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dermatitis.jpg|
Eczema
ICD-10 L20-L30
ICD-9 692
OMIM 603165
DiseasesDB 4113
MedlinePlus 000853
eMedicine Derm/38 Ped/2567
MeSH {{{MeshNumber}}}

Eczema is a form of dermatitis, or inflammation of the upper layers of the skin.

The term "eczema" is broadly applied to a range of persistent or recurring skin rashes characterized by redness, skin edema, itching and dryness, with possible crusting, flaking, blistering, cracking, oozing, or bleeding. Areas of temporary skin discoloration sometimes characterize healed lesions, though scarring is rare.

Psychological effects

Eczema often comes and goes in cycles, meaning that at some times of the year sufferers are able to feel normal, while at other times they will distance themselves from social contact. Sufferers with visible marks generally feel fine (physically) and can act normal, but when it is mentioned they may become withdrawn and self-conscious. Since it is a condition made worse by scratching, a sufferer with highly visible sores aggravated by scratching often feels as if everyone is looking at the marks and that they are self-induced. Although scratching does give a sense of relief, it is usually a temporary solution and can lead to problems with constant scratching. Sufferers often shy away from scratching in public, but the solution is to scratch in privacy. In cases of children with eczema, visible scars or scratch marks can lead to suspicion of home abuse or self-mutilation, which causes possible peer rejection and may add to a general level of stress.

Types

ICD-10 codes are provided where available. The term eczema refers to a set of clinical characteristics. Classification of the underlying diseases has been haphazard and unsystematic, with many synonyms used to describe the same condition. A type of eczema may be described by location (e.g. hand eczema), by specific appearance (eczema craquele or discoid), or by possible cause (varicose eczema). Further adding to the confusion, many sources use the term eczema and the term for the most common type of eczema (atopic eczema) interchangeably.

Eczema-arms

More severe eczema

The European Academy of Allergology and Clinical Immunology (EAACI) has published a position paper which simplifies the nomenclature of allergy-related diseases including atopic and allergic contact eczemas (Johansson et al., 2001, Allergy 56:813). Non-allergic eczemas are not affected by this proposal.

The classification below is clustered by incidence frequency.

More common eczemas

  • Atopic eczema (aka infantile e., flexural e., atopic dermatitis) is believed to have a hereditary component, and often runs in families whose members also have hay fever and asthma. Itchy rash is particularly noticeable on face and scalp, neck, inside of elbows, behind knees, and buttocks. Experts are urging doctors to be more vigilant in weeding out cases that are in actuality irritant contact dermatitis. It is very common in developed countries, and rising. (L20)
  • Contact dermatitis is of two types: allergic (resulting from a delayed reaction to some allergen, such as poison ivy or nickel), and irritant (resulting from direct reaction to a solvent, for example). Some substances act both as allergen and irritant (e.g. wet cement). Other substances cause a problem after sunlight exposure, bringing on phototoxic dermatitis. About three quarters of cases of contact eczema are of the irritant type, which is the most common occupational skin disease. Contact eczema is curable provided the offending substance can be avoided, and its traces removed from one’s environment. (L23; L24; L56.1; L56.0)
Eczema

A patch of eczema that has been scratched

  • Xerotic eczema (aka asteatotic e., e. craquele or craquelatum, winter itch, pruritus hiemalis) is dry skin that becomes so serious it turns into eczema. It worsens in dry winter weather, and limbs and trunk are most often affected. The itchy, tender skin resembles a dry, cracked, river bed. This disorder is very common among the older population. Ichthyosis is a related disorder. (L85.3; L85.0)
  • Seborrhoeic dermatitis (aka cradle cap in infants, dandruff) causes dry or greasy scaling of the scalp and eyebrows. Scaly pimples and red patches sometimes appear in various adjacent places. In newborns it causes a thick, yellow crusty scalp rash called cradle cap which seems related to lack of biotin, and is often curable. (L21; L21.0)

