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慢性肝病相关骨软化症中继发性甲状旁腺功能亢进的证据。

Evidence for secondary hyperparathyroidism in the osteomalacia associated with chronic liver disease.

作者信息

Dibble J B, Sheridan P, Hampshire R, Hardy G J, Losowsky M S

出版信息

Clin Endocrinol (Oxf). 1981 Oct;15(4):373-83. doi: 10.1111/j.1365-2265.1981.tb00677.x.

Abstract

Previous reports have suggested that secondary hyperparathyroidism is extremely uncommon in hepatic osteomalacia. This, together with other findings, has led to suggestions that in chronic liver disease there may be selective resistance of bone to vitamin D or a specific bone mineralization defect unrelated to Vitamin D. To examine these possibilities, twenty-five patients with chronic liver disease have been studied by bone biopsy, serum calcium and inorganic phosphate, plasma 25-hydroxyvitamin D, plasma immunoreactive parathormone (iPTH), fasting urine cAMP, fasting renal tubular maximal reabsorptive capacity for phosphate (TmP/GFR) and fine grain hand x-rays. Nine of the patients had osteomalacia on bone biopsy, eight of these had subnormal levels of plasma 25-hydroxyvitamin D and the other had a borderline result. Based on the consensus of all the tests, five of these had evidence of secondary hyperparathyroidism. Plasma iPTH was higher in patients with osteomalacia than in patients without osteomalacia (P less than 0.01) or controls (P less than 0.01). Urine cAMP was higher in patients with osteomalacia than in patients without osteomalacia (P less than 0.001) or controls (P less than 0.01). TmP/GFR was significantly lower in patients with osteomalacia than in controls (P less than 0.05) but not significantly different from patients without osteomalacia. The findings of this study indicate that hyperparathyroidism occurs in a substantial proportion of patients with the osteomalacia of chronic liver disease. Moreover, osteomalacia in chronic liver disease is clearly related to reduced levels of plasma 25-hydroxyvitamin D. We conclude that hepatic osteomalacia is a vitamin D deficiency state and there is no need to suggest an unusual aetiology.

摘要

以往的报告表明,继发性甲状旁腺功能亢进在肝性骨软化症中极为罕见。这一情况以及其他发现提示,在慢性肝病中,骨骼可能对维生素D存在选择性抵抗,或者存在与维生素D无关的特定骨矿化缺陷。为了探究这些可能性,我们对25例慢性肝病患者进行了研究,检测项目包括骨活检、血清钙和无机磷、血浆25-羟维生素D、血浆免疫反应性甲状旁腺激素(iPTH)、空腹尿环磷腺苷(cAMP)、空腹时肾小管对磷的最大重吸收能力(TmP/GFR)以及手部细颗粒X线检查。骨活检显示9例患者存在骨软化症,其中8例血浆25-羟维生素D水平低于正常,另1例结果处于临界值。基于所有检测结果的综合判断,其中5例有继发性甲状旁腺功能亢进的证据。骨软化症患者的血浆iPTH水平高于无骨软化症的患者(P<0.01)或对照组(P<0.01)。骨软化症患者的尿cAMP水平高于无骨软化症的患者(P<0.001)或对照组(P<0.01)。骨软化症患者的TmP/GFR显著低于对照组(P<0.05),但与无骨软化症的患者无显著差异。本研究结果表明,在相当一部分慢性肝病所致骨软化症患者中会发生甲状旁腺功能亢进。此外,慢性肝病中的骨软化症显然与血浆25-羟维生素D水平降低有关。我们得出结论,肝性骨软化症是一种维生素D缺乏状态,无需提出异常病因。

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