Atopic dermatitis

(medicine) A chronic eruption of red patches accompanied by intense itching that usually begins in infancy but may continue into adult life; the disease has a genetic predisposition, but its expression is modified by environmental factors.

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Definition

Atopic dermatitis (AD) is a chronic skin disorder associated with biochemical abnormalities in the patient's body tissues and immune system. It is characterized by inflammation, itching, weepy skin lesions, and an individual or family history of asthma, hay fever, food allergies, or similar allergic disorders. Atopic dermatitis is also known as infantile eczema or atopic eczema. The word atopic comes from atopy, which is derived from a Greek word that means "out of place." Atopy is a genetic predisposition to type I (immediate) hypersensitivity reactions to various environmental triggers. It includes bronchial asthma and food allergies as well as atopic dermatitis.

Description

AD varies in severity but in general is characterized by red, weeping, crusted patches of inflamed skin that itch constantly. The distribution of the skin lesions depends on the child's age. In infants, the skin lesions are usually found on the face, scalp, diaper area, body folds, hands, and feet, and tend to be exudative (oozing fluid that has escaped from blood vessels as a result of inflammation). Infants old enough to crawl may have patches of inflamed skin on the neck and trunk as well. In older children, the affected areas are usually located on the wrists, ankles, back of the neck, insides of the elbows, and the backs of the knees. The skin lesions in older children are more likely to be lichenified than exudative. Lichenification is the medical term for a leather- or bark-like thickening of the outermost layer of skin cells (the epidermis) as a result of long-term scratching or rubbing of itching lesions. In addition, the normal markings of the skin are exaggerated in lichenification.

The lesions of AD are accompanied by intense pruritus, which is the medical term for itching. Children with atopic dermatitis often have a lowered threshold of sensitivity to itching, which means that they feel itching sensations more intensely than children without the disorder. The pruritus often creates a vicious cycle of itching and scratching, which leads to more widespread rash, which leads to more itching. The child may scratch the affected skin only intermittently during the day, however. It is common for children with AD to do more scratching in the early evening and at night; moreover, disruptions of normal sleep patterns are common in these children.

Transmission

Atopic dermatitis is not contagious but may affect several members of the same family at the same time.

Demographics

Atopic dermatitis is a very common condition in the general population. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), about 15 million people in the United States have one or more symptoms of the disease. It accounts for 15 to 20 percent of all visits to dermatologists (doctors who specialize in treating diseases of the skin). About 20 percent of infants develop symptoms of atopic dermatitis. Moreover, the proportion of people affected by AD is increasing; the American Academy of Allergy, Asthma, and Immunology (AAAAI) began a long-term study in 1999 that indicates that a larger percentage of children are affected by AD than was the case in the 1980s. This rise in prevalence is true of all developed countries, not just the United States and Canada. People who immigrate to Europe or North America from under-developed countries have increased rates of atopic dermatitis, which suggests that environmental factors play a role in the development or triggering of the disorder.

Atopic dermatitis begins early in life; about 65 percent of patients with AD develop symptoms during the first 12 months of life, with 90 percent showing symptoms before five years of age. The most common age for the onset of symptoms in infants is between six and 12 weeks of age. It is unusual for adults over the age of 30 to develop AD for the first time.

There is some disagreement among researchers with regard to race or ethnicity as risk factors for atopic dermatitis. Some studies indicate that all races and ethnic groups are equally at risk, while others suggest that Asians and Caucasians have slightly higher rates of AD than African Americans or Native Americans. Some skin lesions typical of AD may be more difficult to evaluate in African Americans because of the underlying skin pigmentation. With regard to sex, males and females appear to be equally at risk.

Atopic dermatitis is a major economic burden on families with children affected by the disorder. One researcher in Australia stated that the stresses on families with children diagnosed with moderate or severe AD are greater than the burdens on families with children with type 1 diabetes. These stresses include loss of sleep, loss of employment for the parents, time taken for direct care of the skin disorder, and the financial costs of treatment. The National Institutes of Health (NIH) estimates that atopic dermatitis costs U.S. health insurance companies more than $1 billion every year.

Causes and Symptoms

Causes

The causes of atopic dermatitis were not completely understood as of 2004 but are thought to be a combination of genetic susceptibility, damaged skin barrier function, and abnormal responses of the child's immune system to environmental triggers. With regard to genetic factors, the disorder has been tentatively linked to loci on chromosomes 11 and 13. A child with one parent with AD has a 60 percent chance of developing the disorder; if both parents are affected, the risk rises to 80 percent. Nearly 40 percent of newly diagnosed children have at least one first-degree relative with atopic dermatitis.

In addition to genetic susceptibility, AD is the end result of a complex inflammatory process involving abnormalities in the child's skin and immune system. Some researchers have noted that the skin of people with AD contains lower levels of fatty acids, which may cause the skin to lose moisture more readily and become more sensitive to chemicals and other irritants. Others point to decreased production of a hormone in the immune system called interferon-gamma that ordinarily helps to regulate the body's response to allergens. People with AD may be hypersensitive to irritants because they have abnormally low levels of interferon-gamma in their systems.

About 80 to 90 percent of children with AD also have unusually high levels of an antibody called IgE in their blood. Antibodies are specialized proteins produced by the immune system that seek out and destroy bacteria, viruses, and other invaders. The high levels of IgE in the blood of AD patients are produced by hyperactive T helper 2 cells reacting against antigens in the environment. Although the role of increased IgE production in the development of atopic dermatitis was not fully understood as of 2004, measuring the level of this antibody in a sample of blood serum may be done to help distinguish AD from other skin diseases with similar symptoms.

Symptoms

The basic symptoms of AD have already been described. Dermatologists classify the lesions of AD into three basic categories:

• Acute lesions: These include extremely itchy reddened papules (small solid eruptions resembling pimples) and vesicles (small blister-like elevations in the skin surface that contain tissue fluid) over erythematous (reddened) skin. Acute lesions produce a watery exudate and are often accompanied by exfoliation (scaling or peeling of layers of skin) and erosion (destruction of the skin surface).
• Subacute lesions: These are characterized by reddening, peeling, and scaling but are less severe than acute lesions and do not produce an exudate.
• Chronic lesions: These are characterized by thickened plaques of skin, lichenification, and fibrous papules.

It is possible for a child or adolescent with chronic atopic dermatitis to have all three types of lesions at the same time.

Associated Symptoms and Disorders

Children and adolescents with AD frequently develop one or more of the following disorders or problems:

• Asthma: About 50 percent of children diagnosed with AD eventually develop asthma.
• Allergic rhinitis: Between 70 and 75 percent of children with AD eventually develop a nasal allergy. Allergic rhinitis, which is sometimes called atopic rhinitis, may be either seasonal (hay fever or rose fever) or nonseasonal (caused by dust, mold spores, pet dander, cigarette smoke, and other household allergens).
• Eye complications: These include such disorders as conjunctivitis (inflammation of the tissue that lines the eyelid), keratoconus (a cone-shaped distortion of the cornea of the eye), and cataracts. Although cataracts are usually associated with older adults, between 4 and 12 percent of children with AD develop rapidly maturing cataracts that may begin to interfere with vision as early as age 20. About 1 percent develop keratoconus.
• Ichthyosis, xerosis (dry skin), lichenification, and other skin abnormalities not caused by infections: Children with AD are likely to develop other skin problems.
• Secondary skin infections: Children and adolescents with AD frequently develop infections from bacteria that live on the skin and multiply when the child's scratching causes breaks or open sores in the skin. Most of these secondary infections are caused by Staphylococcus aureus and Streptococcus pyogenes.
• Psychosocial problems: Children with atopic dermatitis may withdraw socially if the lesions are extensive or otherwise noticeable. In addition, children with severe cases may have frequent absences from school. Adolescents may suffer depression or anxiety related to concerns about their appearance or the need to avoid participating in sports in order to minimize sweating.

