Melnik B, Plewig G
Universitäts-Hautklinik Düsseldorf.
Z Hautkr. 1988 Jul 15;63(7):591-2, 595-6.
Follicular hyperkeratinization of the epithelium of the acroinfundibulum of sebaceous follicles is one of the primary events in the pathogenesis of acne vulgaris. Oral treatment with 13-cis-retinoic acid can reduce these hyperkeratoses. In order to determine whether follicular hyperkeratinization is related to disturbances of epidermal follicular lipids, we analyzed the lipids of initial comedones from 10 patients with nodulocystic acne before and after a 6th weeks oral therapy with 13-cis-retinoic acid (0.7 mg/kg body weight). The treatment with retinoid resulted in a significant increase of epidermal lipids (free sterols: +34%; ceramides: +19%, whereas the lipids of sebaceous origin decreased (glycerides: -36%). The mass ratio of free sterols to cholesterol sulfate increased by 86% compared to pre-treatment levels. These findings support the hypothesis that local follicular deficiencies of epidermal lipids due to increased sebum secretion might induce abnormal follicular keratinization.
皮脂腺毛囊顶漏斗部上皮的滤泡性过度角化是寻常痤疮发病机制中的主要事件之一。口服13 - 顺式维甲酸治疗可减轻这些过度角化。为了确定滤泡性过度角化是否与表皮滤泡脂质紊乱有关，我们分析了10例结节囊肿性痤疮患者在口服13 - 顺式维甲酸（0.7 mg/kg体重）6周治疗前后初发粉刺的脂质情况。维甲酸治疗导致表皮脂质显著增加（游离固醇：增加34%；神经酰胺：增加19%），而皮脂腺来源的脂质减少（甘油酯：减少36%）。与治疗前水平相比，游离固醇与硫酸胆固醇的质量比增加了86%。这些发现支持了以下假设：由于皮脂分泌增加导致局部滤泡表皮脂质缺乏可能会诱发异常的滤泡角化。
