鱼鳞病
银屑病
洛伐他汀
吉非罗齐
医学
辛伐他汀
脂质代谢
普伐他汀
HMG-CoA还原酶
胆固醇
角化过度
还原酶
皮肤病科
药理学
内分泌学
生物化学
生物
酶
出处
期刊:Hautarzt
[Springer Nature]
日期:1995-02-01
卷期号:46 (2): 76-80
被引量:27
标识
DOI:10.1007/s001050050213
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI