Kalevi Laitinen , Riitta Tähtelä , Kimmo Luomanmäki , Matti J. Välimäki
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引用次数: 36
摘要
对重度饮酒者经常遇到的低钙血症和骨质疏松症的研究,以前曾在已经从酒精中毒中恢复的酗酒者身上进行过。中毒期间和中毒后的骨和矿物质代谢可能不同。我们测量了26名酒精中毒男性和19名健康对照男性的骨和矿物质代谢血清参数。虽然血清游离钙为12% (P <0.0001)低于对照组,研究组血清完整甲状旁腺激素相似。血清骨钙素水平下降(- 43%;P & lt;0.001),患者的骨形成受到抑制。血清I型胶原交联羧基末端末端肽(ICTP)是骨基质降解的新参数,患者血清ICTP比对照组高9% (P = 0.03)。对照组血清骨钙素与ICTP呈正相关(r = 0.59, P <P = 0.8, r = 0.05。我们得出结论,在酒精中毒的酒精使用者中,甲状旁腺对低钙刺激没有正常反应,骨形成的抑制与骨吸收的加速无关。
Mechanisms of hypocalcemia and markers of bone turnover in alcohol-intoxicated drinkers
Studies of hypocalcemia and osteoporosis frequently encountered in heavy users of alcohol have previously been performed on alcoholic people who have already recovered from alcohol intoxication. Bone and mineral metabolism during and after the intoxication may be different. We measured serum parameters of bone and mineral metabolism in 26 alcohol-intoxicated men and in 19 healthy control men. Although serum ionized calcium was 12% (P < 0.0001) lower in the patients than in the controls, serum intact parathyroid hormone was similar in the study groups. As reflected by decreased serum levels of osteocalcin (−43%; P < 0.001), bone formation was depressed in the patients. Serum cross-linked carboxyterminal telopeptide of human type I collagen (ICTP), a novel parameter of bone matrix degradation, was 9% higher in the patients (P = 0.03) than controls. The positive correlation between serum osteocalcin and ICTP in the controls (r = 0.59, P < 0.01) was absent in the patients (r = 0.05, P = 0.8). We conclude that in alcohol-intoxicated alcohol users, the parathyroid glands do not respond normally to a hypocalcemic stimulus, and that depressed bone formation is uncoupled from accelerated bone resorption.