has led to sustained remission in more than one-third of patients. Randomized controlled trials comparing stem cell transplants to monthly cyclophosphamide therapy are underway in Europe and the U.S.

Although the risk of death from having a transplant is now less than 10%, the procedure has serious side effects. Experts suggest that the best candidates are those at high risk for complications from scleroderma. In general, such patients would have diffuse scleroderma, experienced their first symptoms within the previous three years, and have evidence of at least mild abnormalities in the heart, lungs, or kidney. In general, patients with advanced scleroderma would not be the best candidates, because the risks of the procedure would outweigh the risks from the disease.

Extracorporeal Photopheresis: Another phototherapy treatment under investigation, extracorporeal photopheresis, involves withdrawing the patient's blood and treating it with ultraviolet light. Little data exists on its effectiveness. One study found that the therapy improved skin and joint symptoms, but the authors say it's possible that a placebo effect was at least partly responsible for the results. Experts do not recommend photopheresis at this time, but some feel that it does hold promise and warrants more research.

Intravenous immunoglobulin (IVIg). Animal studies have found that administration of IVIg, an agent that modifies the immune system, may reduce the severity of scleroderma and other autoimmune diseases. So far, only extremely small studies including fewer than 10 patients have been conducted, but the treatment is showing promise for relieving joint pain and tenderness and improving function. The exact role of this therapy in scleroderma treatment, if any, has yet to be determined.

Because of the difficulty in treating scleroderma, many patients are tempted to try high-dose supplements or other alternative treatments. Some natural treatments have been evaluated for the treatment of scleroderma, including para-aminobenzoic acid, vitamin E, evening primrose oil, and an avocado/soybean extract. However, these treatments have not been proven effective, and using alternative remedies can be dangerous.

There is almost no published research on the use of herbal remedies for patients with scleroderma. 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 numerous reported cases of serious and even deadly side effects from herbal products. Always check with your doctor before using any herbal remedies or dietary supplements.

Treatment for Raynaud's Phenomenon

The following are some lifestyle tips for managing Raynaud's phenomenon:

Keeping warm is the primary goal for preventing the onset of Raynaud's phenomenon. Air-conditioning and exposure to refrigeration can trigger this syndrome. If patients go out in cold weather, they should dress warmly with many layers. Wearing a hat is essential.
Living in a warm climate may help relieve symptoms, although a recent study found that weather changes themselves had little effect on the disorder.
Exercise is helpful for maintaining a sense of well-being, keeping warm, and sustaining skin flexibility. Patients with Raynaud's phenomenon may want to avoid exercising outdoors in cold weather, however.
Quitting smoking is, of course, essential for anyone, but it is critical for people with scleroderma.
Learning relaxation and anti-stress techniques might help reduce some triggers of Raynaud's phenomenon.
Using moisturizers and antibiotic ointments may be helpful for keeping skin flexible and preventing infections in the fingers.
Avoiding medications such as nonselective beta blockers (such as propranolol), certain common cold preparations, and narcotics, can help avoid aggravating Raynaud's phenomenon.

Vasodilators. Vasodilators open blood vessels and so are important for Raynaud's phenomenon.

Calcium-channel blockers, including diltiazem (Cardizem, Dilacor) and nifedipine (Adalat, Procardia) are the standard vasodilating drugs used for Raynaud's phenomenon. Nifedipine is the best studied of these drugs, but there are also newer dihydropyridines, including felodipine, amlodipine, and isradipine.

Nitrates, available in topical or oral forms, are vasodilators that are also used for Raynaud's phenomenon, and for short-term relief.

Prostacylins. Iloprost and other prostacylins are proving to be effective agents for Raynaud's phenomenon. Small but well done studies seem to show these drugs to be helpful for this condition, and possibly as effective as calcium channel blocker drugs such as nifedipine. Evidence shows that intravenous iloprost given at progressively increasing doses over 3-month cycles can reduce the duration and frequency of attacks. In general, these drugs are used when a patient's symptoms are severe, particularly when the doctor is considering amputating a finger.

Endothelin receptor agonists have also been shown to help with Raynaud's phenomenon.

