Endocrine aspects of menopause.

Abstract

Oocyte depletion and ovarian aging results in profound alterations at the biological level. The reduction in numbers of follicles leads to reduction of circulating inhibin and increased serum FSH, characteristic marker of ovarian failure. The remaining follicles are overstimulated and premature ovulation may ensue. This, leads to luteal deficiency and reduction in progesterone production and relative hyperestrogenemia. The above changes characterize the premenopausal period. In a second phase, anovulatory cycles interchange with premature and occasionally normal ovulatory cycles. This phase is characterized by increased FSH and LH and decreased progesterone/estradiol ratio resulting in irregular bleeding, endometrial hyperplasia, polyps, fibromas, mammary dystrophies, disturbance of mood, appetite and thermoregulation. Lastly, the sensitivity of ovarian follicles to FSH and LH is lost with a decline of E2 below 20 pg/ml produced almost exclusively from peripheral conversion from circulating androgens. The beneficial effects of E2 are lost resulting in atrophy of the sensitive tissues, decreased calcium absorption, increased bone resorption, accelerated bone loss and osteoporosis, rise in serum triglycerides, increased VLDL and LDL lipoproteins, increased LDL/HDL cholesterol, a profile which favors atherosclerosis.