Adashi E Y
Division of Reproductive Endocrinology, University of Maryland School of Medicine, Baltimore.
Endocrinol Metab Clin North Am. 1988 Dec;17(4):649-66.
There is little doubt that disordered gonadotropin economy plays a central role in the pathophysiology of PCOD. However, the nature of the mechanism(s) responsible for altered gonadotropin release remains somewhat controversial. Most importantly, it is difficult to unequivocally determine at this time whether or not the disordered release of gonadotropins is due to a primary central nervous system (for example, hypothalamic) disorder as opposed to constituting a secondary phenomenon reflecting abnormal modulation of gonadotropin release by peripheral glandular input (for example, sex steroids). Regardless of the exact mechanism(s) at play, it is clear that both gonadotropin pulse frequency and amplitude are involved. These alterations combine to produce an overall increase in LH secretion. This hyperactivity, coupled with the apparent secretion of highly bioactive LH molecule(s), is undoubtedly responsible for the intense stimulation of the ovarian androgen-producing cells. It remains to be determined whether this latter phenomenon is consequential to abnormal gonadotropin release or whether it merely represents an epiphenomenon. In contrast, the central role of estrogens in modulating gonadotropin release appears highly likely. However, whether this effect is merely exerted at the level of the pituitary or possibly involves modulation at higher regulatory centers remains the subject of future investigation.
毫无疑问，促性腺激素分泌紊乱在多囊卵巢综合征（PCOD）的病理生理学中起着核心作用。然而，导致促性腺激素释放改变的机制的本质仍存在一定争议。最重要的是，目前很难明确确定促性腺激素的紊乱释放是否归因于原发性中枢神经系统（例如，下丘脑）疾病，而非构成反映外周腺体输入（例如，性类固醇）对促性腺激素释放异常调节的继发性现象。无论起作用的具体机制如何，促性腺激素脉冲频率和幅度显然都参与其中。这些改变共同导致促黄体生成素（LH）分泌总体增加。这种活性过高，再加上明显分泌具有高生物活性的LH分子，无疑是卵巢雄激素生成细胞受到强烈刺激的原因。尚待确定后一种现象是促性腺激素释放异常的结果，还是仅仅是一种附带现象。相比之下，雌激素在调节促性腺激素释放中的核心作用似乎很有可能。然而，这种作用是仅在垂体水平发挥，还是可能涉及更高调节中心的调节，仍是未来研究的课题。
