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Atopic Eczema

Atopic eczema (AD) is a characteristic type of chronic dermatitis frequently associated with atopy and an elevated IgE level. There are no single distinguishing features of AD; however, the diagnosis can be made on a combination of history, and morphological findings.

  1. Epidemiology
    AD has a world-wide distribution and affects all races. About 3% of children under age 5 years had AD with a male to female ratio of 1.2 : 1. Majority of patients presents within the first 5 years. AD runs in family. About 75% of patients have a personal or family history of other atopic diseases, e.g., allergic rhinitis, asthma, hay fever.
  2. Aetiology and Pathogenesis
    The aetiology is unknown and the pathogenetic mechanisms are speculative. However, a number of clinical, pathological and immunological abnormalities are frequently observed in these patients and are briefly discussed below:
  3. Elevated IgE
    Occur in about 80 percent of AD patients and are directed against a wide variety of antigen like pollens, molds, foods, house dust mites (HDM) and bacterial antigens etc. A high IgE level is not a unique feature of AD but appears to correlate with the clinical severity and falls with remission. Atopic diathesis, atopic features without IgE level.
  4. Skin Prick Test and Rast
    Patients with AD often show positive Prick test and RAST to common household allergens like egg, milk, wheat, fish, soy, peanut, pollens, HDM and animal danders etc. However, avoidance of such allergens does not necessarily bring about a clinical response.
  5. Bacterial Antigens
    Staph. aureus colonization occurs in over 50% of AD patients and compared to less than 5% in normal individuals, and is frequently isolated (> 90%) from acute exudative lesions and lichenified plaques. The density of the organism correlates with the severity of eczema and antibiotics that clear Staph. aureus improve eczema.
  6. Impaired Cellular Immunity
    This includes a reduced CD8+ suppressor T cells, a reduced natural killer cell function, a reduced IFN-g production, a reduced response to mitogens; peripheral eosinophilia in some and abnormal neutrophil chemotaxis.
  7. Inflammatory Cells and Mediators
    A very characteristic feature of AD is intense pruritus. It has been shown that an increased population of mast cells occurs in the skin of AD patients which releases histamine, leukotrienes and cytokines much more readily compared with normal subjects.
  8. Abnormal Vascular Responses
    Disturbed vascular reactivity like white dermographism, nicotine blanching, and delayed blanch with methacholine are well documented.
  9. Sweat And Sebum Production
    AD patients tend to produce more sweating than nonatopic controls. It has been suggested that an increase in transepidermal water loss, and a possible deficiency of lipids in the epidermis account for the skin dryness.

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