Baker H W, Burger H G, de Kretser D M, Dulmanis A, Hudson B, O'Connor S, Paulsen C A, Purcell N, Rennie G C, Seah C S, Taft H P, Wang C
Q J Med. 1976 Jan;45(177):145-78.
The clinical features and hormonal abnormalities were surveyed in 117 men with cirrhosis of the liver. Compared with healthy men of similar ages, the patients had significantly lower metabolic clearance rates, plasma production rates and total and free levels of testosterone, reduced testosterone responses to human chorionic gonadotrophin stimulation, higher oestradiol, luteinizing hormone and follicle stimulating hormone levels and higher binding capacities of sex steroid binding globulin. The peripheral conversion of testosterone to oestradiol was also found to be significantly increased. However, the metabolic clearance and plasma production rates of oestradiol were not significantly different from those of healthy men. Patients who were severely ill with liver failure and one with haemochromatosis had low levels of luteinizing hormone and follicle stimulating hormone and sub-normal responses to clomiphene and luteinizing hormone-releasing hormone. Higher plasma oestradiol levels were found in patients with gynaecomastia and spider naevi than in those without these signs. However, the clinical features of androgen deficiency--that is, testicular atrophy, impotence and loss of secondary sex hair--were only poorly related to the low testosterone levels, and production rates and longtitudinal studies indicated that the hormonal levels, endocrine features and severity of the liver disease could change independently. It is concluded that the clearance of oestradiol from plasma is not limited by liver disease in all patients, and that reduced degradation of oestrogens is not the initial event in the sequence leading to the hormonal abnormalities of cirrhosis. While gonadotrophin deficiency occurs with liver failure and in some patients with haemochromatosis, the more usual findings are of elevated gonadotrophin levels and a poor Leydig cell response to chorionic gonadotrophin. These suggest that the hypogonadism is primary in most patients with cirrhosis. The causes of the high oestradiol levels were not discovered. Increased peripheral conversion of precursors to oestradiol or increased testicular secretion of oestradiol are possibilities. The high binding capacities of sex steroid binding globulin were not significantly correlated with either the low testosterone or high oestradiol level and the cause of this abnormality remains uncertain. The low metabolic clearance rates of testosterone appeared to result from the increased plasma protein binding of testosterone. The discrepancies in the expected relationships between the hormone and clinical changes suggest that factors other than those studied are also involved in the genesis of the endocrine features of hepatic cirrhosis.
对117例肝硬化男性患者的临床特征和激素异常情况进行了调查。与年龄相仿的健康男性相比，这些患者的代谢清除率、血浆生成率以及睾酮的总量和游离水平显著降低，对人绒毛膜促性腺激素刺激的睾酮反应减弱，雌二醇、促黄体生成素和促卵泡生成素水平升高，性类固醇结合球蛋白的结合能力增强。还发现睾酮向雌二醇的外周转化显著增加。然而，雌二醇的代谢清除率和血浆生成率与健康男性相比无显著差异。患有严重肝功能衰竭的患者以及1例血色素沉着症患者的促黄体生成素和促卵泡生成素水平较低，对克罗米芬和促黄体生成素释放激素的反应低于正常水平。有男子女性型乳房和蜘蛛痣的患者血浆雌二醇水平高于无这些体征的患者。然而，雄激素缺乏的临床特征，即睾丸萎缩、阳痿和第二性征毛发脱落，与低睾酮水平的相关性较差，并且长期研究表明激素水平、内分泌特征和肝脏疾病的严重程度可能独立变化。得出的结论是，并非所有患者血浆中雌二醇的清除都受肝脏疾病限制，雌激素降解减少并非导致肝硬化激素异常过程中的初始事件。虽然促性腺激素缺乏在肝功能衰竭患者和一些血色素沉着症患者中出现，但更常见的发现是促性腺激素水平升高以及睾丸间质细胞对绒毛膜促性腺激素反应不佳。这些表明大多数肝硬化患者的性腺功能减退是原发性的。雌二醇水平升高的原因尚未明确。前体向雌二醇的外周转化增加或睾丸雌二醇分泌增加都有可能。性类固醇结合球蛋白的高结合能力与低睾酮水平或高雌二醇水平均无显著相关性，这种异常的原因仍不确定。睾酮代谢清除率低似乎是由于睾酮与血浆蛋白结合增加所致。激素与临床变化之间预期关系的差异表明，除了所研究的因素外，其他因素也参与了肝硬化内分泌特征的发生。