When to Call the Doctor

Atopic dermatitis is rarely a medical emergency and can often be treated by the child's pediatrician. Parents should, however, consider consulting a dermatologist, allergist, or immunologist under any of the following circumstances:

• The child's AD has been diagnosed as severe. This classification means that 20 percent of the body's skin surface has been affected or 10 percent of the skin area in addition to involvement of the eyes, hands, and body folds.
• There is extensive exfoliation (peeling and scaling) of the skin.
• The child has eye complications.
• The child has recurrent secondary bacterial infections.
• The child is frequently absent from school, has developed psychosocial complications, or has impaired quality of life. In many cases the entire family's quality of life is affected by the stresses and frustrations of coping with the disease, and other family members' reactions may in turn upset the child with AD.
• The child has had to be hospitalized for treatment of the AD.
• The child has had to take more than one course of oral steroid drugs.
• The diagnosis is uncertain.

Diagnosis

History and Physical Examination

Diagnosis of atopic dermatitis begins with a history-taking and physical examination by the child's doctor. In the case of infants or very young children, the doctor will ask the parents for information about a family history of atopic disorders as well as information about the onset of the symptoms. The doctor will then examine the child's skin and assess the following factors:

• physical appearance of the lesions and their distribution on the child's body
• timing, which includes seasonal variations in the severity of the rash as well as its chronic or recurrent nature
• environmental factors, which includes foods as well as such common triggers of AD as dust, pet dander, household cleaning agents, plastics, nail polish remover, and other cosmetics or chemicals
• presence of such other conditions associated with AD as eye complications or bacterial infections of the skin

The doctor will ask older children and adolescents directly whether their skin lesions are affected by such factors as pets in the household; smoking; using perfumes, shampoos, deodorants, or other personal care products; taking certain prescription medications; wearing wool or other rough-textured fabrics; using laundry detergents or fabric softeners; being exposed to extremes of temperature or humidity; athletic activity; emotional stress; and (in females past puberty) hormonal changes related to menstruation.

There are no laboratory tests that can confirm the diagnosis of AD; in some cases, the doctor may need to examine the child more than once in order to distinguish between atopic and seborrheic dermatitis. In most cases, the doctor will make the diagnosis on the basis of criteria established by the AAAAI in the 1990s. To be considered atopic dermatitis, the child's symptoms must at total at least three major and three minor symptom criteria.

There are four major criteria for AD:

• pruritus
• typical form and distribution of skin lesions
• chronic or recurrent dermatitis
• a personal or family history of atopic disorders

There are about two dozen minor criteria for atopic dermatitis. The most common minor characteristics are early age of onset, food intolerance, wool intolerance, susceptibility to skin infections, immediate type I response to skin test, elevated total serum IgE, eczema of the nipples, xerosis or dry skin, dermatitis of the hands and feet, recurrent conjunctivitis, sensitivity to emotional stress, and ichthyosis.

Family practitioners often refer patients with AD to an allergist for consultation, particularly if the child has developed asthma or has acute reactions to foods.

Laboratory Tests

In addition to a general physical examination, the doctor may order a blood test to look for the presence of elevated IgE levels in the blood serum. The doctor may also test tissue fluid or smears from the child's lesions to rule out skin parasites or infections that mimic atopic dermatitis, such as bacterial infections, scabies, or herpesvirus infections.

The doctor may recommend skin prick testing to determine whether certain specific substances or foods trigger the child's AD. These tests are usually given only to children with moderate or severe cases of atopic dermatitis. The child must discontinue taking oral antihistamine medications for one week before the tests and discontinue using topical steroid creams for two weeks. The test is performed by pricking the surface of the skin with a thin needle containing a small amount of a suspected allergen.

Treatment

The AAAAI recommends a four-part approach to the treatment of atopic dermatitis. Children with AD should take the following steps:

• Avoid foods or other factors that trigger symptoms, avoid such irritating fabrics as wool and synthetic fibers, wear 100 percent cotton underwear, trim fingernails short to minimize damage to the skin from scratching, keep the skin moist with proper use of emollient creams or oils after bathing, avoid the use of fabric softeners or scented detergents when laundering clothes and rinse clothes completely, and try to reduce emotional stress.
• Use appropriate medications as prescribed. The types of medications used vary depending on the severity of the child's symptoms and the presence of other infections. Most children are given both oral and topical (applied to the skin) medications. Topical medications include corticosteroid creams (Aristocort, Kenalog, Halog, Topicort, and many other brand names) and ointments containing immunomodulators, usually tacrolimus (Protopic) or pimecrolimus (Elidel). Corticosteroid creams are used to suppress inflammation, while the immunomodulator creams work by reducing the reactivity of the child's immune system. Although the corticosteroid creams have been used in both prescription-strength and over-the-counter (OTC) formulations for many years to treat AD, they may cause such side effects as thinning of the skin or stretch marks when used for long periods. They may also make skin infections worse. For these reasons, doctors recommend using the least powerful corticosteroid creams that control the symptoms. With regard to oral medications, antihistamines are often prescribed to stop itching at night so that the child can sleep. Oral or injected corticosteroids are sometimes used for short-term treatment of severe cases of AD that have not responded to topical medications; however, these drugs often have severe side effects, including stunted growth, thinning or weakening of the bones, high blood sugar levels, infections, and an increased risk of cataracts. Children with skin infections are usually given oral rather than topical antibiotics, most commonly penicillin or a cephalosporin.
• Regarding asthma or allergic rhinitis, the child should be evaluated for immunotherapy.
• The child's family and friends need to be educated about the condition, and the child needs to maintain a schedule of regular follow-ups. In addition to followup visits with the pediatrician and allergist, the child should have regular eye examinations as a safeguard against cataracts or other eye complications.

Other treatments that are sometimes used for atopic dermatitis are tar preparations and ultraviolet light therapy (phototherapy). Tar preparations are messy but were still as of 2004 considered useful for treating patients with chronic lichenified areas of skin. Phototherapy with ultraviolet A or B light waves, or a combination of both, may be used to treat older children or adolescents with mild or moderate atopic dermatitis; it is not suitable for infants or younger children. Some patients who do not respond to ultraviolet light alone benefit from a combination of phototherapy and an oral medication known as psoralen, which makes the skin more sensitive to the light. Phototherapy has two potential side effects from long-term use: premature aging of the skin and an increased risk of skin cancer.

Children or adolescents with AD must use extra care when bathing or showering. The doctor may recommend a non-soap skin cleanser, as standard bath soaps tend to dry and irritate the skin. If soaps are used, they should never be applied directly to broken or eroded areas of skin. The water should be lukewarm rather than hot, and the skin should be allowed to air-dry or be gently patted with a towel; brisk rubbing or the use of bath brushes must be avoided. After the skin has dried, the patient should apply a skin lubricant to seal moisture in the skin and create a barrier against further dryness or irritation.

Children with AD should also avoid unnecessary exposure to extremely hot, cold, moist, or dry outdoor environments. They should take care to avoid getting sunburned and should avoid participating in sports that involve physical contact or cause heavy perspiration.

Alternative Treatment

There are a number of different complementary and alternative (CAM) approaches that have been used to treat atopic dermatitis, in part because the disorder is so widespread among children. In fact, infantile eczema is one of the most common conditions for which parents seek help from alternative practitioners. Most alternative therapies for atopic dermatitis fall into one of the following groups.

NATUROPATHY. Naturopathy is a commonly used form of alternative treatment for AD; in one British study it was found effective for 19 out of 46 children in the subject group. Naturopaths favor food elimination diets as a way of managing AD, as well as lowering the child's overall intake of animal products. They recommend adding fish oil, flaxseed oil, or evening primrose oil to the child's diet to improve the condition of the skin, as many naturopaths believe that deficient intake of essential fatty acids is a major cause of AD. With regard to botanical products, a naturopath may suggest herbal preparations taken by mouth as well as topical creams made from herbs. Oral preparations may include extracts of hawthorn berry, blackthorn, or licorice root, while topical preparations to relieve itching typically include licorice or German chamomile. One German study found that a cream made with an extract of St. John's wort relieved the symptoms of AD better than a placebo, but the herbal preparation had not as of 2004 been compared to a standard corticosteroid cream.