Anti-Platelet Drugs. Aspirin, dipyridamole, and other drugs that prevent blood clotting and keep blood flowing freely are sometimes recommended to patients with Raynaud's phenomenon. However, these drugs haven't shown much benefit in studies.

Estrogen Therapy in Women. Short-term treatment with estrogen may benefit older women with Raynaud's phenomenon and scleroderma. It is important to note, however, that hormone replacement therapy for more than 5 years can increase a woman's risk for breast cancer, heart attacks, strokes, and blood clots.

PDE5 Inhibitors. Studies have suggested that a class of drugs called PDE5 inhibitors, which includes sildenafil, helps improve symptoms and blood flow, and speeds ulcer healing in patients with Raynaud's phenomenon. This treatment is still experimental.

Sympathectomy and Hand Surgeries. Sympathectomy uses procedures that block or remove the nerve responsible for narrowing blood vessels in the hand. The result is increased blood flow in the hand.

The local anesthetics lidocaine or bupivacaine may be very effective in temporarily restoring blood flow and reducing pain.

For finger ulcers that won't heal and are resistant to standard treatments, sympathectomy surgery may be done.

Treatment for Skin Thickening

Nitroglycerin is a quick acting nitrate and is used as an ointment (Nitro-Bid, Nitrol, Nitrong, Nitrostat) to treat hardened skin. Before applying it, remove any ointment that remains from the previous application.

UVA-1 Phototherapy. Phototherapy (light therapy) is now considered by some experts to be the treatment of choice for local scleroderma. Specifically, doctors favor an approach called ultraviolet A-1 (UVA-1) radiation. This treatment produces long UVA wave lengths that do not cause sunburn and may actually repair DNA in damaged skin cells. Research suggests that UVA-1 therapy blocks inflammatory immune factors and the process leading to over-production of collagen, addressing the underlying mechanisms of scleroderma. The procedure is effective for all stages of morphea. It increases skin elasticity and in some cases, completely clears up symptoms. In one small study, patients with localized scleroderma received 30 phototherapy treatments over a period of 12 weeks. In the majority of patients, 80% of the skin patches disappeared or significantly improved. There were no side effects.

UVA-1 phototherapy is quite expensive and requires a special light source not available everywhere. In addition, studies are reporting an increased risk with UVA radiation. Whether this applies to UVA-1 phototherapy is not yet clear. Nonetheless, phototherapy is still an effective and important treatment of scleroderma. It may prove to be even more beneficial when combined with certain medications, such as calcipotriene (Dovonex), a form of vitamin D3.

PUVA. An alternative phototherapy regimen called PUVA uses drugs called psoralens taken by mouth before UVA treatment. PUVA has been used for other skin diseases, including psoriasis. It may prove useful for patients with early-onset diffuse scleroderma. In one study, most patients treated with PUVA 2 days a month for up to 8 years experienced improvement or stabilization in nearly all scleroderma symptoms. Tests for kidney function remained normal. This treatment is known to increase the risk for skin cancer.

Phototherapy with Psoralen Water Bath. Yet another procedure uses UVA light therapy after patients take a bath containing a solution of psoralen 8-methoxypsoralen (8-MOP). This treatment is safe and well tolerated, although benefits appear to be minor and occur only in a small subset of patients.

A form of vitamin D3, calcipotriene (Dovonex), appears to help block skin cell production. This vitamin is called calcipotriol in Europe. It also has anti-inflammatory properties, and is being investigated as a rub-on treatment and oral treatment for local scleroderma. It may prove beneficial when combined with low-dose ultraviolet A1 phototherapy.

D-penicillamine is proving to be an effective agent for softening skin and reducing thickness. (Improvements in thickness with this drug have also been associated with improved survival.)

Methotrexate (Rheumatrex) is another commonly used drug, and may be even more effective than penicillamine.

Corticosteroids taken by mouth, such as prednisolone and prednisone, are also often used.

Pilocarpine (Salagen) has been approved for treating dry mouth in people with scleroderma and Sjögren syndrome. In one study, patients with Sjögren syndrome experienced increased salivation after the first dose. Patients reported improvement in speaking, sleeping, and swallowing food without drinking. Side effects of this drug include sweating, increased need to urinate, chills, and flushing.

