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脂溢性皮炎与马拉色菌酵母。

Seborrhoeic dermatitis and Pityrosporum yeasts.

作者信息

Bergbrant I M

机构信息

Department of Dermatology, University of Gothenburg, Sahlgrenska Hospital, Götborg, Sweden.

出版信息

Curr Top Med Mycol. 1995;6:95-112.

PMID:8724243
Abstract

The connection between P. ovale and seborrhoeic dermatitis has been clearly demonstrated in a number of treatment studies but we still do not know how P. ovale induces skin lesions. An enhanced growth of P. ovale cannot be the cause, because a number of studies with quantitative determinations of P. ovale have not been able to show any difference in the number of yeast cells between patients and healthy controls. The number of P. ovale is probably only important for the individuals who are susceptible to seborrhoeic dermatitis. An abnormal immune response to P. ovale could be another explanation. Sohnle et al. have shown that P. ovale can activate complement by both the classical and the alternative pathway. A defective cell-mediated immunity to P. ovale in patients with seborrhoeic dermatitis has been demonstrated by Wikler et al. In patients with AIDS, who are known to have a diminished T-cell function, a high incidence of seborrhoeic dermatitis has been found. Activation of the alternative complement pathway by P. ovale, which does not require T-cell function, could be an explanation for the inflammatory response. I also believe that the skin lipids are important in the pathogenesis. An improvement of seborrhoeic dermatitis has been demonstrated after treatment with drugs that reduce the sebum excretion. Pityrosporum has lipase activity and may generate free fatty acids, which could also contribute to the inflammatory response. There are a number of factors which are probably important in the pathogenesis of seborrhoeic dermatitis, that is, the number of P. ovale, P. ovale lipase activity, skin lipids, immune function, heredity, atmospheric humidity and emotional state. A reduction in the number of P. ovale in patients suffering from seborrhoeic dermatitis and being treated with antimycotic treatment is, at the present state of knowledge, the best way to treat the disease.

摘要

在一些治疗研究中已明确证实卵形糠秕孢子菌与脂溢性皮炎之间的关联,但我们仍不清楚卵形糠秕孢子菌是如何诱发皮肤病变的。卵形糠秕孢子菌生长增强并非病因,因为多项对卵形糠秕孢子菌进行定量测定的研究未能显示患者与健康对照之间酵母细胞数量有任何差异。卵形糠秕孢子菌的数量可能仅对易患脂溢性皮炎的个体重要。对卵形糠秕孢子菌的异常免疫反应可能是另一种解释。索恩勒等人已表明,卵形糠秕孢子菌可通过经典途径和替代途径激活补体。维克勒等人已证实脂溢性皮炎患者对卵形糠秕孢子菌的细胞介导免疫存在缺陷。在已知T细胞功能减退的艾滋病患者中,已发现脂溢性皮炎的高发病率。卵形糠秕孢子菌激活不依赖T细胞功能的替代补体途径可能是炎症反应的一种解释。我也认为皮肤脂质在发病机制中很重要。在用减少皮脂分泌的药物治疗后,脂溢性皮炎已得到改善。糠秕孢子菌具有脂肪酶活性,可能产生游离脂肪酸,这也可能导致炎症反应。脂溢性皮炎发病机制中可能有许多因素很重要,即卵形糠秕孢子菌的数量、卵形糠秕孢子菌脂肪酶活性、皮肤脂质、免疫功能、遗传、大气湿度和情绪状态。就目前的知识水平而言,对患有脂溢性皮炎且正在接受抗真菌治疗的患者减少卵形糠秕孢子菌数量是治疗该病的最佳方法。

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