HOMEOPATHY. Homeopathy is the single most common CAM approach to atopic dermatitis in Europe, although it is frequently used in the United States as well. One German study followed a group of 2800 adults and 1130 children diagnosed with AD who were treated by homeopathic practitioners. The researchers found that over 600 different homeopathic remedies were recommended for the patients, although Sepia , Lycopodium, Sulphur, and Natrum muriaticum were the remedies most frequently prescribed. Most homeopathic practitioners in the United States as well as Europe consider AD a chronic condition that should be treated by constitutional homeopathic prescribing rather than by what is known as acute prescribing. In constitutional prescribing, the remedy is selected for long-term treatment of the patient's underlying susceptibility or constitutional weakness rather than short-term relief of present symptoms.

TRADITIONAL SYSTEMS OF MEDICINE. According to Kenneth Pelletier, the former director of the alternative medicine program at Stanford University School of Medicine, both traditional Chinese remedies and Ayurvedic medicines benefit some people with atopic dermatitis. The British study of the use of CAM treatments in children with AD found that parents of Indian or Afro-Caribbean background were more likely to use these traditional approaches than Caucasian parents.

MIND/BODY APPROACHES. Because flare-ups of AD are often related to increased emotional stress, some researchers have hypothesized that alternative approaches to lowering stress might help in treating the disorder. There is disagreement, however, about the effectiveness of such treatments as hypnosis or autogenic training. While some studies have reported that self-hypnosis, biofeedback, or autogenic training helped children with AD to manage their skin lesions with lower levels of steroid medications, other studies have reported that there is no conclusive evidence of the effectiveness of mind/body approaches in treating atopic dermatitis.

Nutritional Concerns

Children and adolescents should avoid foods that trigger their AD. The most common offenders in flareups are peanuts and peanut butter, eggs and milk, seafood, soy, and chocolate. Long-term food elimination diets as a strategy for controlling AD are discussed below.

Children with moderate or severe AD often develop eroded areas or open cracks in the skin around the mouth from licking their lips or from allergic reactions to specific foods. They should apply a thin layer of petroleum jelly around the mouth before a meal to avoid irritation from citrus fruits, tomatoes, and other highly acidic foods.

Prognosis

As of the early 2000s, there is no cure for atopic dermatitis. People diagnosed with AD have highly individual combinations of symptoms that may vary greatly in severity over time. A significant percentage of children diagnosed with the condition, however, remain atopic into adulthood; one source states that 20 to 40 percent of children with infantile eczema continue to be affected, while NIAMS gives a figure of 60 percent. Some children included in these figures, however, outgrow the more severe forms of atopic dermatitis and suffer flare-ups in adult life only when they are exposed to high stress levels, chemical irritants, or other triggers in the environment. Other children may have only mild symptoms of AD until adolescence, when changes in hormone levels may cause a sudden worsening of symptoms.

Prevention

While atopic dermatitis in children cannot be completely prevented, NIAMS offers the following tips to parents as they try to help control the severity and frequency of flare-ups:

• Keep the child from scratching or rubbing the affected areas whenever possible.
• Avoid dressing the child in rough or scratchy fabrics and protect his or her skin from high levels of moisture.
• Keep the house at a cool, stable temperature with a consistent humidity level, using a humidifier during the heating season in colder climates.
• Quit smoking and do not allow others to smoke inside the house.
• Limit the child's exposure to dust, pollen, and animal dander. Some doctors recommend installing special filters in the house to remove dust and pollen from the air, removing carpets from the floors, or encasing mattresses and pillows with special covers to control dust mites.
• Recognize when the child is under stress and lower the stress level in the household if possible.

Nutritional Concerns

The doctor may suggest a food challenge in order to identify a food or foods that may be triggering the child's skin rash. In a food challenge, a particular food is eliminated from the child's diet for a few weeks and then reintroduced. In some cases, a child with AD may benefit from a longer-term diet that eliminates problem foods entirely. In these cases, however, the child's height and weight should be carefully monitored to make sure that the diet is nutritionally adequate, and the diet itself should be reevaluated every four to six months. The doctor may recommend vitamin supplements or a consultation with a dietitian.

Parental Concerns

Parental concerns about atopic dermatitis extend to the possible long-term consequences of the disorder as well as the child's present discomfort and sleeping problems. Depending on the severity and location of the skin rash, the child may withdraw from social activities to avoid teasing or resent restrictions on athletic or other outdoor activities. In addition to such possible complications of AD as eye disorders and skin infections, parents must also be attentive to signs of long-term side effects caused by medications or other forms of treatment for the AD. To cope with the impact of AD on other family members, parents may find counseling and support groups helpful. Because atopic dermatitis is so widespread in the general population, many support groups have been formed, particularly in the larger cities.

See also Allergic rhinitis; Allergies; Asthma.

Resources

Books

"Atopic Dermatitis." Section 10, Chapter 111 in The Merck Manual of Diagnosis and Therapy, edited by Mark H. Beers and Robert Berkow. Whitehouse Station, NJ: Merck Research Laboratories, 2002.

"Hypersensitivity Disorders." Section 12, Chapter 148 in The Merck Manual of Diagnosis and Therapy, edited by Mark H. Beers and Robert Berkow. Whitehouse Station, NJ: Merck Research Laboratories, 2002.

Pelletier, Kenneth R. "CAM Therapies for Specific Conditions: Eczema." In The Best Alternative Medicine, Part II. New York: Simon & Schuster, 2002.

Periodicals

Ernst, E., et al. "Complementary/Alternative Medicine in Dermatology: Evidence-Assessed Efficacy of Two Diseases and Two Treatments." American Journal of Clinical Dermatology 3 (2002): 341–48.

Johnston, G. A., et al. "The Use of Complementary Medicine in Children with Atopic Dermatitis in Secondary Care in Leicester." British Journal of Dermatology 149 (September 2003): 566–71.

Kemp, A. S. "Cost of Illness of Atopic Dermatitis in Children: A Societal Perspective." Pharmacoeconomics 21 (2003): 105–13.

Leung, D. Y., et al. "New Insights into Atopic Dermatitis." Journal of Clinical Investigation 113 (March 2004): 651–57.

Ross, S. M. "An Integrative Approach to Eczema (Atopic Dermatitis)." Holistic Nursing Practice 17 (January-February 2003): 56–62.

Schempp, C. M., et al. "Topical Treatment of Atopic Dermatitis with St. John's Wort Cream: A Randomized, Placebo-Controlled, Double-Blind Half-Side Comparison." Phytomedicine 10 (2003), Supplement 4: 31–7.

Organizations

American Academy of Allergy, Asthma, and Immunology (AAAAI). 611 East Wells Street, Milwaukee, WI 53202. Web site: www.aaaai.org.

American Academy of Dermatology (AAD). PO Box 4014, Schaumburg, IL 60168–4014. Web site: www.aad.org.

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). 1 AMS Circle, Bethesda, MD 20892–3675. Web site: www.niams.nih.gov.

Web Sites

Krafchik, Bernice R. "Atopic Dermatitis." eMedicine, January 23, 2002. Available online at www.emedicine.com/derm/topic38.htm (accessed November 22, 2004).

Other

"Handout on Health: Atopic Dermatitis". NIH Publication No. 03–4272. National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Bethesda, MD: NIAMS, 2003.

[Article by: Rebecca Frey, PhD]

1. a general term for any superficial inflammatory process involving primarily the epidermis, marked early by redness, itching, minute papules and vesicles, weeping, oozing and crusting, and later by scaling, lichenification and often pigmentation.
2. atopic dermatitis.