Less common eczemas

  • Dyshidrosis (aka dyshidrotic e., pompholyx, vesicular palmoplantar dermatitis, housewife’s eczema) only occurs on palms, soles, and sides of fingers and toes. Tiny opaque bumps called vesicles, thickening, and cracks are accompanied by itching which gets worse at night. A common type of hand eczema, it worsens in warm weather. (L30.1)
  • Discoid eczema (aka nummular e., exudative e., microbial e.) is characterized by round spots of oozing or dry rash, with clear boundaries, often on lower legs. It is usually worse in winter. Cause is unknown, and the condition tends to come and go. (L30.0)
  • Venous eczema (aka gravitational e., stasis dermatitis, varicose e.) occurs in people with impaired circulation, varicose veins and edema, and is particularly common in the ankle area of people over 50. There is redness, scaling, darkening of the skin and itching. The disorder predisposes to leg ulcers. (I83.1)
  • Dermatitis herpetiformis (aka Duhring’s Disease) causes intensely itchy and typically symmetrical rash on arms, thighs, knees, and back. It is directly related to celiac disease, and can often be put into remission with appropriate diet. (L13.0)
  • Neurodermatitis (aka lichen simplex chronicus, localized scratch dermatitis) is an itchy area of thickened, pigmented eczema patch that results from habitual rubbing and scratching. Usually there is only one spot. Often curable through behavior modification and anti-inflammatory medication. Prurigo nodularis is a related disorder showing multiple lumps. (L28.0; L28.1)
  • Autoeczematization (aka id reaction, autosensitization) is an eczematous reaction to an infection with parasites, fungi, bacteria or viruses. It is completely curable with the clearance of the original infection that caused it. The appearance varies depending on the cause. It always occurs some distance away from the original infection. (L30.2)
  • There are also eczemas overlaid by viral infections (e. herpeticum, e. vaccinatum), and eczemas resulting from underlying disease (e.g. lymphoma). Eczemas originating from ingestion of medications, foods, and chemicals, have not yet been clearly systematized. Other rare eczematous disorders exist in addition to those listed here.

Diagnosis

Eczema diagnosis is generally based on the appearance of inflamed, itchy skin in eczema sensitive areas such as face, chest and other skin crease areas. For evaluation of the eczema, a scoring system can be used (for example, SCORAD, a scoring system for atopic dermatitis).

Given the many possible reasons for eczema flare ups, a doctor is likely to ascertain a number of other things before making a judgment:

  • An insight to family history
  • Dietary habits
  • Lifestyle habits
  • Allergic tendencies
  • Any prescribed drug intake
  • Any chemical or material exposure at home or workplace

To determine whether an eczema flare is the result of an allergen, a doctor may test the blood for the levels of antibodies and the numbers of certain types of cells. In eczema, the blood may show a raised IgE or an eosinophilia.

The blood can also be sent for a specific test called Radioallergosorbent Test (RAST) or a Paper Radioimmunosorbent Test (PRIST). In the test, blood is mixed separately with many different allergens and the antibody levels measured. High levels of antibodies in the blood signify an allergy to that substance.

Another test for eczema is skin patch testing. The suspected irritant is applied to the skin and held in place with an adhesive patch. Another patch with nothing is also applied as a control. After 24 to 48 hours, the patch is removed. If the skin under the suspect patch is red and swollen, the result is positive and the person is probably allergic to that substance.

Occasionally, the diagnosis may also involve a skin biopsy: removal of a small piece of affected skin for microscopic examination in a pathology laboratory.

Blood tests and biopsies are not always necessary for eczema diagnosis. However, doctors will at times require them if the symptoms are unusual, severe or in order to identify particular triggers.

Treatment

Moisturizing

Dermatitis severely dries out the skin, and keeping the affected area moistened can promote healing and retain natural moisture. This is the most important self-care treatment that one can use in atopic eczema. The use of anything that may dry out the skin or that remove the natural oils from the skin should be discontinued.

Soap removes dirt but also removes natural oils from the skin; making the skin dry, irritated and itchy. The removal of soap altogether and the use of soap-free body washes will maintain natural skin oils and may reduce some of the need to moisturize the skin.

Moistening agents are called 'emollients'. The rule for use is this: match the thicker ointments to the driest, flakiest skin. Light emollients like aqueous cream may dry the skin if it is very flaky, so heavier ointment should be used.

