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特发性高钙尿症患者的骨密度和骨骼代谢会发生改变。

Bone density and skeletal metabolism are altered in idiopathic hypercalciuria.

作者信息

Giannini S, Nobile M, Sartori L, Calò L, Tasca A, Dalle Carbonare L, Ciuffreda M, D'Angelo A, Pagano F, Crepaldi G

机构信息

Institute of Internal Medicine and National Research Council-Centre for Aging Studies of Padova, Italy.

出版信息

Clin Nephrol. 1998 Aug;50(2):94-100.

PMID:9725780
Abstract

OBJECTIVE

To study bone density in hypercalciuric patients, when classified according to the main metabolic defect.

METHODS

We studied 49 patients, aged 19-60 years with calcium stones and idiopathic hypercalcuria. All subjects underwent an evaluation of mineral metabolism and a spinal and femoral DEXA measurement. Then, patients were classified as having Fasting (FH, 31 subjects) or Absorptive (AH, 18 patients) Hypercalciuria according to a standard oral calcium load.

RESULTS

Spinal bone density was lower only in FH patients as compared to controls (p <0.001). Bone alkaline phosphatase and urine hydroxyproline were higher with respect to controls only in patients with FH (p <0.005 and p <0.015, respectively). After low calcium diet, hydroxyproline excretion continued to be higher in FH patients (p <0.05). Although in the normal range, serum and urine uric acid were higher in hypercalciuric subjects (p <0.03 and p <0.005, respectively); blood pH was lower in hypercalciuric patients than in controls (p <0.01). In FH patients urine hydroxyproline negatively correlated with spinal and femoral density (p <0.001 and p <0.005, respectively), and blood pH positively correlated with spinal density.

CONCLUSIONS

a disordered bone metabolism and bone loss are present only in patients with fasting hypercalciuria. An excessive acid load, possibly of dietary origin, might be involved as a pathogenetic factor.

摘要

目的

根据主要代谢缺陷对高钙尿症患者进行分类,研究其骨密度。

方法

我们研究了49例年龄在19至60岁之间、患有钙结石和特发性高钙尿症的患者。所有受试者均接受了矿物质代谢评估以及脊柱和股骨的双能X线吸收测定(DEXA)。然后,根据标准口服钙负荷,将患者分为空腹高钙尿症(FH,31例受试者)或吸收性高钙尿症(AH,18例患者)。

结果

与对照组相比,仅FH患者的脊柱骨密度较低(p<0.001)。仅在FH患者中,骨碱性磷酸酶和尿羟脯氨酸相对于对照组更高(分别为p<0.005和p<0.015)。低钙饮食后,FH患者的羟脯氨酸排泄仍较高(p<0.05)。尽管在正常范围内,但高钙尿症受试者的血清和尿酸水平较高(分别为p<0.03和p<0.005);高钙尿症患者的血液pH值低于对照组(p<0.01)。在FH患者中,尿羟脯氨酸与脊柱和股骨密度呈负相关(分别为p<0.001和p<0.005),而血液pH值与脊柱密度呈正相关。

结论

仅空腹高钙尿症患者存在骨代谢紊乱和骨质流失。过量的酸负荷,可能源于饮食,可能是一个致病因素。

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