Other Surgeries. Disabling deformity of the hand is a common feature of scleroderma. Various surgical procedures can relieve pain, prevent tissue loss, protect hand function, and improve the appearance of the hands.

Treatment for Lung Complications

Cyclophosphamide. Cyclophosphamide (Cytoxan), an immunosuppressive drug, may be effective for preventing lung deterioration and is the important medication for treating pulmonary fibrosis, particularly when given early in the course of the disease.

Use of this drug may improve survival in patients who show early signs of lung deterioration, notably inflammation in the small lung airways (alveolitis). The drug is not recommended for patents with existing stable pulmonary fibrosis and no signs of inflammation. In one study, patients with early signs of lung inflammation were given a course of intravenous pulses of the corticosteroid methylprednisolone (MP) and cyclophosphamide. Nearly all patients experienced improvement or stabilization during the first year, although the disease had progressed in two-thirds of them after 2 years.

Other Treatments. Lung transplantation may offer hope for people with advanced pulmonary hypertension or interstitial fibrosis that does not respond to conservative treatments.

Several types of drugs are used to treat pulmonary hypertension. Anticoagulants taken by mouth, such as warfarin (Coumadin), are a standard treatment used to prevent blood clots from forming. Diuretic treatment and supplemental oxygen are recommended for patients with fluid retention and low blood oxygen, respectively.

Vasodilators help open blood vessels and relieve pressure in arteries of the lungs. Vasodilators used to treat pulmonary hypertension fall into several different drug classes:

Calcium Channel Blockers (CCBs). Some patients with pulmonary hypertension benefit from these drugs. They help relax blood vessels in the heart and lungs, and increase the supply of oxygen. However, calcium channel blockers are only appropriate for patients who meet certain diagnostic criteria, including those who don't have right-sided heart failure. Long-acting nifedipine or diltiazem, or amlodipine, are the preferred calcium channel blockers.

Prostacyclins (Prostaglandins). Prostacyclins, which open blood vessels, are now the primary agents for treating pulmonary hypertension.

Iloprost (Ventavis) is available in inhaled and intravenous forms. Studies suggest that the inhaled form improves exercise capacity and survival in some patients with pulmonary hypertension. In addition, infusions of iloprost remain effective over long periods (up to 3 years) of use.
Treprostinil (Remodulin) is similar to epoprostenol but is more stable. It can also be administered using a portable pump that delivers the drug under the skin. This is less expensive, cumbersome, and invasive than the delivery methods for epoprostenol.
Epoprostenol (Flolan), which is administered intravenously, has improved exercise capacity and symptoms in both the short and long term in a number of patients. In some patients, survival is increased significantly. However, not all patients respond to this drug. The implanted catheter needed to deliver the drug can also cause serious complications.

Endothelin Receptor Antagonists. Bosentan (Tracleer) was the first drug taken by mouth that was approved for pulmonary hypertension. Bosentan controls endothelin, a powerful substance that causes blood vessels to narrow. Studies have reported improved exercise capacity in patients with pulmonary hypertension. Sitaxsentan and ambrisentan (Letairis) are two new drugs being studied.

PDE5 Inhibitors. Sildenafil (Revatio) was approved in 2005 as the first pill for patients with early-stage pulmonary hypertension. Sildenafil is the same medication contained in the erectile dysfunction drug Viagra. However, Revatio is prescribed at a lower dosage than Viagra, and is a different color and shape than Viagra pills.

Other Treatments. Lung transplantation may offer hope for people with advanced pulmonary hypertension that does not respond to conservative measures.

Treatment for Gastrointestinal Problems

Treatments for abnormalities in the esophagus and stomach are generally the same as those for gastroesophageal reflux (GERD) or heartburn. Many non-prescription agents are available for the relief of heartburn.