• facial e. — see facial eczema.
• miliary e. — see feline miliary dermatitis.
• moist e. — see acute moist dermatitis.
• nasal e. — see solar dermatitis. Called also Collie nose.
• watery e. — exudative epidermitis.

Atopic eczema characterized by the distinctive phenomenon of atopy, a familial related allergic response associated with IgE antibody.

Atopic dermatitis
Classification and external resources
Atopic dermatitis
ICD-10	L20
ICD-9	691.8
OMIM	603165
eMedicine	emerg/130 derm/38 ped/2567 oph/479
MeSH	D003876

Atopic dermatitis (AD, a type of eczema) is an inflammatory, chronically relapsing, non-contagious and pruritic (that is, itchy) skin disorder.^[1] It has been given names like "prurigo Besnier," "neurodermitis," "endogenous eczema," "flexural eczema," "infantile eczema," and "prurigo diathésique".^[2]

Contents 1 Signs and symptoms 2 Causes 2.1 Epidermal Barrier Dysfunction 2.2 Allergy 2.3 Microwave radiation 2.4 Food allergy 2.5 Histamine intolerance 2.6 Biological 3 Prevention 3.1 Diet 3.2 Environment and lifestyle 3.3 Allergen/irritant evasion 4 Treatment 4.1 Maintaining the skin barrier 4.2 Prescription drugs 4.3 Light (UV) therapy 4.4 Alternative treatments 4.5 Future research 5 Epidemiology 6 See also 7 References 8 External links

Signs and symptoms

Atopic dermatitis of the anterior flextural crease of the elbow.

Pattern of atopic eczema varies with age

The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food, and environmental allergens and becomes red, flaky and very itchy. It also becomes vulnerable to surface infections caused by bacteria. The skin on the flexural surfaces of the joints (for example inner sides of elbows and knees) are the most commonly affected regions in people.

Atopic dermatitis often occurs together with other atopic diseases like hay fever, asthma and allergic conjunctivitis. It is a familial and chronic disease and its symptoms can increase or disappear over time. Atopic dermatitis in older children and adults is often confused with psoriasis. Atopic dermatitis afflicts humans, particularly young children; it is also a well-characterized disease in domestic dogs.

Although there is no cure for atopic eczema, and its cause is not well understood, it can be treated very effectively in the short term through a combination of prevention (learning what triggers the allergic reactions) and drug therapy.

Atopic dermatitis most often begins in childhood before age 5 and may persist into adulthood. For some, it flares periodically and then subsides for a time, even up to several years.^[3] Yet, it is estimated that 75% of the cases of atopic dermatitis improve by the time children reach adolescence, whereas 25% continue to have difficulties with the condition through adulthood.^[4]

Although atopic dermatitis can theoretically affect any part of the body, it tends to be more frequent on the hands and feet, on the ankles, wrists, face, neck and upper chest. Atopic dermatitis can also affect the skin around the eyes, including the eyelids.^[5]

In most patients, the usual symptoms that occur with this type of dermatitis are aggravated by a Staphylococcus aureus infection, dry skin, stress, low humidity and sweating, dust or sand or cigarette smoke. Also, the condition can be worsened by having long and hot baths or showers, solvents, cleaners or detergents and wool fabrics or clothing.

Atopic dermatitis is also known as infantile eczema, when it occurs in infants. Infantile eczema may continue into childhood and adolescence and it often involves an oozing, crusting rash mainly on the scalp and face, although it can occur anywhere on the body.^[6] The appearance of the rash tends to modify, becoming dryer in childhood and then scaly or thickened in adolescence while the itching is persistent.

Approximately 50% of the patients who develop the condition display symptoms before the age of 1, and 80% display symptoms within the first 5 years of life.^[4]

Symptoms may vary from person to person but they are usually present as a red, inflamed, and itchy rash and can quickly develop into raised and painful bumps.^[7] The first sign of atopic dermatitis is the red to brownish-gray colored patches that are usually very itchy. Itching may become more intense during the night. The skin may present small and raised bumps which may be crusting or oozing if scratched, which will also worsen the itch. The skin tends to be more sensitive and may thicken, crack or scale.

When appearing in the area next to the eyes, scratching can cause redness and swelling around them and sometimes, rubbing or scratching in this area causes patchy loss of eyebrow hair and eyelashes.^[3]

The symptoms of atopic dermatitis vary with the age of the patients. Usually, in infants, the condition causes red, scaly, oozy and crusty cheeks and the symptoms may also appear on their legs, neck and arms. Symptoms clear in about half of these children by the time they are 2 or 3 years old.^[8] In older children, the symptoms include dry and thick, scaly skin with a very persistent itch, which is more severe than in infants. Adolescents are more likely to develop thick, leathery and dull-looking lesions on their face, neck, hands, feet, fingers or toes.

Causes

Epidermal Barrier Dysfunction

More recently, a theory involving the role of Epidermal Barrier Dysfunction has been proposed as an explanation on the physiopathology of atopic dermatitis. Changes in at least 3 groups of genes encoding structural proteins, epidermal proteases and protease inhibitors predispose to a defective epidermal barrier and increase the risk of developing atopic dermatitis. The strong association between both genetic barrier defects and environmental insults to the barrier with atopic dermatitis suggests that epidermal barrier dysfunction is a primary event in the development of this disease.^[9]

Allergy

Although it is an inherited disease, eczema is primarily aggravated by contact with or intake of allergens. It can also be influenced by other factors that affects the immune system such as stress or fatigue. Atopic eczema consists of chronic inflammation; it often occurs in people with a history of allergy disorders such as asthma or hay fever. There is no certain cause of atopic dermatitis. In dogs, atopic dermatitis can be caused by or aggravated by inhaled allergens, food allergens, and flea bites; however, in humans, such relationships are not well established.

Microwave radiation

Exposure to microwave radiation from a cell phone can worsen existing allergies to house dust mite and Japanese Cryptomeria pollen.^[10][11] In a randomized controlled trial, exposure to a cell phone that was actively transmitting increased allergen specific IgE production, whereas sham exposure did not.^[12] The use of a microwave oven at home has been associated with an increased risk of eczema as well.^[13] Mast cell activation is seen in children suffering from eczema.^[14] Electrohypersensitive individuals suffer from increased levels of mast cells in their skin.^[15]

Food allergy

While no cause of atopic dermatitis, food allergy is often present in atopic children, and children with food allergy often present with skin dermatitis indistinguishable from atopic dermatitis. New-onset atopic dermatitis patients at a later age or severe atopic dermatitis often warrant referral to an allergist for food allergy testing. Many dermatologists and physicians test for food allergy in their office. The test is often done as a "pin prick" or "needle prick." A drop of food extract is placed on the skin, and a small prick in the epidermis is performed. A "wheal" is produced with a positive test.

Common food allergen causing eczematous dermatitis include peanuts, tree nuts, shellfish, fish, milk, and egg. While food allergy induced eczematous dermatitis might present independent of atopic dermatitis, some children with atopic dermatitis also have concurrent food allergies.

Histamine intolerance

For a subset of people afflicted with atopic dermatitis are affected by exogenous sources of histamine,^[16] meaning histamine from outside the body. About one-third (33%) of atopic eczematics significantly improve their symptoms after following a histamine-free diet. This diet excludes various foods high in histamine content including cheeses, hard cured sausages, alcohol, and other fermented foods.^[16] Other histamine-free diets also exclude fish, shellfish, tomatoes, spinach, and eggplant as well. Fish is known to succumb to bacterial degradation quickly thus forming high amounts of histamine in the fish which can cause Scombroid poisoning. Certain vegetables like tomatoes, spinach and eggplant naturally contain histamine.

Histamine intolerance is related to an inability for the body to degrade the histamine. This decreased ability to break down histamine may be related to a deficiency in an enzyme called diamine oxidase (DAO). It is unknown whether a deficiency in DAO or another mechanism is responsible for the impaired histamine processing.