Typical emollients are: Oilatum or Balneum bath oils, Medi Oil, aqueous cream for washing with. Diprobase or Doublebase pump-action creams can also be used for washing and may be applied directly to the skin after bathing.Sebexol, Epaderm ointment and Eucerin lotion or cream may be helpful with itching. Moisturizing gloves can be worn while sleeping. Emollient bath oils should be added to bath water and then suitable agents applied after patting the skin dry. Generally twice daily applications of emollients work best and while creams are easy to apply, they are quickly absorbed into the skin, therefore needing frequent re-application. Ointments, with less water content, stay on the skin for longer and need fewer applications.

As an alternative to therapy for rehydrating unbroken skin, for broken skin direct application of waterproof tape for an extended period, with or without other medicinal balms, can stop dryness and prevent skin cracking and mechanical abrasions of the itch-cycle and reduce lichenification.

One alternative treatment, fashionable in the Victorian and Edwardian eras, was sulfur. Recently sulfur has regained some popularity as a homeopathic alternative to steroids and coal tar. However, there is currently no scientific evidence for the claim that sulfur treatment relieves eczema.[1]

Eczema and detergents

The first and primary recommendation is that people suffering from eczema shouldn't use detergents of any kind unless absolutely necessary. Current medical thought is that people wash too much and that eczema sufferers should use cleansers only when water is not sufficient to remove dirt from skin.

Another point of view is that detergents are so ubiquitous in modern environments and so persistent in tissues and surfaces, safe soaps are necessary to remove them in order to eliminate the eczema in a percentage of cases. Although most recommendations use the terms "detergents" and "soaps" interchangeably, and tell eczema sufferers to avoid both, detergents and soaps are not the same and are not equally problematic to eczema sufferers. Detergents increase the permeability of skin membranes in a way that soaps and water alone do not. Sodium lauryl sulfate, the most common household detergent, has been shown to amplify the allergenicity of other substances ("increase antigen penetration").[2]

The use of detergents in recent decades has increased dramatically, while the use of soaps began to decline when detergents were invented, and leveled off to a constant around the '60s. Complicating this picture is the recent development of mild plant-based detergents for the natural products sector.

Unfortunately there is no one agreed-upon best kind of cleanser for eczema sufferers. Different clinical tests, sponsored by different personal product companies, unsurprisingly tout various brands as the most skin friendly based on specific properties of various products and different underlying assumptions as to what really determines skin friendliness. The terms "hypoallergenic" and "doctor tested" are not regulated,[3] and no research has been done showing that products labeled "hypoallergenic" are in fact less problematic than any others.

Dermatological recommendations in choosing a soap generally include:

  • Avoid harsh detergents or drying soaps.
  • Choose a soap that has an oil or fat base; a "superfatted" soap is best.
  • Use an unscented soap.
  • Patch test your soap choice, by using it only on a chosen area until you are sure of its results.
  • Use a non-soap based cleanser.

How to use soap when one must

  • Use soap sparingly
  • Avoid using washcloths, sponges, or loofahs
  • Use soap only on areas where it is necessary
  • Soap up only at the very end of your bath
  • Use a fragrance-free barrier type moisturizer such as vaseline or aquaphor before drying off
  • Use care when selecting lotion, soap, or fragrance, avoiding suspected allergens. Ask your doctor for recommendations.
  • Never rub your skin dry, or else your skin's oil/moisture will be on the towel and not your body

Itch relief

Anti-itch drugs, often antihistamine, may reduce the itch during a flare up of eczema, and the reduced scratching in turn reduces damage & irritation to the skin (the Itch cycle).

Capsaicin applied to the skin acts as a counter irritant (see Gate control theory of nerve signal transmission). Other agents that act on nerve transmissions, like menthol, also have been found to mitigate the body's itch signals, providing some relief. Recent research suggests Naloxone hydrochloride and dibucaine suppress the itch cycle in atopic-dermatitis model mice as well.

