Gynecomastia and cirrhosis of the liver.

Gynecomastia and cirrhosis of the liver.
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男性乳房发育症和肝硬化。

DOI:
10.1001/archinte.1990.00390150061012
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发表时间:
1990
影响因子:
--
通讯作者:
Frank Q. Nuttall
Frank Q. Nuttall
中科院分区:
--
文献类型:
--
作者:
John Cavanaugh;Catherine B. Niewoehner;Frank Q. Nuttall

文献摘要

被引文献

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肝硬化经常被列为男性乳房发育症的原因。我们之前发现,在住院男性中,男性乳房发育症的患病率与体重指数和年龄相关。肝硬化受试者(非水肿)的平均体重指数和男性乳房发育症患病率与总体人群没有差异。由于患有腹水、外周水肿或两者兼而有之的更严重的肝硬化受试者通常都很瘦,因此我们检查了 18 名更严重的肝硬化受试者和 18 名非肥胖者(平均体重指数,20.9 +/- 0.6 kg/m2)年龄匹配的对照受试者,了解可触及的男性乳房发育的患病率。还测量了总睾酮、游离睾酮、总雌激素和雌二醇浓度。百分之五十的对照受试者患有男性乳房发育症。乳腺组织直径与体重指数相关。肝硬化受试者中男性乳房发育症的患病率为 44%。在这些受试者中,乳腺组织直径和体重指数之间没有发现显着相关性,可能是因为体液潴留导致体重指数增加。结果无法根据药物来解释。肝硬化患者的血清游离睾酮浓度低于对照组(0.11 +/- 0.02 vs 0.22 +/- 0.03 nmol/L)。肝硬化患者的总无雌激素睾酮比率较高(10.3 +/- 2.5 vs 2.6 +/- 0.5),无雌二醇睾酮比率也较高(2.2 +/- 0.7 vs 0.5 +/- 0.1)。这些比率在患有或不患有男性乳房发育症的肝硬化受试者中没有显着差异。因此,这些数据表明,除了雌激素-睾酮比率之外的因素在肝硬化受试者和对照者的男性乳房发育中发挥着作用,或者乳腺组织对雌激素-睾酮比率升高的敏感性高度可变。
Hepatic cirrhosis is frequently listed as a cause of gynecomastia. We found previously that in hospitalized men the prevalence of gynecomastia was correlated with body mass index and with age. The mean body mass index and the prevalence of gynecomastia in the cirrhotic subjects (nonedematous) did not differ from those in the overall population. Because more severely cirrhotic subjects with ascites, peripheral edema, or both usually are thin, we examined 18 more severely cirrhotic subjects and 18 nonobese (mean body mass index, 20.9 +/- 0.6 kg/m2), age-matched control subjects for the prevalence of palpable gynecomastia. Total testosterone, free testosterone, total estrogen, and estradiol concentrations also were measured. Fifty percent of the control subjects had gynecomastia. Breast tissue diameter was correlated with body mass index. The prevalence of gynecomastia in the cirrhotic subjects was 44%. In these subjects no significant correlation was noted between breast tissue diameter and body mass index, presumably because the body mass index was increased owing to fluid retention. The results could not be accounted for based on medications. Serum free testosterone concentrations were lower in the cirrhotic patients than in the controls (0.11 +/- 0.02 vs 0.22 +/- 0.03 nmol/L). The total estrogen-free testosterone ratio was higher in cirrhotic patients (10.3 +/- 2.5 vs 2.6 +/- 0.5), as was the estradiol-free testosterone ratio (2.2 +/- 0.7 vs 0.5 +/- 0.1). These ratios did not differ significantly in cirrhotic subjects with and without gynecomastia. Therefore, these data indicate that factors other than the estrogen-testosterone ratio are playing a role in the development of gynecomastia in both cirrhotic subjects and controls or that breast tissue sensitivity to an elevated estrogen-testosterone ratio is highly varible.