![]() Although the transepidermal water loss (TEWL) values as marker of the inside-outside skin barrier function improved significantly more in the betamethasone valerate-treated group, the important skin barrier structures (lamellar bodies and formation of the lipid bilayers in the lower stratum corneum) did not normalize. Skin atrophy in the betamethasone group was already noticeable after 3 weeks of treatment. In our recent randomized, double-blinded right–left arm study comparing topical treatment with 0.1% betamethasone valerate cream and 1% pimecrolimus cream (PIM) for 3 weeks in AD patients with symmetrical lesions we found a good clinical response to both treatment regimens (15). pimecrolimus) primarily emerged as topical anti-inflammatory drugs without the risk of skin thinning and without displacement of epidermal Langerhans’ cells (16, 17). In recent years calcineurin inhibitors (e.g. The side-effects of corticosteroid treatment, skin atrophy and immune suppression leading to bacterial infection, are well known (2, 15). The most established treatment for AD is topical corticosteroids of different strengths, focussing on immune intervention. It is well known that those patients with dry skin conditions benefit from treatment with emollients as the time between episodes of disease recurrence can be extended. These findings correlate with the dry skin type or ichthyosis vulgaris frequently seen in atopic patients. Since 2004 (14) we have consistently seen reduced hydration values in lesional skin in different skin conditions when there are enhanced TEWL values. ![]() ![]() In earlier studies we and others found a disturbed epidermal barrier function in patients with AD not only in lesional skin, but already in non-lesional skin (14). The intercellular lipid bilayers are formed during the extrusion of the epidermal lamellar body into the transition zone between stratum granulosum and stratum corneum (for review see 13). The skin barrier is mainly localized in the lower stratum corneum and is maintained by corneocytes and a lipid-enriched intercellular domain. Recently it has been suggested that allergen penetration into the skin due to a defect in skin barrier function leads to sensitization and causes the development of AD and even hay fever and asthma (11, 12). The ”atopic march” describes the development of asthma in patients with AD (9, 10). Mutations in the filaggrin gene are strong risk factors for ichthyosis vulgaris, AD and asthma (4–8). The pathogenesis of AD is still largely unknown, but an interaction of genetic and environmental factors is likely to play a major role (1–3). The dysfunctional skin barrier allows invasion of allergens and pathogens to occur, which triggers immunological reaction of the TH-2-mediated pathway (allergy development) and thereafter the TH-1-mediated pathway (inflammation). The resulting pruritus and burning sensations lead to scratching and self-perpetuation of the disease. E-mail: with atopic dermatitis (AD) have epidermal barrier dysfunction and inflammation of the skin. Jens-Michael Jensen, Department of Dermatology, University Hospitals of Schleswig-Holstein, Campus Kiel, University of Kiel, Arnold-Heller-Str. Īccepted Epub ahead of print Apr 10, 2013 Key words: calcineurin inhibitor epidermis topical corticosteroid epidermal barrier. Clinical score and TEWL were more improved after treatment with TA, whereas the lamellar bodies were more normal after treatment with PIM. An increase in lamellar bodies also occurred with TA treatment (46% p < 0.05) however, significantly less than with PIM ( p < 0.05). A significantly higher number of normal lamellar bodies was found after 3 weeks of treatment with PIM (58% p < 0.005). The TEM revealed a strong reduction in lamellar bodies in lesional skin of AD only 32% of the lamellar bodies were normal. The pEASi was significantly more improved with TA compared with PIM, whereas stratum corneum hydration was slightly more improved after treatment with PIM. Partial Eczema Area and Severity Index (pEASi), stratum corneum hydration, and transepidermal water loss (TEWL) were monitored on days 1, 8 and 22. In punch biopsies, before and after treatment, skin lipid bilayer and lamellar body structure were examined by transmission electron microscopy (TEM). In a controlled, randomized, double-blinded, right–left comparison study we investigated the effect of pimecrolimus (PIM) cream compared with triamcinolone acetonide cream (TA) on the skin barrier in 15 patients with symmetrical elbow lesions of AD. Stratum corneum skin barrier is formed by corneocytes and extracellular lipids extruded from the epidermal lamellar bodies. Patients with atopic dermatitis (AD) have an epidermal barrier dysfunction, which allows invasion of allergens to occur.
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