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多囊卵巢疾病作为女性生殖轴的一种神经内分泌紊乱疾病。

Polycystic ovarian disease as a neuroendocrine disorder of the female reproductive axis.

作者信息

Hall J E

机构信息

Department of Medicine, Harvard Medical School, Boston, Massachusetts.

出版信息

Endocrinol Metab Clin North Am. 1993 Mar;22(1):75-92.

PMID:8095452
Abstract

Despite many years of investigation, the benign syndrome(s) of hyperandrogenic amenorrhea, commonly known as PCOD, remains an enigma. Although hyperinsulinemia and hyperandrogenemia from any cause may produce many of the signs and symptoms common to PCOD secondarily, there exists a subset of patients in whom the major abnormality is neuroendocrine. These patients have a gonadotropin profile characterized by an elevated amplitude of LH pulsations in association with normal to low levels of FSH and a fast frequency of pulsatile LH secretion. A major question still remaining is whether the neuroendocrine abnormality is primary or secondary to abnormal ovarian feedback by androgens, or more likely, estrogens. Some evidence suggests that the pattern of secretion of LH and FSH from the pituitary may be owing solely to an increased frequency of GnRH stimulation, but there is little evidence of a specific primary abnormality of neurotransmitters. Subsequent studies in which the various subgroups of PCOD are carefully delineated will be required to clarify these relationships and in so doing provide patients with optimal therapeutic choices.

摘要

尽管经过多年研究,高雄激素性闭经这种良性综合征(通常称为多囊卵巢综合征)仍然是个谜。虽然任何原因导致的高胰岛素血症和高雄激素血症都可能继发产生许多多囊卵巢综合征常见的体征和症状,但有一部分患者的主要异常在于神经内分泌。这些患者的促性腺激素特征为促黄体生成素(LH)脉冲幅度升高,同时促卵泡生成素(FSH)水平正常或偏低,且促黄体生成素呈快速脉冲式分泌。仍然存在的一个主要问题是,神经内分泌异常是原发性的,还是雄激素,更有可能是雌激素对卵巢异常反馈的继发性结果。一些证据表明,垂体分泌促黄体生成素和促卵泡生成素的模式可能仅仅是由于促性腺激素释放激素(GnRH)刺激频率增加,但几乎没有证据表明存在特定的神经递质原发性异常。后续需要对多囊卵巢综合征的各个亚组进行仔细划分的研究,以阐明这些关系,从而为患者提供最佳治疗选择。

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Progesterone treatment inhibits and dihydrotestosterone (DHT) treatment potentiates voltage-gated calcium currents in gonadotropin-releasing hormone (GnRH) neurons.孕激素治疗抑制促性腺激素释放激素(GnRH)神经元的电压门控钙电流,而二氢睾酮(DHT)治疗增强其电流。
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