Gennari C, Agnusdei D
Institute of Medical Semeiotics, University of Siena, Italy.
J Steroid Biochem Mol Biol. 1990 Nov 20;37(3):451-5. doi: 10.1016/0960-0760(90)90497-9.
Estrogen deficiency following natural or surgical menopause, is thought to be the main factor leading to postmenopausal bone loss. Furthermore, after estrogen failure a significant reduction of intestinal calcium absorption and a negativization of calcium balance has been observed. The mechanism of estrogen effect on skeletal tissue is not yet fully elucidated. Recently, specific receptors for estrogens in osteoblastic cells have been described; however their low density does not give a full explanation about their functional role. Therefore estrogens act, at least in part, indirectly through calciotropic hormones. In order to further elucidate this issue, we performed some studies in postmenopausal osteoporotic patients and in fertile oophorectomized women. In the first double blind placebo controlled study, after a 1-year estrogen treatment period we observed an increase in bone mineral content in the hormone-treated patients. Furthermore, in all treated patients an improvement of intestinal calcium absorption was detected, while 1,25-dihydroxy-vitamin D serum levels did not show significant changes. To further analyse the relationship between estrogens (E) and calcitonin (CT) in postmenopausal osteoporosis, we performed a double blind placebo controlled study to evaluate the effects of 1-yr estro-progestative treatment on CT secretory reserve, evaluated by calcium infusion test. Blood levels of CT showed a progressive increase during the study period in the hormone-treated group, with a significant increase in the CT response to calcium stimulation test, suggesting a modulation of CT secretion by E. Recently, we performed two studies in fertile oophorectomized women. In the first, we followed longitudinally 24 fertile women for 1 yr. In these patients we measured, before and after oophorectomy, biochemical indexes of bone metabolism and bone mass. During the observation period a significant increase in bone resorption and a significant drop in intestinal calcium absorption was observed. In the second study, performed on 14 women before and 6 months after oophorectomy, a treatment with conjugated estrogens allowed the correction of the primary intestinal defect responsible for the reduced calcium absorption.(ABSTRACT TRUNCATED AT 400 WORDS)
自然绝经或手术绝经后的雌激素缺乏被认为是导致绝经后骨质流失的主要因素。此外,雌激素功能衰退后,已观察到肠道钙吸收显著减少且钙平衡呈负性。雌激素对骨骼组织的作用机制尚未完全阐明。最近,已描述了成骨细胞中雌激素的特异性受体;然而,其低密度并不能完全解释其功能作用。因此,雌激素至少部分地通过钙调节激素间接发挥作用。为了进一步阐明这个问题,我们对绝经后骨质疏松患者和生育期卵巢切除的女性进行了一些研究。在第一项双盲安慰剂对照研究中,经过1年的雌激素治疗期后,我们观察到接受激素治疗的患者骨矿物质含量增加。此外,在所有接受治疗的患者中均检测到肠道钙吸收有所改善,而血清1,25 - 二羟维生素D水平未显示出显著变化。为了进一步分析绝经后骨质疏松中雌激素(E)与降钙素(CT)之间的关系,我们进行了一项双盲安慰剂对照研究,以评估1年雌孕激素治疗对通过钙输注试验评估的CT分泌储备的影响。在研究期间,激素治疗组的CT血水平呈逐渐上升趋势,对钙刺激试验的CT反应显著增加,提示雌激素对CT分泌有调节作用。最近,我们对生育期卵巢切除的女性进行了两项研究。在第一项研究中,我们对24名生育期女性进行了为期1年的纵向跟踪。在这些患者中,我们在卵巢切除前后测量了骨代谢和骨量的生化指标。在观察期内,观察到骨吸收显著增加且肠道钙吸收显著下降。在第二项研究中,对14名女性在卵巢切除前和切除后6个月进行了研究,使用结合雌激素治疗可纠正导致钙吸收减少的原发性肠道缺陷。(摘要截选至400字)