Atopic dermatitis clinical features

Dry, scaly skin is characterized by a decrease in the water retention capacity of the stratum corneum (SC),1 with water content diminished to less than 10%. Barrier function of the SC is usually declined, and transepidermal water loss (TEWL) is increased because of an abnormality on barrier homeostasis.2 People feel tightness of their skin, and the skin surface becomes rough, scaly, and sensitive. Hyperkeratosis, abnormal scaling, and epidermal hyperplasia are usually observed in the dry skin.2 Keratinization also shows abnormal features.2 These phenomena are commonly observed in atopic dermatitis and psoriasis.3 Dermatitis induced by environmental factors such as exposure to chemicals, low humidity, and UV radiation also shows these features. Thus, many researchers have been investigating the cause and treatment of dry skin, and there is currently great interest in adequate model systems for dry skin studies. In this chapter, I will describe several model systems of dry skin for clinical research of dermatitis associated with skin surface dryness and also mention recent studies to improve the dry skin. 

As described previously, one can induce dry, scaly skin, which shows features very similar to dermatitis such as atopic dermatitis and psoriasis. Use of this experimentally induced dry skin should enable the discovery of a new clinical methodology to cure or care for skin problems. Recently, several excellent in vitro skin models have been reported. Although they are also very useful models for the study of cutaneous metabolism, their function and microstructure are still different from those of intact skin. On the other hand, the mechanisms underlying abnormal desquamation, that is, scaling in the dry skin such as atopic dermatitis, are not completely known. Sato et al. reported55 the inhibition of protease in the SC induced scale without affecting epidermal mitosis. This result seems to be no direct relationship between skin surface appearance and epidermal proliferation. However, decline of SC barrier function induced epidermal hyperplasia, as described earlier.30 The loss of water content from SC also induced epidermal DNA synthesis.30 Further mechanistic studies on each of the dry skin features are required. 

Burr and Burr reported in 1929 a new deficiency disease produced by the rigid exclusion of fat from the diet. 1 Rodents fed a fat-free diet showed reduced growth and reproductive failure, accompanied by two prominent changes in the skin, that is, increased scaliness and impaired barrier function.1,2 Reversal of the features of deficiency by administration of linoleic acid (LA), led to the concept of essential fatty acids (EFA) that cannot be synthesized by the higher animals.2 Similarities between the clinical features of EFA deficiency and atopic dermatitis led Hansen in 1937 to discover low blood levels of unsaturated fat in atopic children,3 and he later reported that EFA-deficient infants developed an eczematous rash, which responded to LA supplements.4 Several studies had previously examined a range of dietary oil supplements in atopic dermatitis,5-8 with generally reported benefit. 

VKC is differentiated from GPC and AKC by its clinical presentation. Distinguishing features include age at onset, male predisposition, geographic distribution, lack of relationship to contact lens use, and absence of atopic dermatitis. 

Allergic disorders of the eyelid include atopic dermatitis, contact dermatitis, and urticaria. Eczema is a common feature of both atopic and contact dermatitis.Table 27-5 summarizes the clinical manifestations and management of each entity. 

Amemiya T, Matsuda H, Uehara M. Ocular findings in atopic dermatitis with special reference to the clinical features of atopic cataract. Ophthaknologica 1980 180 129-132. 

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