Cosman F, Shen V, Xie F, Seibel M, Ratcliffe A, Lindsay R
Regional Bone Center, Helen Hayes Hospital, West Haverstraw, New York.
Ann Intern Med. 1993 Mar 1;118(5):337-43. doi: 10.7326/0003-4819-118-5-199303010-00003.
Because parathyroid hormone (PTH) stimulates bone resorption, resistance to its actions might help maintain bone mass. We tested the hypothesis that the effects of estrogen on bone are accomplished in part by decreasing the sensitivity of the skeleton to the resorbing effects of PTH.
Comparison of response to PTH infusion in untreated and estrogen-treated postmenopausal women with osteoporosis.
(1-34) human PTH, 0.55 U/(kg.h), was infused intravenously over 20 hours.
The inpatient clinical research unit of a referral hospital.
Women with primary postmenopausal osteoporosis who were untreated (n = 15) or treated with estrogen (n = 17).
Skeletal turnover indices including hydroxyproline, deoxypyridinoline, pyridinoline, tartrate-resistant acid phosphatase, alkaline phosphatase, bone Gla protein, and insulin-like growth factor-1.
All basal indices were higher in untreated than in estrogen-treated women, but statistical differences were seen only for deoxypyridinoline and pyridinoline. During the 20-hour infusion, hydroxyproline/creatinine increased 0.023 mumol/mumol in untreated women but only 0.010 mumol/mumol in estrogen-treated women (P < 0.05). Corresponding changes for deoxypyridinoline/creatinine were 14.6 mumol/mumol and 3.5 mumol/mumol (P = 0.06). Tartrate-resistant acid phosphatase and pyridinoline increased only in untreated group. A circadian rhythm in circulating bone Gla protein was seen in both groups without clear PTH-induced effects or differences between groups. Alkaline phosphatase levels decreased and insulin-like growth factor-1 levels increased in both groups with no distinction between untreated and estrogen-treated women [corrected].
The estrogenized postmenopausal osteoporotic skeleton is less sensitive to the bone resorbing effects of acutely administered PTH. There are no differential effects on bone formation.
由于甲状旁腺激素（PTH）刺激骨吸收，对其作用产生抵抗可能有助于维持骨量。我们检验了这样一个假说，即雌激素对骨骼的作用部分是通过降低骨骼对PTH吸收作用的敏感性来实现的。
比较未经治疗和接受雌激素治疗的绝经后骨质疏松妇女对PTH输注的反应。
以0.55 U/（kg·h）的剂量静脉输注（1-34）人PTH，持续20小时。
一家转诊医院的住院临床研究科室。
未经治疗（n = 15）或接受雌激素治疗（n = 17）的原发性绝经后骨质疏松妇女。
骨转换指标，包括羟脯氨酸、脱氧吡啶啉、吡啶啉、抗酒石酸酸性磷酸酶、碱性磷酸酶、骨钙素和胰岛素样生长因子-1。
未经治疗的妇女所有基础指标均高于接受雌激素治疗的妇女，但仅脱氧吡啶啉和吡啶啉存在统计学差异。在20小时的输注过程中，未经治疗的妇女羟脯氨酸/肌酐增加0.023 μmol/μmol，而接受雌激素治疗的妇女仅增加0.010 μmol/μmol（P < 0.05）。脱氧吡啶啉/肌酐的相应变化分别为14.6 μmol/μmol和3.5 μmol/μmol（P = 0.06）。抗酒石酸酸性磷酸酶和吡啶啉仅在未经治疗的组中增加。两组均观察到循环骨钙素的昼夜节律，无明显的PTH诱导效应或组间差异。两组碱性磷酸酶水平均降低，胰岛素样生长因子-1水平均升高，未经治疗和接受雌激素治疗的妇女之间无差异[校正后]。
雌激素化的绝经后骨质疏松骨骼对急性给予的PTH的骨吸收作用敏感性较低。对骨形成没有差异影响。
