Seborrhoeic dermatitis and Pityrosporum yeasts.

Current topics in medical mycology Pub Date : 1995-01-01
I M Bergbrant
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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.

脂溢性皮炎和糠皮孢子菌。
卵形疟原虫与脂溢性皮炎之间的联系已经在许多治疗研究中得到了清楚的证明,但我们仍然不知道卵形疟原虫是如何诱发皮肤病变的。卵形假单胞菌的生长增强不可能是原因,因为许多对卵形假单胞菌进行定量测定的研究未能显示出患者与健康对照组之间酵母菌细胞数量的任何差异。卵圆杆菌的数量可能只对易患脂溢性皮炎的个体重要。卵形疟原虫的异常免疫反应可能是另一种解释。Sohnle等人已经证明,卵形圆孢杆菌可以通过经典途径和替代途径激活补体。Wikler等人证实了脂溢性皮炎患者对卵形疟原虫的细胞介导免疫缺陷。在已知t细胞功能降低的艾滋病患者中,脂溢性皮炎的发病率很高。卵形蛋白激活替代补体途径,不需要t细胞功能,这可能是炎症反应的一个解释。我也认为皮肤脂质在发病机制中起重要作用。脂溢性皮炎的改善已被证明治疗后,减少皮脂排泄的药物。Pityrosporum具有脂肪酶活性,并可能产生游离脂肪酸,这也可能有助于炎症反应。脂溢性皮炎的发病机制中可能有许多重要的因素,即卵泡磷脂的数量、卵泡磷脂酶活性、皮肤脂质、免疫功能、遗传、大气湿度和情绪状态。减少患有脂溢性皮炎并正在接受抗真菌治疗的患者的卵形疟原虫数量,就目前的知识状况而言,是治疗该疾病的最佳方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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