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[抗血脂药物引起的皮肤表现]

[Antilipemic drug-induced skin manifestations].

作者信息

Proksch E

机构信息

Universitäts-Hautklinik, Kiel.

出版信息

Hautarzt. 1995 Feb;46(2):76-80. doi: 10.1007/s001050050213.

Abstract

Systemically administered lipid-lowering drugs can induce eczema, ichthyosis, or psoriasis as side effects. Common abnormalities in these diseases are a rough, scaly skin, a disturbed permeability barrier and disturbed epidermal proliferation and differentiation. The disturbed epidermal differentiation is accompanied by changes in the keratin composition and the cornified envelope proteins as well as by changes in the lipid composition. Lipid-lowering drugs do not necessarily all cause the same diseases, because they inhibit different steps in the cholesterol synthetic pathway. The lipid-lowering drugs lovastatin (Mevacor), simvastatin (Zocor) and pravastatin (Selipram) can cause eczema; these drugs inhibit an early step of cholesterol biosynthesis, viz. HMG CoA reductase activity. The lipid-lowering drugs triparanol and diazacholesterol inhibit a late step in cholesterol biosynthesis, delta-24-sterol reductase, and they can induce ichthyosis or palmoplantar hyperkeratosis. In contrast, systemically applied gemfibrozil, which mainly lowers triglycerides, can cause an exacerbation of psoriasis. These observations show the importance of the lipid metabolism in the pathogenesis of eczema, ichthyosis, and psoriasis.

摘要

全身给药的降脂药物可诱发湿疹、鱼鳞病或银屑病等副作用。这些疾病常见的异常表现为皮肤粗糙、脱屑,通透性屏障受损以及表皮增殖和分化紊乱。表皮分化紊乱伴随着角蛋白组成和角质包膜蛋白的变化以及脂质组成的改变。降脂药物不一定都会引发相同的疾病,因为它们抑制胆固醇合成途径中的不同步骤。降脂药物洛伐他汀(美降之)、辛伐他汀(舒降之)和普伐他汀(普拉固)可引发湿疹;这些药物抑制胆固醇生物合成的早期步骤,即HMG CoA还原酶活性。降脂药物曲帕拉醇和氮杂胆固醇抑制胆固醇生物合成的后期步骤,即δ-24-甾醇还原酶,它们可诱发鱼鳞病或掌跖角化过度。相比之下,主要降低甘油三酯的全身应用药物吉非贝齐可使银屑病病情加重。这些观察结果表明脂质代谢在湿疹、鱼鳞病和银屑病发病机制中的重要性。

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