Proton-pump or acid-pump inhibitors are probably the best drug treatments for reflux symptoms related to scleroderma. They work by inhibiting the so-called gastric acid pump that is required for the cells of the stomach to release acid. The standard drug has been omeprazole (Prilosec). Newer drugs -- including lansoprazole (Prevacid), pantoprazole (Protonix), esomeprazole (Nexium), and rabeprazole (Aciphex) -- are more potent, but few comparison studies have been done on them.

Side Effects. Side effects are uncommon, but can include allergic reaction, headache, stomach pain, diarrhea, and flatulence. Of some concern was a report of a very severe and widespread skin rash caused by omeprazole in a woman with scleroderma. It should be noted that this is only one incident, but patients should be cautious about any skin change when taking this medication.

Metoclopramide. Metoclopramide (Reglan) is sometimes used for patients who have delayed stomach emptying.

Octreotide. Octreotide (Sandostatin) is related to a natural hormone that suppresses growth hormone, and may prove to be very helpful for scleroderma patients. Small studies have reported that this drug improved weight and nutrition. It may even help other symptoms of scleroderma.

Prokinetics. Prokinetics improve the muscle action of the esophagus and enhance stomach emptying. Prucalopride is an investigative pro-kinetic agent that significantly improved symptoms and relieved constipation. Similar medications, such as cisapride (Propulsid), are showing promise; however these types of drugs can have serious side effects.

Antibiotics may be effective for the malabsorption syndrome associated with an increase in bacteria. Octeotride may also be used for this problem.

Strictures (abnormally narrowed regions in the esophagus) may need to be opened with surgery.

Resources

www.scleroderma.org -- Scleroderma Foundation
www.srfcure.org -- Scleroderma Research Foundation
www.arthritis.org -- The Arthritis Foundation
www.niams.nih.gov -- National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.rheumatology.org -- American College of Rheumatology
www.sclero.org -- International Scleroderma Network
www.sctc-online.org -- Scleroderma Clinical Trials Consortium
www.phassociation.org -- Pulmonary Hypertension Association
www.thoracic.org -- American Thoracic Society

References

Badesch DB, Abman SH, Simonneau G, Rubin LJ, McLaughlin VV. Medical therapy for pulmonary arterial hypertension: updated ACCP evidence-based clinical practice guidelines. Chest. 2007;131:1917-1928.

Feldman M, Friedman LS, Brandt LJ. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 8th ed. Philadelphia, Pa: Saunders; 2006.

Goldman L, Ausiello D. Goldman: Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders, 2007.

Grader-Beck T, Wigley FM. Raynaud's phenomenon in mixed connective tissue disease. Rheum Dis Clin North Am. 2005;31:465-481.

Henness S, Wigley FM. Current drug therapy for scleroderma and secondary Raynaud's phenomenon: evidence-based review. Curr Opin Rheumatol. 2007;19:611-618.

Knobler RM, French LE, Kim Y, Bisaccia E, Graninger W, Nahavandi H, et al. A randomized, double-blind, placebo-controlled trial of photopheresis in systemic sclerosis. J Am Acad Dermatol. 2006;54:793-799.

Kreuter A, Hyun J, Stücker M, Sommer A, Altmeyer P, Gambichler T. A randomized controlled study of low-dose UVA1, medium-dose UVA1, and narrowband UVB phototherapy in the treatment of localized scleroderma. J Am Acad Dermatol. 2006;54:440-447.

Mason RJ, Murray JF, Broaddus VC, Nadel JA. Mason: Murray & Nadel's Textbook of Respiratory Medicine. 4th ed. Philadelphia, Pa: Saunders; 2005.

Nash RA, McSweeney PA, Crofford LJ, Abidi M, Chen CS, Godwin JD, et al. High-dose immunosuppressive therapy and autologous hematopoietic cell transplantation for severe systemic sclerosis: long-term follow-up of the US multicenter pilot study. Blood. 2007;110:1388-1396.

Ostojic P, Cerinic MM, Silver R, Highland K, Damjanov N. Interstitial lung disease in systemic sclerosis. Lung. 2007;185:211-220.

Pfizenmaier DH 2nd, Kavros SJ, Liedl DA, Cooper LT. Use of intermittent pneumatic compression for treatment of upper extremity vascular ulcers. Angiology. 2005 Jul-Aug;56(4):417-22.

