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.
Eczema classification remains haphazard and unsystematized, and the proliferation of synonyms hinders understanding. At times, there is focus on the location (e.g. hand eczema), or on the specific appearance (eczema craquele or discoid), and other times on possible cause (varicose eczema). Herpetiformis and dyshidrosis are misnomers. Further adding to the confusion, many sources use the term eczema and the term for the most common type of eczema (atopic eczema) interchangeably.
This classification is clustered by incidence frequency.
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 lesion biopsy: removal of a small piece of skin for microscopic examination in a 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.
The use of anything that may dry out the skin should be discontinued and this includes both normal soaps and bubble baths that remove the natural oils from the skin.
The moistening agents are called 'emollients'. The rule to use is: match the thicker ointments to the driest, flakiest skin. Light emollients like Aqueous Cream may dry the skin if it is very flaky and whilst it is the moisturiser traditionally prescribed by doctors in the UK, it is in fact only licensed for use as a soap substitute on washing
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 whilst creams are easy to apply, they are quickly absorbed into the skin and so need frequent re-application. Ointments, with their lesser water content, stay on the skin for longer and so need fewer applications but they must be applied sparingly if to avoid a sticky mess.
Typical emollients in the U.K. are: Oilatum or Balneum bath oils, Aqueous cream for washing with, Diprobase or Doublebase pump-action creams also used for washing and may be later applied directly to the skin. The preferred moisturiser of dermatologists is a mix of liquid and white-soft paraffins. Sebexol, Epaderm ointment and Eucerin lotion or cream may be helpful with itching. Moisturizing gloves can be worn while sleeping.
Some report improvement of symptoms after treatment of the skin with porridge oats, either directly or with an extract.
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"). (For example, Corazza M, Virgili A, Allergic contact dermatitis from ophthalmic products: can pre-treatment with sodium lauryl sulfate increase patch test sensitivity? Contact Dermatitis. 2005 May;52(5):239-41.)
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 (according to Consumer Reports), 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:
How to use soap when one must
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. Whilst research has suggested Naloxone hydrochloride and dibucaine suppress the itch cycle in atopic-dermatitis model mice.
Hence a steroid of an appropriate strength to promptly settle an episode of eczema should be sparingly applied. Once the desired response has been achieved, it should be discontinued and not used for long-term prevention.
Light therapy using ultraviolet light can help. PUVA, UVB, and Narrow Band UVB are all used. Current research seems to show that Narrow Band UVB is the most effective, in addition to having lowest risk of skin cancer.
When light therapy alone is found to be ineffective, it is combined with a drug called Psoralen. This treatment is termed as photo-chemotherapy.
It might be necessary to avoid processed foods to remove these allergens from the diet. This is because many processed foods contain milk-derived products such as whey powder, which is added to the food as a filler. Processed meats (for example: ham, salami and bacon) often contain preservatives in very high doses. Many fizzy drinks also contain preservatives.
The symptoms of Biotin deficiency include Seborrheic dermatitis, a skin disorder which is similar to eczemaCurrent research has found that taking biotin alleviates the symptoms of eczema [http://www.althealth.co.uk/services/info/supplements/vitamin_h_1.php.
Patients should inform their doctor/allergist/dermatologist if they are pursuing one of these treatment routes.
An article by Cookson et al. (2004), that appeared in Nature Reviews Immunology, has shed some much needed light onto the immunogenetics and pathogenesis of eczema. Many individuals with eczema are known to have high IgE titres (immunoglobulin levels) specific for allergens from the ubiquitous house dust mite, Dermatophagoides pteronyssinus. This litter critter, received its name because it feeds on human skin that is shed from the outermost layer of human skin. It comes from the Greek word meaning “eater of skin.” These dust-mites contain numerous proteins that allow them to survive. Der p I, Der p II are the main house dust-mite allergens. These allergens are present in the mites faecal pellets and are proteases that have profound effects on epithelial cells and the skin. These proteases are known to disrupt intercellular adhesion molecules, increase paracellular permeability, and also initiate cell death. Basically, these proteins damage the barrier effect of the skin, by releasing more skin cells, of which the dust mite can now consume. This in turn, leads to an easier entry point for bacteria to penetrate the skin, and subsequently leads to the well-known inflammatory response of eczema; redness, itchiness, and pain. Other well-known allergens are proteases that damage the skin barrier; Fel d I, the main cat allergen, degrades denatured collagens and cleaves fibronectin and the main grass allergen Phl p V is an RNAase. Damage from these allergens is usually prevented by endogenous protease inhibitors, such the gene SPINK5. Mutations in this gene are known to cause Netherton’s syndrome, which is a generalized congenital erythroderma. These patients always develop atopic disease, including hay fever, food allergy, urticaria and asthma. Such evidence clearly supports the hypothesis that skin damage from allergens may be the cause of eczema.
The March 2006 issue of the journal Nature Genetics, reports on research at the University of Dundee identifying 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.
Autoimmune diseases | Dermatology
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