Taylor A E
Harvard Medical School, Reproductive Endocrine Unit, National Center for Infertility Research, Massachusetts General Hospital, Boston 02114, USA.
J Pediatr Endocrinol Metab. 2000;13 Suppl 5:1281-4.
Polycystic ovary syndrome (PCOS) is a common reproductive disorder that is first clinically diagnosable approximately 3 years after menarche. Women with PCOS have exaggerated gonadotropin secretion, with an elevated LH/FSH ratio, as well as an increased frequency and amplitude of LH pulsations. Since the elevated pulse frequency is a marker of unusually rapid hypothalamic GnRH secretion, these results imply a defect at the level of the hypothalamus. Such an abnormality could theoretically be a primary defect that could cause PCOS, and if so, would be expected to be detectable at the onset of puberty. How these abnormalities of hypothalamic and pituitary function relate to other, seemingly disparate, organ defects has not yet been delineated. We studied 99 PCOS patients and 42 normal controls with 8 to 12 hours of q10 min frequent blood sampling. Women with PCOS had significantly elevated mean LH levels, LH pulse amplitude, LH pulse frequency, and LH/FSH ratios compared to normal women. However, these abnormalities were not randomly distributed. All gonadotropin secretion parameters tended to be normal in PCOS patients when measured during the luteal phase or first 7 days after an ovulatory menses. There was a strong inverse relationship of mean LH, LH/FSH ratio, and LH pulse amplitude, but not frequency, with BMI. We hypothesize that this effect of body size occurs at the pituitary level. Several investigators have performed similar investigations in adolescent girls with regular and irregular menstrual cycles. Taken together, this evidence suggests that the gonadotropin defects appear as a very early finding in the development of PCOS, but the presence of abnormalities in both gonadotropin secretion and androgen secretion does not allow one to conclude that the gonadotropin defects are causal. We conclude that gonadotropin defects, particularly excess of serum LH, is a predominant finding in hyperandrogenic women, whether they are young peripubertal adolescents, or older perimenopausal women. Whether there is a primary neuroendocrine abnormality driving excess gonadotropin secretion that causes the hyperandrogenic condition, or whether the excess gonadotropin secretion reflects abnormal feedback of another factor, still remains unknown.
多囊卵巢综合征（PCOS）是一种常见的生殖系统疾病，通常在初潮后约3年临床上首次可诊断。患有PCOS的女性促性腺激素分泌亢进，LH/FSH比值升高，同时LH脉冲频率和幅度增加。由于升高的脉冲频率是下丘脑GnRH分泌异常快速的标志，这些结果提示下丘脑水平存在缺陷。从理论上讲，这种异常可能是导致PCOS的原发性缺陷，如果是这样，预计在青春期开始时就可以检测到。下丘脑和垂体功能的这些异常与其他看似不同的器官缺陷之间的关系尚未明确。我们对99例PCOS患者和42例正常对照进行了研究，每10分钟频繁采血8至12小时。与正常女性相比，PCOS患者的平均LH水平、LH脉冲幅度、LH脉冲频率和LH/FSH比值显著升高。然而，这些异常并非随机分布。在黄体期或排卵性月经后的前7天测量时，PCOS患者的所有促性腺激素分泌参数往往正常。平均LH、LH/FSH比值和LH脉冲幅度（而非频率）与BMI呈强烈负相关。我们假设这种体型的影响发生在垂体水平。几位研究人员对月经周期规律和不规律的青春期女孩进行了类似的研究。综合来看，这些证据表明促性腺激素缺陷在PCOS的发展过程中是一个非常早期的发现，但促性腺激素分泌异常和雄激素分泌异常的同时存在并不能得出促性腺激素缺陷是病因的结论。我们得出结论，促性腺激素缺陷，尤其是血清LH过多，是高雄激素女性的主要表现，无论她们是青春期早期的年轻女性，还是围绝经期的老年女性。是存在原发性神经内分泌异常驱动促性腺激素分泌过多导致高雄激素状态，还是促性腺激素分泌过多反映了另一个因素的异常反馈，仍然未知。