Biological

Although it is such a common disease, relatively little is understood about the underlying causes of atopic eczema.^[17] While atopic eczema is associated with asthma and allergic rhinitis, the connection between the diseases has not been established.^[17] Twin studies have consistently shown that the disease has a higher rate of concordance in identical as compared to fraternal twins, which also indicates that genetics plays a role in its development.^[17] However, the rate of concordance between identical twins is far from 100%, and the changing frequency of the disease over time points to the environmental factors—nutrition or hygiene, for instance—that also play a role in disease susceptibility.^[18]

Genomic research into the cause of multigenic diseases is still in its infancy: few genes have ever been identified that contribute to multigenic human disorders.^[18] Researchers have attempted to do this in past whole-genome screens for AE and related diseases, but their results have been inconsistent. A few of the pertinent loci have been validated by replication in further studies (chromosome 2q, chromosome 6p, and chromosome 12q, for example),^[19] but most have not been.

Associations with ATOD1, ATOD2, ATOD3, ATOD4, ATOD5 and ATOD6 have been identified.^[20]

In a publication in Nature Genetics from April 6, 2009, Young-Ae Lee of the Max Delbrück Center for Molecular Medicine in Berlin and her colleagues report a strong association between atopic dermatitis and a common genetic variant, a new locus on chromosome 11, potentially associated with the gene C11orf30.^[21]

Prevention

Since there is no cure for atopic eczema, treatment should mainly involve discovering the triggers of allergic reactions and learning to avoid them.

Diet

Originally controversial, the association of food allergy with atopic dermatitis has now been clearly demonstrated. Many common food allergens can trigger an allergic reaction: such as milk, nuts, cheese, tomatoes, wheat, yeast, soy, and corn. Many of these allergens are common ingredients in grocery store products. Specialty health food stores often carry products that do not contain common allergens.

It has also been established that about a third of people afflicted with atopic dermatitis may have histamine intolerance^[16] and benefit from a histamine-free diet. Various foods commonly associated with allergies also happen have high histamine content. Foods such as cheeses, yogurt, alcohol, fish, shellfish, tomatoes, and fermented foods (soy, yeast, etc.) all have high histamine content. Other histamine foods include spinach, and eggplant, hard-cured sausages, and other processed meats. Various food additives including benzoates and food coloring have also been shown to release endogenous histamine.^[22] Avoiding high histamine foods and processed foods may be beneficial in improving symptoms.

Breastfeeding has been demonstrated to help prevent the development of allergic disease, but if that is unavailable, then hydrolyzed formulas are preferred to cow's milk.^[23] The use of organic dairy products by children and breastfeeding or pregnant mothers reduces the risk of atopic dermatitis in young children.^[24] The avoidance of common food allergens including milk and dairy products, egg, fish, beef and peanut during pregnancy and lactation has also been shown to enhance the preventive beneficial effect of exclusive breast feeding on the incidence of atopic eczema among infants at high risk.^[25]

Environment and lifestyle

Since dust is a very common allergen and irritant, adults with atopic eczema should avoid smoking, as well as the inhalation of dust in general. The dander from the fur of dogs and cats may also trigger an inflammatory response. It is a common misconception that simply removing an animal from a room will prevent an allergic reaction from occurring. A room must be completely free of animal dander in order to prevent an allergic reaction. Anger, stress, and lack of sleep are also factors that are known to aggravate eczema. Excessive heat (especially with humidity) and coldness are known to provoke outbreaks, as well as sudden and extreme temperature swings.

Allergen/irritant evasion

An allergy skin-patch or "scratch" test, given by an allergist, can often pinpoint the triggers of allergic reactions. Once the causes of the allergic reactions are discovered, the allergens should be eliminated from the diet, lifestyle, and/or environment. If the eczema is severe, it may take some time (days to weeks depending on the severity) for the body's immune system to begin to settle down after the irritants are withdrawn.

Treatment

Maintaining the skin barrier

The primary treatment involves prevention, includes avoiding or minimizing contact with (or intake of) known allergens. Once that has been established, topical treatments can be used. Topical treatments focus on reducing both the dryness and inflammation of the skin.

To combat the severe dryness associated with atopic dermatitis, a high-quality, dermatologist-approved moisturizer should be used daily. Moisturizers should not have any ingredients that may further aggravate the condition. Moisturizers are especially effective if applied 5–10 minutes after bathing. As a rule of thumb the thicker the moisturizer the better it is at retaining moisture. Petroleum jelly is considered one of the most effective moisturizers by reducing transepidermal water loss by up to 98%.^[26]

Atopic dermatitis has also been linked to a ceramide deficiency. Ceramide is one of the three key lipids that comprise the skin barrier.^[27] The "stratum corneum ceramide deficiency" is possibly "the putative cause of the barrier abnormality"^[28] in atopic dermatitis. There are various ceramide based creams available including the prescription drug Epiceram as well as other non-prescription options like Cerave and Aveeno for Eczema.

A doctor might prescribe lotion containing sodium hyaluronate to improve skin dryness. One brand of sodium hyaluronate lotion is Hylira.^[29][30]

Most commercial soaps wash away all the oils produced by the skin that normally serve to prevent drying. Using a soap substitute such as aqueous cream helps keep the skin moisturized. A non-soap cleanser can be purchased usually at a local drug store. Showers should be kept short and at a lukewarm/moderate temperature.

Prescription drugs

If moisturizers on their own don't help and the eczema is severe, a doctor may prescribe topical corticosteroid ointments, creams, or injections. Corticosteroids have traditionally been considered the most effective method of treating severe eczema. Disadvantages of using steroid creams include stretch marks and thinning of the skin. Higher-potency steroid creams must not be used on the face or other areas where the skin is naturally thin; usually a lower-potency steroid is prescribed for sensitive areas. The use of the finger tip unit may be helpful in guiding how much topical cream is required to cover different areas. If the eczema is especially severe, a doctor may prescribe prednisone or administer a shot of cortisone or triamcinolone. In some countries, over-the-counter hydrocortisone can be purchased for treatment of mild eczema.

If complications include infections (often of Staphylococcus aureus), antibiotics may be employed.

The immunosuppressants tacrolimus and pimecrolimus can be used as a topical preparation in the treatment of severe atopic dermatitis instead of or in addition to traditional steroid creams. There can be unpleasant side effects in some patients such as intense stinging, itching or burning, which mostly get better after the first week of treatment.^[31] However, the risk of developing skin cancer from the use of these drugs^[32] (especially when combined to UV exposure, such as sunrays) was not ignored by the FDA, which issued a "black box warning."^[33]

In severe cases that do not respond to other treatments, oral immunosuppressant medications are sometimes prescribed, such as ciclosporin, azothioprine and methotrexate. However, these treatments require patients to take regular blood tests as they can have significant side effects on the kidneys and liver.

Light (UV) therapy

A more novel form of treatment involves exposure to broad or narrow-band ultraviolet light. UV radiation exposure has been found to have a localized immunomodulatory effect on affected tissues and may be used to decrease the severity and frequency of flares.^[34] In particular, Meduri et al. have suggested that the usage of UVA1 is more effective in treating acute flares, whereas narrow-band UVB is more effective in long-term management scenarios.^[35] However, UV radiation has also been implicated in various types of skin cancer,^[36] and thus UV treatment is not without risk.

