OVARIAN-STEROID TREATMENT BLOCKS A POSTMENOPAUSAL INCREASE IN BLOOD MONOCYTE INTERLEUKIN-1 RELEASE
OVARIAN-STEROID TREATMENT BLOCKS A POSTMENOPAUSAL INCREASE IN BLOOD MONOCYTE INTERLEUKIN-1 RELEASE
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DOI：
10.1073/pnas.86.7.2398
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发表时间：
1989-04-01
影响因子：
11.1
通讯作者：
PECK, WA
中科院分区：
文献类型：
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作者：
PACIFICI, R;RIFAS, L;PECK, WA
在之前的研究中，我们发现血液中白细胞介素1 （IL-1）的单核细胞精化（IL-1是一种已知的骨吸收刺激因子）在骨质疏松症患者中，骨转换快的患者比骨转换慢的患者和非骨质疏松症患者更高。由于绝经后骨质流失加速会增加女性骨质疏松的风险，我们研究了绝经和卵巢类固醇治疗对非骨质疏松和骨质疏松女性单核细胞IL-1释放的影响。未经治疗的绝经后妇女（非骨质疏松和骨质疏松）单核细胞培养基中IL-1活性高于未经治疗的绝经前妇女或经雌激素/黄体酮治疗的绝经后妇女培养基。在健康（r = -0.75; P < 0.005）和骨质疏松（r = -0.61; P < 0.01）未接受治疗的绝经后妇女中，IL-1与绝经时间呈显著负相关。两斜率差异有统计学意义（P < 0.05）。绝经前IL-1水平在非骨质疏松症患者绝经后8年内达到，但在骨质疏松症患者中没有，骨质疏松症患者的IL-1水平在绝经后15年内明显升高。定量计算机断层扫描显示，IL-1也与椎体矿物质密度呈负相关（r = -0.37; P < 0.05）。在前瞻性研究中，雌激素-孕酮治疗1个月后，3名非骨质疏松患者和5名骨质疏松患者的IL-1活性均显著降低，证实了横断面分析中观察到的激素治疗的明显效果。虽然因果关系尚未确定，但我们的假设是，基于这些数据，IL-1产生的改变可能是绝经后骨质流失加速和卵巢类固醇抑制骨质流失的基础。IL-1分泌的持续升高似乎是绝经后骨质疏松症的一个特征。
In previous studies, we showed that blood monocyte elaboration of interleukin 1 (IL-1), a known stimulator of bone resorption, was higher in osteoporotic patients with rapid bone turnover than in those with slow turnover and in nonosteoporotic subjects. Since an acceleration of bone loss following menopause contributes to the risk of osteoporosis in women, we have studied the effects of menopause and ovarian steroid treatment on IL-1 release by monocytes obtained from nonosteoporotic and osteoporotic women. IL-1 activity in the monocyte culture medium derived from untreated postmenopausal women (nonosteoporotic and osteoporotic) was higher than in the medium derived from either untreated premenopausal or estrogen/progesterone-treated postmenopausal women. A significant negative correlation was found between IL-1 and years since menopause in both the healthy (r = -0.75; P < 0.005) and the osteoporotic (r = -0.61; P < 0.01) untreated postmenopausal women. The difference between the two slopes was significant at P < 0.05. Premenopausal IL-1 levels were achieved within 8 years of menopause in the nonosteoporotic, but not in the osteoporotic, subjects in whom increases were evident as long as 15 years after menopause. IL-1 also correlated inversely with vertebral mineral density (r = -0.37; P < 0.05), as measured by quantitative computed tomography. In prospective studies, treatment with estrogen progesterone for 1 month caused a substantial highly significant decrease in IL-1 activity in each of three nonosteoporotic and five osteoporotic women, confirming the apparent effect of hormone therapy observed in the cross-sectional analysis. Although a cause-effect relationship has not been established, it is our hypothesis, bsed on these data, that alterations in IL-1 production may underlie the postmenopausal acceleration in bone loss and its inhibition by ovarian steroids. Persistent elevation of IL-1 secretion appears to be a feature of postmenopausal osteoporosis.