Burger Henry G, Dudley Emma C, Robertson David M, Dennerstein Lorraine
Prince Henry's Institute of Medical Research at Monash Medical Centre, Clayton, Victoria, Australia.
Recent Prog Horm Res. 2002;57:257-75. doi: 10.1210/rp.57.1.257.
The menopause is the permanent cessation of menstruation resulting from the loss of ovarian follicular activity. It is heralded by the menopausal transition, a period when the endocrine, biological, and clinical features of approaching menopause begin. A common initial marker is the onset of menstrual irregularity. The biology underlying the transition to menopause includes central neuroendocrine changes as well as changes within the ovary, the most striking of which is a profound decline in follicle numbers. Follicle-stimulating hormone (FSH) is an established indirect marker of follicular activity. In studies of groups of women, its concentration, particularly in the early follicular phase of the menstrual cycle, begins to increase some years before there are any clinical indications of approaching menopause. The rise in FSH is the result of declining levels of inhibin B (INH-B), a dimeric protein that reflects the fall in ovarian follicle numbers, with or without any change in the ability of the lining granulosa cells to secrete INH-B. Estradiol levels remain relatively unchanged or tend to rise with age until the onset of the transition and are usually well preserved until the late perimenopause, presumably in response to the elevated FSH levels. During the transition, hormone levels frequently vary markedly - hence, measures of FSH and estradiol are unreliable guides to menopausal status. Concentrations of testosterone have been reported to fall by about 50% during reproductive life, between the ages of 20 and 40. They change little during the transition and, after menopause, may even rise. Dehydroepiandrosterone (DHEA) and DHEAS, its sulphate, on the other hand, decline with age, without any specific influence of the menopause. Symptoms of the menopause can be interpreted as resulting primarily from the profound fall in estradiol, occurring over a 3- to 4-year period around final menses, a fall that presumably contributes importantly to the beginning, in the late perimenopause, of loss of bone mineral density.
绝经是由于卵巢卵泡活动丧失导致的月经永久性停止。它以绝经过渡期为先导，在这个时期，接近绝经的内分泌、生物学和临床特征开始出现。一个常见的初始标志是月经不规律的开始。向绝经过渡的生物学机制包括中枢神经内分泌变化以及卵巢内的变化，其中最显著的是卵泡数量的大幅下降。促卵泡生成素（FSH）是卵泡活动的既定间接标志物。在对女性群体的研究中，其浓度，特别是在月经周期的卵泡早期，在接近绝经的任何临床迹象出现前几年就开始升高。FSH升高是抑制素B（INH - B）水平下降的结果，抑制素B是一种二聚体蛋白，反映卵巢卵泡数量的减少，无论颗粒细胞分泌INH - B的能力有无变化。雌二醇水平相对保持不变或随年龄增长而趋于升高，直到过渡期开始，并且通常在围绝经期晚期仍保持良好，这可能是对FSH水平升高的反应。在过渡期，激素水平经常显著变化——因此，FSH和雌二醇的测量对于绝经状态来说是不可靠的指标。据报道，睾酮浓度在20至40岁的生殖期内下降约50%。在过渡期变化不大，绝经后甚至可能升高。另一方面，脱氢表雄酮（DHEA）及其硫酸盐DHEAS随年龄下降，不受绝经的任何特定影响。绝经症状可主要解释为在末次月经前后3至4年期间雌二醇的大幅下降所致，这种下降可能在围绝经期晚期对骨矿物质密度的丧失起重要作用。