If ultraviolet light therapy is employed, initial exposure should be no longer than 5–10 minutes, depending on skin type. UV therapy should only be moderate, and special care should be taken to avoid sunburn (sunburn will only aggravate the eczema). It does not necessarily have to be administered in a hospital; it can be done at a tanning salon or in natural sunlight, as long as it's done under the direction and supervision of a dermatologist.^[37]

Alternative treatments

Four small and low-quality randomized clinical trials found beneficial effects from a Traditional Chinese medicine herbal formulation called Zemaphyte, which is no longer manufactured.^[38] A randomized clinical trial published in 2007 found that another Chinese herbal formulation increased quality of life and reduced topical corticosteroid use.^[39]

Alternative medicines may (illegally) contain corticosteroids, which are standard treatments for atopic dermatitis, raising a question of whether these illicit substances cause the effects;^[40] however, a 2006 study did not find corticosteroids in a PentaHerbs concoction that had shown beneficial effects.^[41]

A study in April 2009 showed that bathing in a dilute household bleach solution (1/2 cup or 120 ml of ordinary household chlorine bleach (sodium hypochlorite) to a bathtub full of water) in combination with nasal application of mupirocin can be beneficial in patients with clinical signs of secondary bacterial infections.^[42] It is believed that the antibacterial effect of these agents prevents the skin's colonization by staphylococcus aureus which can cause infections in an existing rash when the skin is broken by scratching; this in turn increases the itching, leading to more scratching and inflammation. If a bath is not available, swab onto reddened skin a dilute solution of 4.5 ml household bleach in 750 ml water. The skin must be moisturised with the patient's preferred moisturiser or oil after the antibacterial swabbing or bath.

Future research

It was less than ten years ago that the researchers discovered the first mouse model to spontaneously developed AE-like lesions, the inbred NC/Nga mouse.^[43] These models have been used for tests that would have been impossible in humans, like the administration of Mycobacterium vaccae for the possible prevention of AE-like lesions.^[44]

Trials are being carried out at the Biotechnology and Biological Science Research Council in the UK to see if applying a naturally occurring molecule on the skin will improve the barrier function. The skin of people who suffer from Atopic Dematitis often lacks an efficient barrier making their skin more susceptible to microbial invasions. The trial is expected to end in Jan 2011 ^[45]

Epidemiology

Since the beginning of the twentieth century, many mucosal inflammatory disorders have become dramatically more common; atopic eczema (AE) is a classic example of such a disease. It now affects 10–20% of children and 1–3% of adults in industrialized countries, and its prevalence in the United States alone has nearly tripled in the past thirty to forty years.^[46]

Atopic dermatitis is a common disease which tends to affect both males and females in the same proportion. It is estimated that this condition accounts for about 20% of all dermatologic referrals. The prevalence of atopic dermatitis is however quite difficult to establish since the diagnostic criteria are not applied universally and are not standard, but it is thought to vary roughly between 10% and 30%. Most of the population-based studies report that at least 80% of the atopic dermatitis populations have mild eczema.^[47]

Atopic dermatitis occurs most often in infants and children, and its onset decreases substantially with age, and it is highly unlikely to develop in patients who are older than 30 years.^[48] The condition appears to primarily affect individuals who live in urban areas and in climates with low humidity. However, specialists claim that there is a genetic factor which may play an important role in the development of atopic dermatitis.