Schachna L, Medsger TA Jr., Dauber JH, Wigley FM, Braunstein NA, White B, et al. Lung transplantation in scleroderma compared with idiopathic pulmonary fibrosis and idiopathic pulmonary arterial hypertension. Arthritis Rheum. 2006;54:3954-3961.

Shoenfeld Y, Katz U. IVIg therapy in autoimmunity and related disorders: our experience with a large cohort of patients. Autoimmunity. 2005 Mar;38(2):123-37.

Steen VD. Pregnancy in scleroderma. Rheum Dis Clin North Am. 2007;33:345-358.

Tashkin DP, Elashoff R, Clements PJ, et al. Cyclophosphamide versus placebo in scleroderma lung disease. N Engl J Med. 2006; 354(25):2655-66.

Thombs BD, Taillefer SS, Hudson M, Baron M. Depression in patients with systemic sclerosis: a systematic review of the evidence. Arthritis Rheum. 2007;57:1089-1097.

Tyndall A, Furst DE. Adult stem cell treatment of scleroderma. Curr Opin Rheumatol. 2007;19:604-610.

van Laar JM. High-dose immunosuppressive therapy and autologous progenitor cell transplantation for systemic sclerosis. Best Pract Res Clin Haematol. 2004; 17(2): 233-45.

Review Date:
1/15/2008
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. Copyright

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Newsletter - Week 18

FitSugar — Wed, 08 Oct 2008 17:34:53 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Welcome To Week 18

Your Baby: Did You Hear A Hiccup?

At about 5 1/2 inches (14 cm) in length and up to 7 ounces (200 g) in weight, the fetus is growing fast and looking more and more babyish. During this week, your baby sense of hearing has become much more acute. The baby can hear noises within the uterus of your bowel moving and even the blood pumping within your vessels. Additionally, the baby can hear things outside the uterus. So if you are talking to your partner, the baby is hearing some sound. (You may even feel the baby get startled inside from noises that take place outside!)

Though you probably won't feel them at this early date, your baby may have the hiccups, which happens before fetal breathing movements become common.

Your Body: Undergoing An Ultrasound

If you're like most women, you'll have a routine ultrasound about now so your caregiver can get information on your baby's health. Though this brief (5 to 10 minutes) and painless test is most often done during the second trimester, it can be performed any time between the fifth week of gestation and delivery.

There are two types of ultrasounds: transvaginal and transabdominal. With both, you lie on your back on an exam table while your belly or a probe is lubed up with a special gel. A transducer (a small microphone-like device) is gently pressed on your belly or inserted into your vagina -- the method depends on how far along you are and what type of equipment is on hand. The transabdominal transducer is moved over your belly and it works by picking up the sound waves that come off the bones and tissues in the body at a higher frequency than we can hear. These sound waves then produce an image on a nearby computer screen. The image on the screen, which for some is crystal clear and for others a big blur, is your baby. Regardless, most expectant moms find this first glimpse thrilling -- and over all too quickly.

Ultrasound is a non-invasive test that provides a tremendous amount of information to your health care provider about your baby's development and health. Some of the things that can be seen by ultrasound include:

Determine an accurate gestational age of the baby
Determine sex of the baby
See any anatomical abnormalities that exist in the baby
Determine if it is just one baby or more than one
See the location of the placenta and the baby's position within the uterus
See the amount of amniotic fluid
Watch how the baby's heart is beating and breathing movements

On That Note: Baby On View

As your next -- or in some cases, your only -- ultrasound draws near, you're eager to get a look at the precious cargo you're carrying. For a sneak preview of what the test entails, click on this ultrasound presentation.

Weekly Tip

Wear loose-fitting separates for the ultrasound exam. That way, you can easily pull the top half up and the bottom half down. And even though you'll mop up the goop on your belly with a towel when it's all over, some of it will surely wind up on your clothes. So whatever you do, don't wear your Sunday best!

Review Date:
2/6/2007
Reviewed By:
Douglas A. Levine, MD, Gynecology Service, Memorial Sloan-Kettering Cancer Center, New York, NY. Review provided by VeriMed Healthcare Network.