Corticosteroids

Dermatitis is often treated by doctors with prescribed Glucocorticoid (a corticosteroid steroid) ointments, creams or lotions. For mild-moderate eczema a weak steroid may be used (e.g. Hydrocortisone or Desonide), whilst more severe cases require a higher-potency steroid (e.g. Clobetasol propionate). Corticosteroids do not cure eczema, but are highly effective in controlling or suppressing symptoms in most cases.[4]

Corticosteroids must be used sparingly to avoid possible side effects, the most common of which is that their prolonged use can cause the skin to thin and become fragile (atrophy).[5] Because of this, if used on the face or other delicate skin, only a low-strength steroid should be used. Additionally, high-strength steroids used over large areas, or under occlusion, may be significantly absorbed into the body, causing hypothalamic-pituitary-adrenal axis suppression (HPA Axis suppression).[6] Finally by their immunosuppressive action they can, if used without antibiotics or antifungal drugs, lead to some skin infections (fungal or bacterial). Care must be taken to avoid the eyes, as topical corticosteroids applied to the eye can cause glaucoma.[7]

Because of the risks associated with this type of drug, a steroid of an appropriate strength should be sparingly applied only to control an episode of eczema. Once the desired response has been achieved, it should be discontinued and replaced with emollients as maintenance therapy. Corticosteroids are generally considered safe to use in the short- to medium-term for controlling eczema, with no significant side effects differing from treatment with non-steroidal ointment.[8]

Immunomodulators

Topical immunomodulators like pimecrolimus (Elidel® and Douglan®) and tacrolimus (Protopic®) were developed after corticosteroid treatments, effectively suppressing the immune system in the affected area, and appear to yield better results in some populations. However, such suppression is believed by alternative health practitioners to have possible adverse health effects. The US Food and Drug Administration has issued a public health advisory[9] about the possible risk of lymph node or skin cancer from use of these products, but many professional medical organizations disagree with the FDA's findings;

  • The postulation is that the immune system may help remove some pre-cancerous abnormal cells which is prevented by these drugs. However, any chronic inflammatory condition such as eczema, by the very nature of increased metabolism and cell replication, has a tiny associated risk of cancer (see Bowen's disease).
  • Current practice by UK dermatologists [10] is not to consider this a significant real concern and they are increasingly recommending the use of these new drugs. The dramatic improvement on the condition can significantly improve the quality of life of sufferers (and families kept awake by the distress of affected children). The major debate, in the UK, has been about the cost of such newer treatments and, given only finite NHS resources, when they are most appropriate to use.[11]
  • In addition to cancer risk, there are other potential side effects with this class of drugs. Adverse reactions including severe flushing, photosensitive reactivity and possible drug interaction in patients who consume even small amounts of alcohol.[12]

Antibiotics

The disruption to the skin's normal barrier protection through dry and cracked skin allows easy entry for bacteria. Scratching by the patient both introduces infection and spreads it from one area to another. Any skin infection further irritates the skin and a rapid deterioration in the condition may ensue; the appropriate antibiotic should be given.

Light therapy

Light therapy using ultraviolet light can help control eczema.[13] UVA is mostly used, but UVB and Narrow Band UVB are also used. Ultraviolet light exposure carries its own risks, particularly eventual skin cancer from exposure.[14]

When light therapy alone is found to be ineffective, the treatment is performed with the application (or ingestion) of a substance called psoralen. This PUVA (Psoralen + UVA) combination therapy is termed photo-chemotherapy. Psoralens make the skin more sensitive to UV light, thus allowing lower doses of UVA to be used. However, the increased sensitivity to UV light also puts the patient at greater risk for skin cancer.[15]

Diet and Nutrition

Recent studies provide hints that food allergy may trigger atopic dermatitis. For these people, identifying the allergens could allow an avoidance diet, although this approach is still in an experimental stage.[16]

Dietary elements reported to trigger Eczema by sufferers include dairy products and coffee (both caffeinated and decaffeinated), soya, eggs, nuts, wheat and maize (sweetcorn).[How to reference and link to summary or text]

Alternative therapies

Non-conventional medical approaches include traditional herbal medicine and others. Patients should inform their doctor/allergist/dermatologist if they are pursuing one of these treatment routes. Patients can also wear clothing designed specifically to manage the itching, scratching and peeling associated with eczema. Sulfur has been used for many years as a treatment in the alleviation of eczema, although this could be suppressive. Many patients find that swimming in the ocean will relieve symptoms and clear up the red patchy scales. Oatmeal is a common kitchen remedy to relieve itching, and can be applied topically as a cream or, as a colloid, in the bath.

