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肝硬化男性性腺功能减退的机制。

Mechanism of hypogonadism in cirrhotic males.

作者信息

Green G R

出版信息

Gut. 1977 Oct;18(10):843-53. doi: 10.1136/gut.18.10.843.

Abstract

Men with chronic liver disease frequently develop clinical signs of hypogonadism and overt feminisation. Associated with these features, they have been found to have a reduced production of testosterone with low plasma concentrations, but only a minority of cirrhotic men would seem to have a marginal increase in circulating biologically potent oestrogens. Furthermore, this latter finding does not correlate with the presence of clinical feminisation. The original hypothesis to explain these changes now seems less likely to be true and no other single hypothesis has, on its own, been found to provide an adequate explanation for all the clinical and biochemical features found in cirrhotic men. It may be that the pathogenesis of endocrine changes in cirrhotic men is multifactorial--for instance, a combination of decreased hepatic clearance of some oestrogenic compounds, an autoimmune mediated primary testicular defect, and a specific potentiation effect by alcohol. Alternatively, it may be that none of these suggested mechanisms is of importance and that the endocrine changes are mediated instead by other mechanisms which remain, as yet, undiscovered or unconsidered. The fascination which this problem has held for clinicians and biochemists for many years seems likely to persist for some time to come.

摘要

患有慢性肝病的男性经常会出现性腺功能减退和明显女性化的临床症状。与这些特征相关的是,他们被发现睾酮分泌减少,血浆浓度较低,但只有少数肝硬化男性的循环生物活性雌激素似乎略有增加。此外,后一项发现与临床女性化的存在并无关联。最初用于解释这些变化的假设现在似乎不太可能成立,而且尚未发现其他单一假设能够充分解释肝硬化男性中发现的所有临床和生化特征。肝硬化男性内分泌变化的发病机制可能是多因素的——例如,某些雌激素化合物的肝脏清除率降低、自身免疫介导的原发性睾丸缺陷以及酒精的特定增强作用共同作用。或者,也可能是这些提出的机制都不重要,内分泌变化是由其他尚未被发现或未被考虑的机制介导的。这个问题多年来一直吸引着临床医生和生物化学家,在未来一段时间内似乎仍将如此。

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