A.D.A.M. Copyright

adam.com

Pregnancy Center Links

Allergy to mold - dander - dust

admin — Wed, 03 Sep 2008 17:52:13 -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

Allergy symptoms

Dust mite-proof pillow cover

HEPA air filter

Yeast and mold

HEALTH GUIDE REFERENCE FROM A.D.A.M

Definition

Allergy-related symptoms can occur after you are around mold, certain animals or animal hair, dust, and other substances. These substances are usually found indoors and do not cause symptoms for most people.

Alternative Names

Indoor allergies; Pet allergies

Causes, incidence, and risk factors

Allergies are relatively common. They are caused by an over-sensitive immune response. The immune system normally protects the body against harmful substances such as bacteria and viruses. Allergy occurs when the immune system reacts to substances (allergens) that are generally harmless and, in most people, do not cause an immune response.

When a person with allergies breathes in an allergen, histamine and other chemicals are released as part of the immune response. This causes itching and swelling, mucus production, and in serious cases, hives and rashes, as well as other symptoms.

Symptoms vary in severity from person to person. Most environmental allergens contact the skin or eyes, or are inhaled. Therefore, most symptoms affect the skin, eyes, or the breathing passages.

You may develop an allergic reaction to particles in the indoor or outdoor environment that leads to hay fever-like symptoms. Common allergy triggers include:

Mold -- Mold spores are carried in the air and may be present all year long. Mold is most common indoors in damp locations such as basements, bathrooms, or washrooms. Fabrics, rugs, stuffed animals, books, or wallpaper can contain mold spores if they are frequently in contact with water or kept in a damp place. Outdoors, mold lives in the soil, on compost, and on damp vegetation.
Animals -- People who are allergic to certain animals are rarely allergic to the animals' fur or feathers. They are actually allergic to the small scales of skin (dander) that the animal sheds. Some people are allergic to the animal's saliva, particularly cats. Cats have saliva that contains a protein known to cause allergy. You can come into contact with animal saliva if the pet licks you, if you touched the pet after it has groomed itself, or if you touch an object that the animal has recently licked or chewed.
Dust -- House dust contains tiny particles of pollen, mold, fibers from clothing and fabrics, detergents, and microscopic insects (mites). Dust mites, including small fragments of dead mites, are the primary cause of dust allergy and are found in the highest numbers in bedding, mattresses, and box springs.

A few people develop allergy-like symptoms to other irritants in the environment, including smoke, fumes from industries or cleaning products, tobacco, powder, and laundry detergents.

Symptoms

Coughing
Difficulty breathing
Hives
Itching of the nose, eyes, throat, or skin
Rash
Redness in the eyes
Runny nose
Sinus pressure
Sneezing
Tearing eyes
Wheezing

Signs and tests

The doctor will perform a physical exam and ask you questions about your symptoms. The history of symptoms is important in diagnosing allergies, including whether the symptoms vary according to time of day or the season and possible exposures such as having a pet in the household.

Allergy testing is done to see identify the specific allergens that are causing your symptoms. Skin testing is the most common and useful method. This may include scratch, patch, or other tests.

If your doctor determines that you cannot undergo skin testing, a RAST blood test (to look for IgE antibodies to a specific allergen) may be helpful.

Having allergies may also alter the results of the following tests:

WBC count, particularly eosinophil count
Serum immunoelectrophoresis

Treatment

The goal of treating allergic rhinitis is to reduce allergy symptoms caused by the inflammation of affected tissues.

The best "treatment" is to avoid what causes the allergic symptoms in the first place. It may be impossible to completely avoid all allergens to which you are sensitive, but you can often take steps to reduce exposure.

