[Sex hormone replacement following menopause--for all women? A plea for prevention using estrogens and gestagens].
After the menopause, a growing proportion of women will have a good chance to add three decades or more to their lifetime. They must decide whether to start long-term hormonal replacement therapy or to accept the risks of osteoporosis, fracture, cardiovascular disease, and a variety of psychological and physical problems as 'natural' destiny. The syndrome of postmenopausal endocrine deficiency is a primary glandular insufficiency, which in principle requires substitution with the secretory product of the gland. Postmenopausal osteoporosis and fractures are consequences of a pathological dysfunction of calcium metabolism. After estrogen withdrawal, the impaired hepatic and renal synthesis of calcitriol will result in a reduced intestinal resorption of calcium. Parathyroid hormone may initiate a vicious circle by acceleration of bone resorption, mobilization of bone calcium and a tendency to hypercalcemia. The failure to preserve circulating calcium due to 'escape' from calcitonin and a decreased renal tubular back-resorption are followed by an increased loss of calcium from a 'renal calcium leak', resulting in hypercalcuria. In order to maintain homeostasis, additional calcium is required, which will be supplied from accelerated bone resorption. Thus, the circle is closed by renewed osteolysis. The process is associated with accelerated bone turnover and a negative balance of calcium and bone. After a variable time interval which depends on the individual bone mass and rate of bone loss, these events will inevitably result in osteoporosis. Estrogen replacement will interrupt the circle, decelerate bone turnover, and re-establish a positive balance of calcium and bone. Estrogen withdrawal also favors an 'atherogenic' set of lipoproteins, which is strongly associated with increased coronary risk. Substitution with estrogens will favor a 'protective' profile of lipoproteins and cut the cardiovascular risk to about one half. Progestogens, in particular the 17 alpha-alkylated 19-nor-steroids, may reduce the favorable effects of estrogens on lipoproteins in a dose-dependent manner; however, they do not impair the antiatherogenic estrogen effects, even in presence of an atherogenic profile of lipoproteins. Thus, these anti-estrogenic effects of progestogens, at least in nonhuman primates, do not have clinical significance.(ABSTRACT TRUNCATED AT 400 WORDS)
D000368:Aged; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000378:metabolism; D001943:Breast Neoplasms / Q000139:chemically induced; D002118:Calcium / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000517:prevention & control; D015914:Estrogen Replacement Therapy; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology*; D006801:Humans; D006949:Hyperlipidemias / Q000517:prevention & control; D008593:Menopause / Q000502:physiology*; D008875:Middle Aged; D010014:Osteolysis / Q000378:metabolism; D010024:Osteoporosis / Q000517:prevention & control; D011372:Progestins / Q000627:therapeutic use
D012739:Gonadal Steroid Hormones; D011372:Progestins; D002118:Calcium
Sexualhormonsubstitution nach der Menopause--für alle Frauen? Plädoyer für die Prävention mit Ostrogenen und Gestagenen.