|
Eczema is a chronic skin condition, characterized by dry, red, flaky patches of skin. Eczema appears most commonly on the face, neck, elbows, wrists, knees, behind the ears, and on the scalp. During acute episodes, the patches become oozing, inflamed, and itchy. There are currently two recognized classifications of dermatitis: atopic and contact. Contact dermatitis is typically aggravated by direct skin contact with allergens, such as chemicals, wool, lanolin, soap, or cosmetics. Atopic eczema is usually triggered by inhaled or ingested allergens, such as certain foods, pollen, dust, or animal dander. Some literature discusses a third classification, "dysregulatory microbial eczemas."(1) This category refers to eczema caused by the introduction of microflora into the horny layer of the skin, and a breakdown in the epidermis, resulting in inflammation.
Eczema is caused by a cascade of immune mechanisms. The itching of eczema is a result of allergens interacting with IgG on the surface of mast cells and macrophages under the skin. This leads to the flooding of histamines, prostaglandins, and other inflammatory components, along with T lymphocytes (type 2 T-helper cells) and macrophages to the skin.
Eczema is an atopic condition, an inherited form of an allergic disorder. It typically appears in infancy or early childhood. Children whose parents both have allergies are twice as likely to develop allergies themselves.(2) The prevalence of atopic allergies, such as asthma and eczema, has risen steadily since the 1960's, perhaps in correlation with increasing levels of pollutants.(2) The risk of developing asthma and allergic rhinitis is higher among children with hereditary eczema.(3)
Evidence exists that eczema may be due to a hereditary impairment of the delta-6-desaturase enzyme.(4) Delta-6 desaturase is responsible for converting dietary linoleic acid to gamma linolenic acid, a precursor of the anti-inflammatory prostaglandin PGE1.
Food allergies appear to play a significant role in atopic dermatitis. The presence of severe eczema has been associated with an increased tendency to produce food-specific IgE antibodies.(3) Although the subject is debated, maternal antigen exposure during pregnancy and lactation may increase the chance of eczema in infancy. Studies have confirmed that women who avoid antigens during pregnancy and lactation, and exclusively breast feed have reduced occurrence of infants with atopic eczema.(5)
There appears to be a strong link between intestinal flora and allergic sensitivity. This relationship begins in infancy, as the colonization of bacteria in the gut begins shortly after birth. Intestinal microorganisms may help regulate inflammation by enhancing the ability of IgA to distinguish between antigens, and by controlling the secretion of type 2 T-helper cells.(6) If normal development of the gut microflora is disrupted in infancy, it may predispose the child to allergic diseases.
|