Herbal Medicine

Historical sources - notably traditional Chinese medicine and Western herbalism - suggest a wide variety of treatments, each of which may vary from individual to individual as to efficacy or harm. Toxicity may be present in some. Some of these remedies are for topical use.

Research

Other than direct treatments of the symptoms, no cure is presently known for most types of dermatitis; even cortisone treatments and immunomodulation may often have only minor effects on what may be a complex problem. As the condition is often related to family history of allergies (and thus heredity), it is probable that gene therapy or genetic engineering might help.

Damage from the enzymatic activity of allergens is usually prevented by the body's own protease inhibitors, such as, LEKTI, produced from the gene SPINK5. Mutations in this gene are known to cause Netherton’s syndrome, which is a congenital erythroderma. These patients nearly always develop atopic disease, including hay fever, food allergy, urticaria and asthma. Such evidence supports the hypothesis that skin damage from allergens may be the cause of eczema, and may provide a venue for further treatment.[17]

Another study identified a gene that the researchers believe to be the cause of inherited eczema and some related disorders. The gene produces the protein filaggrin, the lack of which causes dry skin and impaired skin barrier function.[18]

Vulnerability to live vaccinia virus

In June, 2007, Science magazine reported[19] that an American soldier who had been vaccinated for smallpox-- the vaccine contains live vaccinia virus-- had transmitted vaccinia virus to his two-year-old son. The soldier and his son both had a history of eczema. The son rapidly came down with a rare side effect, eczema vaccinatum, which had been seen during the 1960s when children were routinely vaccinated against smallpox. The child developed a severe full-body pustular rash; his abdomen filled with fluid; and his kidneys nearly failed. Intense consultation with experts from the Centers for Disease Control and Prevention, and a donation of an experimental antiviral drug by SIGA Technologies, saved the child's life. Those with a family history of eczema are advised not to accept the smallpox vaccination, or any other that contains live vaccinia virus.

See also

References

  1. [1]
  2. Corazza, M., Virgili, A. (2005) Allergic contact dermatitis from ophthalmic products: can pretreatment with sodium lauryl sulfate increase patch test sensitivity? Contact Dermatitis 52(5), 239-41. PMID 15898995
  3. Murphy, L.A., White, I.R., Rastogi, S.C.(2004) Is hypoallergenic a credible term? Clinical and Experimental Dermatology, 29(3), 325-7. PMID 15115531
  4. Hoare C., Li Wan Po A., Williams H. (2000) Systematic reviews of treatments for atopic eczema. Health Technology Assessment 4, 1-191.
  5. [2]
  6. Lee, N. P., Arriola, E. R. (1999) Topical corticosteroids: back to basics. Western Journal of Medicine, 171(5-6), 351–353.
  7. [3]
  8. Van Der Meer, J. B., Glazenburg, E. J., Mulder, P. G., Eggink, H. F., Coenraads, P.J. (1999) The management of moderate to severe atopic dermatitis in adults with Fluticasone Propionate. British Journal of Dermatology, 140, 1114-21.
  9. [4]
  10. [5]
  11. [6]
  12. Martins, G. A., Arruda, L. (2004) Systemic treatment of psoriasis - Part I: methotrexate and acitretin. Anais Brasileiros de Dermatologia, 79(3), 263-278
  13. Polderman M., Wintzen, M., le Cessie, S., Pavel, S. (2005). UVA-1 cold light therapy in the treatment of atopic dermatitis: 61 patients treated in the Leiden University Medical Center. Photodermatology, Photoimmunology, Photomedicine, 21(2), 93.
  14. [7]
  15. Stern, R. S. (2001). The Risk of Melanoma in Association with Long-term Exposure to PUVA. Journal of the American Academy of Dermatology, 44(5), 755-61.
  16. Kanny G. Atopic dermatitis in children and food allergy: combination or causality? Should avoidance diets be initiated? Ann Dermatol Venereol 2005; 132 Spec No 1: 1S90-103. PMID 15984300
  17. Walley, A.J. et al. (2001) Gene polymorphism in Netherton and common atopic disease. Nature Genetics 29(2), 175-8. PMID 11544479
  18. Palmer, C.N. et al. (2006) Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nature Genetics 38(4), 441-6. PMID 16550169
  19. Kaiser, J. (2007) A tame virus runs amok Science 316(5830), 1418-9.

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