See also

• SCORAD

References

1. ^ De Benedetto, A; Agnihothri, R; McGirt, LY; Bankova, LG; Beck, LA (2009). "Atopic dermatitis: a disease caused by innate immune defects?". The Journal of investigative dermatology 129 (1): 14–30. doi:10.1038/jid.2008.259. PMID 19078985. 
2. ^ Abels, C; Proksch, E (2006). "Therapy of atopic dermatitis". Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete 57 (8): 711–725. doi:10.1007/s00105-006-1176-x. PMID 16816954. 
3. ^ ^{a b} "Atopic dermatitis (eczema)". http://www.mayoclinic.com/health/eczema/ds00986/dsection=symptoms. Retrieved June 16, 2010. 
4. ^ ^{a b} "Atopic Dermatitis – Symptoms, Diagnosis". http://www.dermatologychannel.net/dermatitis/atopic-dermatitis-symptoms.shtml. Retrieved June 16, 2010. 
5. ^ "Factors that worsen atopic dermatitis". http://www.mayoclinic.com/health/eczema/ds00986/dsection=symptoms. Retrieved June 16, 2010. 
6. ^ "Infantile eczema". http://www.mayoclinic.com/health/eczema/ds00986/dsection=symptoms. Retrieved June 16, 2010. 
7. ^ "Dermatitis Atopic Eczema". http://www.dermatitisatopic.net/. Retrieved June 16, 2010. 
8. ^ "Signs and Symptoms". http://www.dermatologychannel.net/dermatitis/atopic-dermatitis-symptoms.shtml. Retrieved June 16, 2010. 
9. ^ Cork MJ, et al. Epidermal Barrier Dysfunction in Atopic Dermatitis. J Inv Dermatol 2009. 129:1892-1908
10. ^ Kimata, H (2002). "Enhancement of allergic skin wheal responses by microwave radiation from mobile phones in patients with atopic eczema/dermatitis syndrome". International archives of allergy and immunology 129 (4): 348–350. doi:10.1159/000067592. PMID 12483040. 
11. ^ Kimata, H (2003). "Enhancement of allergic skin wheal responses in patients with atopic eczema/dermatitis syndrome by playing video games or by a frequently ringing mobile phone". European journal of clinical investigation 33 (6): 513–517. doi:10.1046/j.1365-2362.2003.01177.x. PMID 12795649. 
12. ^ Kimata, H. (2005). "Microwave radiation from cellular phones increases allergen-specific IgE production". Allergy 60 (6): 838–839. doi:10.1111/j.1398-9995.2005.00802.x. PMID 15876318. 
13. ^ Wang, IJ; Guo, YL; Weng, HJ; Hsieh, WS; Chuang, YL; Lin, SJ; Chen, PC (2007). "Environmental risk factors for early infantile atopic dermatitis". Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology 18 (5): 441–447. doi:10.1111/j.1399-3038.2007.00550.x. PMID 17617812. 
14. ^ Øymar, K; Aksnes, L (2004). "Urinary 9alpha,11beta-prostaglandin F(2) in children with atopic eczema/dermatitis syndrome: an indicator of mast cell activation?". Acta dermato-venereologica 84 (5): 359–362. doi:10.1080/00015550410035515. PMID 15370701. 
15. ^ Johansson, Olle (2006). "Electrohypersensitivity: State-of-the-Art of a Functional Impairment". Electromagnetic Biology and Medicine 25 (4): 245–258. doi:10.1080/15368370601044150. PMID 17178584. http://adante.vingar.se/electrohypersensitivity1.pdf. 
16. ^ ^{a b c} . pp. 52–56. doi:10.2340/00015555-0565. 
17. ^ ^{a b c} Kluken, H.; Wienker, T.; Bieber, T. (2003). "Atopic eczema/dermatitis syndrome – a genetically complex disease. New advances in discovering the genetic contribution". Allergy 58 (1): 5–12. doi:10.1034/j.1398-9995.2003.02162.x. PMID 12580800. 
18. ^ ^{a b} Schreiber, Stefan; Rosenstiel, Philip; Albrecht, Mario; Hampe, Jochen; Krawczak, Michael (2005). "Genetics of Crohn disease, an archetypal inflammatory barrier disease". Nature Reviews Genetics 6 (5): 376–388. doi:10.1038/nrg1607. PMID 15861209. 
19. ^ Palmer, L. J.; Cookson, WO (2000). "Genomic Approaches to Understanding Asthma". Genome Research 10 (9): 1280–1287. doi:10.1101/gr.143400. PMID 10984446. 
20. ^ "OMIM – DERMATITIS, ATOPIC". http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=603165. Retrieved 2008-09-19. 
21. ^ Esparza-Gordillo, Jorge; Weidinger, Stephan; F lster-Holst, Regina; Bauerfeind, Anja; Ruschendorf, Franz; Patone, Giannino; Rohde, Klaus; Marenholz, Ingo et al. (2009). "A common variant on chromosome 11q13 is associated with atopic dermatitis". Nature Genetics 41 (5): 596–601. doi:10.1038/ng.347. PMID 19349984. 
22. ^ Histamine Restricted Diet—ICUS – International Chronic Urticaria Society. Urticaria.thunderworksinc.com. Retrieved on 2011-01-05.
23. ^ Odijk, J.; Kull, I.; Borres, M. P.; Brandtzaeg, P.; Edberg, U.; Hanson, L. A.; Host, A.; Kuitunen, M. et al. (2003). "Breastfeeding and allergic disease: a multidisciplinary review of the literature (1966–2001) on the mode of early feeding in infancy and its impact on later atopic manifestations". Allergy 58 (9): 833–843. doi:10.1034/j.1398-9995.2003.00264.x. PMID 12911410. 
24. ^ KOALA Birth Cohort Study, University of Maastricht, the Netherlands (Dutch language only)
25. ^ Chandra, RK; Puri, S; Suraiya, C; Cheema, PS (1986). "Influence of maternal food antigen avoidance during pregnancy and lactation on incidence of atopic eczema in infants". Clinical allergy 16 (6): 563–569. doi:10.1111/j.1365-2222.1986.tb01995.x. PMID 3791630. 
26. ^ Petroleum Jelly: Facts and Myths. Articlesbase.com. Retrieved on 2011-01-05.
27. ^ Ceramide Barrier Repair
28. ^ Chamlin, SL; Kao, J; Frieden, IJ; Sheu, MY; Fowler, AJ; Fluhr, JW; Williams, ML; Elias, PM (2002). "Ceramide-dominant barrier repair lipids alleviate childhood atopic dermatitis: changes in barrier function provide a sensitive indicator of disease activity". Journal of the American Academy of Dermatology 47 (2): 198–208. doi:10.1067/mjd.2002.124617. PMID 12140465. Lay summary – Medscape (August 12, 2002). 
29. ^ Hylira Gel Facts and Comparisons at. Drugs.com. Retrieved on 2011-01-05.
30. ^ "Hylira Gel Facts and Comparisons at". Drugs.com. 2010-05-05. http://www.drugs.com/cdi/hylira-lotion.html. Retrieved 2010-06-19. 
31. ^ Jasek, W, ed (2007) (in German). Austria-Codex (62 ed.). Vienna. pp. 2720, 6770. ISBN 3-85200-181-4. 
32. ^ Wooltorton, E. (2005). "Eczema drugs tacrolimus (Protopic) and pimecrolimus (Elidel): cancer concerns". Canadian Medical Association Journal 172 (9): 1179–1180. doi:10.1503/cmaj.050373. PMC 557066. PMID 15817641. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=557066. 
33. ^ Food and Drug Administration (United States) (2005-03-10). "Safety information on Protopic (tacrolimus), Elidel (pimecrolimus)". http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm152565.htm. Retrieved 2009-10-21. 
34. ^ Beattie, P.E.; Finlan, L.E.; Kernohan, N.M.; Thomson, G.; Hupp, T.R.; Ibbotson, S.H. (2005). "The effect of ultraviolet (UV) A1, UVB and solar-simulated radiation on p53 activation and p21Waf1/Cip1". British Journal of Dermatology 152 (5): 1001–1008. doi:10.1111/j.1365-2133.2005.06557.x. PMID 15888160. 
35. ^ Meduri, N. Bhavani; Vandergriff, Travis; Rasmussen, Heather; Jacobe, Heidi (2007). "Phototherapy in the management of atopic dermatitis: a systematic review". Photodermatology, Photoimmunology & Photomedicine 23 (4): 106–112. doi:10.1111/j.1600-0781.2007.00291.x. 
36. ^ Jans, J.; Garinis, G. A.; Schul, W.; Van Oudenaren, A.; Moorhouse, M.; Smid, M.; Sert, Y.-G.; Van Der Velde, A. et al. (2006). "Differential Role of Basal Keratinocytes in UV-Induced Immunosuppression and Skin Cancer". Molecular and Cellular Biology 26 (22): 8515–8526. doi:10.1128/MCB.00807-06. PMC 1636796. PMID 16966369. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1636796. 
37. ^ Scheinfeld, NS; Tutrone, WD; Weinberg, JM; Deleo, VA (2003). "Phototherapy of atopic dermatitis". Clinics in dermatology 21 (3): 241–248. doi:10.1016/S0738-081X(02)00364-4. PMID 12781441. 
38. ^ Zhang, W; Leonard, T; Bath-Hextall, F; Chambers, CA; Lee, C; Humphreys, R; Williams, HC; Zhang, Weiya (2004). "Chinese herbal medicine for atopic eczema". In Zhang, Weiya. Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD002291.pub3. 
39. ^ Hon, K.L.E.; Leung, T.F.; Ng, P.C.; Lam, M.C.A.; Kam, W.Y.C.; Wong, K.Y.; Lee, K.C.K.; Sung, Y.T. et al. (2007). "Efficacy and tolerability of a Chinese herbal medicine concoction for treatment of atopic dermatitis: a randomized, double-blind, placebo-controlled study". British Journal of Dermatology 157 (2): 357–363. doi:10.1111/j.1365-2133.2007.07941.x. PMID 17501956. 
40. ^ Ramsay, H M; Goddard, W; Gill, S; Moss, C (2003). "Herbal creams used for atopic eczema in Birmingham, UK illegally contain potent corticosteroids". Archives of Disease in Childhood 88 (12): 1056–1057. doi:10.1136/adc.88.12.1056. PMC 1719403. PMID 14670768. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1719403. 
41. ^ Hon, Kam-Lun E.; Lee, Vivian W. Y.; Leung, Ting-Fan; Lee, Kenneth K. C.; Chan, Andrew K. W.; Fok, Tai-Fai; Leung, Ping-Chung (November 2006). "Corticosteroids are not present in a traditional Chinese medicine formulation for atopic dermatitis in children". Annals of the Academy of Medicine, Singapore 35 (11): 759–63. PMID 17160188. http://www.annals.edu.sg/pdf/35VolNo11Nov2006/V35N11p759.pdf. 
42. ^ Huang, J. T.; Abrams, M.; Tlougan, B.; Rademaker, A.; Paller, A. S. (2009). "Treatment of Staphylococcus aureus Colonization in Atopic Dermatitis Decreases Disease Severity". Pediatrics 123 (5): e808–e814. doi:10.1542/peds.2008-2217. PMID 19403473. 
43. ^ Gutermuth, Jan; Ollert, Markus; Ring, Johannes; Behrendt, Heidrun; Jakob, Thilo (2004). "Mouse Models of Atopic Eczema Critically Evaluated". International Archives of Allergy and Immunology 135 (3): 262–276. doi:10.1159/000082099. PMID 15542938. 
44. ^ Arkwright, Peter D.; Fujisawa, Chie; Tanaka, Akane; Matsuda, Hiroshi (2005). "Mycobacterium vaccae Reduces Scratching Behavior but not the Rash in NC Mice with Eczema: A Randomized, Blinded, Placebo-Controlled Trial". Journal of Investigative Dermatology 124 (1): 140–143. doi:10.1111/j.0022-202X.2004.23561.x. PMID 15654967. 
45. ^ ISRCTN97515110 – Investigating whether topical application of a non toxic molecule improves epidermal pH and barrier function in atopic dermatitis
46. ^ Saito, Hirohisa (2005). "Much Atopy about the Skin: Genome-Wide Molecular Analysis of Atopic Eczema". International Archives of Allergy and Immunology 137 (4): 319–325. doi:10.1159/000086464. PMID 15970641. 
47. ^ "Eczema". http://www.medscape.com/viewarticle/451667_2. Retrieved June 16, 2010. 
48. ^ "How common is atopic dermatitis?". http://www.medicinenet.com/atopic_dermatitis/page2.htm#3howcommon. Retrieved June 16, 2010. 

