Spratt D I, Bigos S T, Beitins I, Cox P, Longcope C, Orav J
Department of Medicine, Maine Medical Center, Portland 04102.
J Clin Endocrinol Metab. 1992 Dec;75(6):1562-70. doi: 10.1210/jcem.75.6.1464665.
Previous reports of hypogonadotropic hypogonadism in critically ill men may not reflect the complexity of changes in the hypothalamic-pituitary-gonadal (HPG) axis during acute illness. We sampled blood throughout hospitalization in 55 men admitted to acute care units to delineate the spectrum of changes in circulating gonadotropin and sex steroid levels at the onset and during recovery from acute illness. Bioactive LH and FSH were measured in a subset of patients. Percent free testosterone was measured to assess changes in binding to sex hormone binding globulin. Medications and serum estrogen and prolactin levels were monitored as potential causes of hypogonadotropism. Sustained suppression of serum testosterone levels below the normal range occurred in 62% of men with varying diagnoses and disease severity. Percent free testosterone remained constant. Hypogonadotropism was observed in most men (60%) and occurred independently from head injury, surgery, medications, or hyperprolactinemia. In a subset of men (n = 16), LH and/or FSH rose transiently above the normal range. Bioactivity of both LH and FSH remained constant while serum testosterone levels decreased. In contrast to serum testosterone levels, mean serum levels of E1, E2 and androstenedione were not less than control values. We conclude that both primary and secondary hypogonadism occur transiently in acutely ill men and cannot be explained solely by medications, hyperprolactinemia, or hyperestrogenemia. Neither biopotency of gonadotropins nor binding of testosterone to SHBG change across the course of acute illness. The hypogonadism, often severe and prolonged, may contribute to the persistent catabolic state observed in many critically ill patients.
先前有关危重症男性低促性腺激素性性腺功能减退的报道可能未反映出急性疾病期间下丘脑 - 垂体 - 性腺（HPG）轴变化的复杂性。我们对入住急性护理病房的55名男性在整个住院期间进行了血液采样，以描绘急性疾病发作时及恢复过程中循环促性腺激素和性类固醇水平的变化范围。在一部分患者中测量了生物活性促黄体生成素（LH）和促卵泡生成素（FSH）。测量了游离睾酮百分比以评估与性激素结合球蛋白结合的变化。监测药物以及血清雌激素和催乳素水平作为低促性腺激素血症的潜在原因。62%患有不同诊断和疾病严重程度的男性血清睾酮水平持续抑制至正常范围以下。游离睾酮百分比保持不变。大多数男性（60%）出现了低促性腺激素血症，且其发生与头部损伤、手术、药物或高催乳素血症无关。在一部分男性（n = 16）中，LH和/或FSH短暂升高至正常范围以上。LH和FSH的生物活性保持不变，而血清睾酮水平下降。与血清睾酮水平相反，E1、E2和雄烯二酮的平均血清水平不低于对照值。我们得出结论，急性病男性会短暂出现原发性和继发性性腺功能减退，且不能仅由药物、高催乳素血症或高雌激素血症来解释。在急性疾病过程中，促性腺激素的生物活性以及睾酮与性激素结合球蛋白的结合均未改变。这种性腺功能减退往往严重且持续时间长，可能导致许多危重症患者出现持续的分解代谢状态。
