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Dermatitis/eczema 

Dermatitis/eczema

Chapter:
Dermatitis/eczema
Author(s):

Peter S. Friedmann

, and Michael J. Arden-Jones

DOI:
10.1093/med/9780199204854.003.2306_update_001

Update:

Pathogenesis—discussion of the phenomenon whereby the skin of atopic dermatitis sufferers helps programme the adaptive T cell-mediated immune response towards Th2.

Updated on 28 Nov 2013. The previous version of this content can be found here.
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date: 29 April 2017

Eczema is a characteristic pattern of skin inflammation that has many subtypes, with some induced by external factors such as irritants or skin sensitizers. Atopic eczema is due partly to a genetic susceptibility, which programmes altered immune responses and skin physiology, together with reactions to exogenous allergens and microbes, but a number of eczema patterns do not appear to have external causes.

The key points in the recognition of eczema are that the skin is reddened, may be thickened as a result of the inflammatory infiltrate and oedema, and the affected areas have ill-defined margins that break up into tiny red papules. Acute or severe eczema bubbles, blisters, and weeps. The distribution of the rash may be diagnostic, both of the type of eczema and the key causal factors.

Management requires identification and avoidance of provoking factors. The inflammation is treated with topical steroids of different potencies, supplemented with moisturizers. Newer therapies include topical calcineurin antagonists, with a range of systemic therapies being used to control the most severe types of disease.

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