External links

• NEA All About Atopic Dermatitis
• Atopic dermatitis picture page at Dermnet
• NIH Handout on Health: Atopic Dermatitis
• Staphy.com a site about atopic eczema
• DermAtlas 9

v d e Diseases of the skin and appendages by morphology Growths Epidermal wart callus seborrheic keratosis acrochordon molluscum contagiosum actinic keratosis squamous cell carcinoma basal cell carcinoma merkel cell carcinoma nevus sebaceous trichoepithelioma Pigmented Freckles lentigo melasma nevus melanoma Dermal and subcutaneous epidermal inclusion cyst hemangioma dermatofibroma keloid lipoma neurofibroma xanthoma Kaposi's sarcoma infantile digital fibromatosis granular cell tumor leiomyoma lymphangioma circumscriptum myxoid cyst Rashes With epidermal involvement Eczematous contact dermatitis atopic dermatitis seborrheic dermatitis stasis dermatitis lichen simplex chronicus Darier's disease glucagonoma syndrome langerhans cell histiocytosis lichen sclerosus pemphigus foliaceus Wiskott-Aldrich syndrome Zinc deficiency Scaling psoriasis tinea (corporis cruris pedis manuum faciei) pityriasis rosea secondary syphillis mycosis fungoides systemic lupus erythematosus pityriasis rubra pilaris parapsoriasis ichthyosis Blistering herpes simplex herpes zoster varicella bullous impetigo acute contact dermatitis pemphigus vulgaris bullous pemphigoid dermatitis herpetiformis porphyria cutanea tarda epidermolysis bullosa simplex Papular scabies insect bite reactions lichen planus miliaria keratosis pilaris lichen spinulosus transient acantholytic dermatosis lichen nitidus pityriasis lichenoides et varioliformis acuta Pustular acne vulgaris acne rosacea folliculitis impetigo candidiasis gonococcemia dermatophyte coccidioidomycosis subcorneal pustular dermatosis Hypopigmented tinea versicolor vitiligo pityriasis alba postinflammatory hyperpigmentation tuberous sclerosis idiopathic guttate hypomelanosis leprosy hypopigmented mycosis fungoides Without epidermal involvement Red Blanchable Erythema Generalized drug eruptions viral exanthems toxic erythema systemic lupus erythematosus Localized cellulitis abscess boil erythema nodosum carcinoid syndrome fixed drug eruption Specialized urticaria erythema (multiforme migrans gyratum repens annulare centrifugum ab igne) Nonblanchable Purpura Macular thrombocytopenic purpura actinic purpura Papular disseminated intravascular coagulation vasculitis Indurated scleroderma/morphea granuloma annulare lichen sclerosis et atrophicus necrobiosis lipoidica Miscellaneous disorders Ulcers Hair telogen effluvium androgenic alopecia trichotillomania alopecia areata systemic lupus erythematosus tinea capitis loose anagen syndrome lichen planopilaris folliculitis decalvans acne keloidalis nuchae Nail onychomycosis psoriasis paronychia ingrown nail Mucous membrane aphthous stomatitis oral candidiasis lichen planus leukoplakia pemphigus vulgaris mucous membrane pemphigoid cicatricial pemphigoid herpesvirus coxsackievirus syphilis systemic histoplasmosis squamous cell carcinoma

v d e Health science - Medicine - Allergic conditions Respiratory system Allergic rhinitis · Asthma · Hypersensitivity pneumonitis · Eosinophilic pneumonia · Churg-Strauss syndrome · Allergic bronchopulmonary aspergillosis · Farmer's lung · Laboratory animal allergy Skin Angioedema · Urticaria · Atopic dermatitis · Allergic contact dermatitis · Hypersensitivity vasculitis Blood and immune system Serum sickness Circulatory system Anaphylaxis Digestive system Coeliac disease · Eosinophilic gastroenteritis · Eosinophilic esophagitis · Food allergy · Milk intolerance Nervous system Eosinophilic meningitis Genitourinary system Acute interstitial nephritis Other conditions Drug allergy · Allergic conjunctivitis · Latex allergy M: LMC cell/phys/auag/auab/comp, igrc imdf/ipig/hyps/tumr proc, drug(L3/4)

v d e Dermatitis and eczema (L20–L30, 690–693,698) Atopic dermatitis Besnier's prurigo Seborrheic dermatitis Pityriasis simplex capillitii · Cradle cap Contact dermatitis (allergic, irritant) plants: Urushiol-induced contact dermatitis · African blackwood dermatitis · Tulip fingers other: Abietic acid dermatitis · Diaper rash · Airbag dermatitis · Baboon syndrome · Contact stomatitis · Protein contact dermatitis Eczema Autoimmune estrogen dermatitis · Autoimmune progesterone dermatitis Breast eczema · Ear eczema · Eyelid dermatitis · Hand eczema (Chronic vesiculobullous hand eczema, Hyperkeratotic hand dermatitis) Autosensitization dermatitis/Id reaction (Candidid, Dermatophytid, Molluscum dermatitis) · Circumostomy eczema · Dyshidrosis · Juvenile plantar dermatosis · Nummular eczema · Nutritional deficiency eczema · Sulzberger–Garbe syndrome · Xerotic eczema Pruritus/Itch/ Prurigo Lichen simplex chronicus/Prurigo nodularis by location: Pruritus ani · Pruritus scroti · Pruritus vulvae · Scalp pruritus Drug-induced pruritus (Hydroxyethyl starch-induced pruritus) · Senile pruritus · Aquagenic pruritus (Aquadynia) Adult blaschkitis · due to liver disease (Biliary pruritus · Cholestatic pruritus) · Prion pruritus · Prurigo pigmentosa · Prurigo simplex · Puncta pruritica · Uremic pruritus Other/ungrouped substances taken internally: Bromoderma · Fixed drug reaction Nummular dermatitis · Pityriasis alba · Papuloerythroderma of Ofuji M: INT, SF, LCT anat/phys/devp noco(i/b/d/q/u/r/p/m/k/v/f)/cong/tumr(n/e/d), sysi/epon proc, drug (D2/3/4/5/8/11)

v d e Immune disorders: hypersensitivity and autoimmune diseases (279.5–6) Type I/allergy/atopy (IgE) Foreign Atopic dermatitis · Allergic urticaria · Hay fever · Allergic asthma · Anaphylaxis · Food allergy (Milk, Egg, Peanut, Tree nut, Seafood, Soy, Wheat), Penicillin allergy Autoimmune none Type II/ADCC (IgM, IgG) Foreign Pernicious anemia · Hemolytic disease of the newborn Autoimmune Cytotoxic Autoimmune hemolytic anemia · Idiopathic thrombocytopenic purpura  · Bullous pemphigoid  · Pemphigus vulgaris · Rheumatic fever · Goodpasture's syndrome "Type 5"/receptor Graves' disease · Myasthenia gravis Type III (Immune complex) Foreign Henoch–Schönlein purpura · Hypersensitivity vasculitis · Reactive arthritis · Farmer's lung · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction Autoimmune Systemic lupus erythematosus · Subacute bacterial endocarditis · Rheumatoid arthritis Type IV/cell-mediated (T-cells) Foreign Allergic contact dermatitis · Mantoux test Autoimmune Diabetes mellitus type 1 · Hashimoto's thyroiditis · Guillain–Barré syndrome  · Multiple sclerosis  · Coeliac disease · Giant-cell arteritis GVHD Transfusion-associated graft versus host disease Unknown/ multiple Foreign Hypersensitivity pneumonitis (Allergic bronchopulmonary aspergillosis) · Transplant rejection · Latex allergy (I+IV) Autoimmune Sjögren's syndrome · Autoimmune hepatitis · Autoimmune polyendocrine syndrome (APS1, APS2) · Autoimmune adrenalitis · Systemic autoimmune disease M: LMC cell/phys/auag/auab/comp, igrc imdf/ipig/hyps/tumr proc, drug(L3/4)

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