Lieberman S A, Holloway L, Marcus R, Hoffman A R
Medical Service Department of Veterans Affairs Medical Center, Palo Alto, California.
J Bone Miner Res. 1994 Nov;9(11):1723-8. doi: 10.1002/jbmr.5650091108.
The mechanisms underlying the effects of recombinant human growth hormone (rhGH) on vitamin D, mineral, and bone metabolism are not known. We examined whether these effects are mediated by parathyroid hormone (PTH) by measuring renal phosphorus (P) and calcium (Ca) handling, serum calcitriol, and markers of bone turnover for 24 h before and 72 h after an infusion of hPTH(1-34) in eight healthy postmenopausal women at baseline and following short-term (1 week) and sustained (5 weeks) rhGH treatment. On short-term rhGH, serum phosphorus and basal TmP/GFR were unaffected, but the fall in TmP/GFR after hPTH infusion was exaggerated (integrated response: -99.2 +/- 22.3 versus -144.1 +/- 15.0 minute-mg/dl, P = 0.0021). Basal calcitriol levels rose from 115 +/- 17 to 163 +/- 16 pM (P = 0.0002), but the increase in calcitriol following hPTH infusion was unaffected by short-term rhGH. The basal Ca excretion index (CEI) rose from 0.054 +/- 0.005 to 0.073 +/- 0.007 mM (P = 0.0095), but markers of bone turnover were unaffected. With sustained rhGH treatment, serum P (1.47 +/- 0.05 mM), basal TmP/GFR (4.29 +/- 0.24 mg/dl), and basal CEI (0.067 +/- 0.005 mM) were elevated compared with control values, and the PTH-induced lowering of TmP/GFR was again enhanced (-158.7 +/- 22.8 minute-mg/dl, P = 0.0021). Basal calcitriol concentrations returned to control levels (108 +/- 10 pM), but the calcitriol response to hPTH remained unchanged. Markers of bone remodeling were elevated with sustained rhGH treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
重组人生长激素(rhGH)对维生素D、矿物质及骨代谢产生影响的潜在机制尚不清楚。我们通过测量8名健康绝经后女性在基线时以及短期(1周)和持续(5周)rhGH治疗后,输注人甲状旁腺激素(hPTH)(1 - 34)前24小时和后72小时的肾脏磷(P)和钙(Ca)处理情况、血清骨化三醇以及骨转换标志物,来研究这些影响是否由甲状旁腺激素(PTH)介导。短期rhGH治疗时,血清磷和基础TmP/GFR未受影响,但hPTH输注后TmP/GFR的下降被夸大(综合反应:-99.2±22.3对-144.1±15.0分钟 - 毫克/分升,P = 0.0021)。基础骨化三醇水平从115±17升至163±16 pM(P = 0.0002),但hPTH输注后骨化三醇的增加不受短期rhGH影响。基础钙排泄指数(CEI)从0.054±0.005升至0.073±0.007 mM(P = 0.0095),但骨转换标志物未受影响。持续rhGH治疗时,血清P(1.47±0.05 mM)、基础TmP/GFR(4.29±0.24毫克/分升)和基础CEI(0.067±0.005 mM)较对照值升高,PTH诱导的TmP/GFR降低再次增强(-158.7±22.8分钟 - 毫克/分升,P = 0.0021)。基础骨化三醇浓度恢复至对照水平(108±10 pM),但骨化三醇对hPTH的反应保持不变。持续rhGH治疗使骨重塑标志物升高。(摘要截短于250字)