Medication options include the following:

Short-acting antihistamines can relieve mild to moderate symptoms, but can cause drowsiness. Many may be bought without a prescription. A pediatrician should be consulted before using these medicines in children, as they may affect learning. Loratadine (Claritin) is now available over the counter. It does not tend to cause drowsiness or affect learning in children.
Longer-acting antihistamines are available by prescription. They cause less drowsiness and can work just as well. They usually do not interfere with learning. These medications include fexofenadine (Allegra), and cetirizine (Zyrtec).
Nasal corticosteroid sprays work very well for people with symptoms not relieved by antihistamines alone. These prescription medications include fluticasone (Flonase), mometasone (Nasonex), and triamcinolone (Nasacort).
Azelastine (Astelin) is a new, nasal antihistamine that is used to treat allergic rhinitis.
Decongestants may also be helpful in reducing symptoms such as nasal congestion, but should not be used for long periods.
Cromolyn sodium is available as a nasal spray (Nasalcrom) for treating hay fever. Eye drop versions of cromolyn sodium and antihistamines are available for itchy or bloodshot eyes.
The leukotriene inhibitor montelukast (Singulair) is a prescription medicine approved to help control asthma and to help relieve the symptoms of seasonal allergies.

The most appropriate medication depends on the type and severity of symptoms. Specific illnesses that are caused by allergies (such as asthma and eczema) may require other treatments.

Allergy shots (immunotherapy) are occasionally recommended if the allergen cannot be avoided and symptoms are hard to control. Immunotherapy includes regular injections of the allergen, given in increasing doses (each dose is slightly larger than the previous dose) that may help the body adjust to the antigen. As mold, animal, and dust avoidance are more feasible than avoiding outdoor pollens, allergy shots are less commonly prescribed for these types of allergies.

Expectations (prognosis)

Most symptoms of allergies to mold, dander, and dust can be readily treated, and regular treatment can minimize the symptoms.

In some cases (particularly in children), people may outgrow an allergy as the immune system becomes less sensitive to the allergen. However, as a general rule, once a substance causes allergies for an individual, it can continue to affect the person long term.

The most severe cases of allergic rhinitis from these allergens may require immunotherapy (allergy shots) or removal of tissue in the nose or sinuses.

Complications

Frequent ear infections (otitis media) in children
Drowsiness and other side effects of antihistamines
Side effects of other medications (see the specific medication)
Sinusitis
Nasal polyps
Hives or other skin rashes
Anaphylaxis (a rare but severe allergic reaction)
Disruption of lifestyle

Calling your health care provider

Call your health care provider if severe symptoms of allergy occur, if previously successful treatment has become ineffective, or if symptoms do not respond to treatment.

Prevention

There is no known way to prevent development of allergies, but recent research has given us clues.

Breastfeeding can be effective at preventing and decreasing allergies. There is also evidence that exposures to certain allergens in the first year of life may prevent some allergies. This is called the "hygiene hypothesis" and sprang from observations that infants on farms tend to have fewer allergies than those in environments that are more sterile. Once allergies have developed, avoiding known allergens may decrease symptoms and prevent other allergies.

Mold spores are everywhere. Minimize exposure by keeping rooms dry, using a dehumidifier if necessary. Discard moldy or mildewed articles (books, toys, shoes, and so on). Use synthetic fabrics for clothing and household furnishings whenever possible. Disinfect bathrooms, basement walls, and furniture with diluted bleach or other appropriate disinfectant solution.

Clean frequently to minimize dust. Vacuum frequently, preferably using a small-pore filter to capture dust mites. Damp-mop and dust often. Eliminate as many "dust catchers" as possible, including rugs, bed ruffles or canopies, and curtains. Bedding and mattresses harbor dust mites.

You can buy special covers for mattresses, box springs, and pillows to reduce dust mite allergens. Wash rugs, bedding, and furniture coverings weekly if possible. Central heating and air-conditioning systems may be helpful, particularly if they include special filters to capture dust.

People who are allergic to animals may need to avoid keeping pets. Frequent bathing and grooming of the pet (preferably by someone who is not allergic to the animal) may help. Allergy to animals may also include wool, which may contain tiny amounts of dander (skin).

Avoid other irritants whenever possible.

Review Date: 10/30/2006

Reviewed By: Donald Accetta, MD, MPH, President, Allergy & Asthma Care, PC, Taunton, MA. Review provided by VeriMed Healthcare Network.

A.D.A.M. Copyright

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