The role of magnesium in the pathogenesis of bone disease in childhood cholestatic liver disease: A preliminary report

被引:18
作者
Heubi, JE
Higgins, JV
Argao, EA
Sierra, RI
Specker, BL
机构
[1] CHILDRENS HOSP,MED CTR,PEDIAT BONE RES CTR,CINCINNATI,OH 45229
[2] CHILDRENS HOSP,MED CTR,GEN CLIN RES CTR,CINCINNATI,OH 45229
关键词
bone mineral density; bone mineralization; cholestasis; magnesium;
D O I
10.1097/00005176-199709000-00010
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Magnesium deficiency may contribute to the metabolic bone disease that complicates chronic cholestatic liver disease. We hypothesized that magnesium deficiency alters vitamin D metabolism by decreasing parathyroid hormone (PTH) response, resulting in decreased serum osteocalcin and decreased bone accretion. Methods: Nine subjects, age 3-22 years, with cholestatic liver disease were evaluated with the magnesium retention test. The response of PTH, 1,25(OH)(2) vitamin D, and osteocalcin to provocative stimuli and dual x-ray absorptiometry measurement of bone mineral density (BMD) of the lumbar spine were assessed. Thereafter, subjects were treated with oral magnesium supplements. Results: All nine subjects were magnesium depleted. Repletion with magnesium was successful in seven subjects, and required 4 to 31 (median 14) months with doses of 6 to 34 (median 11) mg/kg/day. Baseline serum PTH was significantly reduced in the cholestatic subjects compared to 15 age-matched controls. Comparison of baseline to repleted provocative testing was performed in six Mg-repleted subjects. Osteocalcin response increased significantly (p = 0.048) with repletion, while PTH response increased (p = 0.061). Lumbar spine BMD increased modestly with repletion (p = 0.093). Conclusions: This preliminary report suggests that magnesium depletion is extremely common in children with chronic cholestasis. We speculate that magnesium supplementation may be warranted to forestall the progression of metabolic bone disease in chronic cholestasis. (C) 1997 Lippincott-Raven Publishers.
引用
收藏
页码:301 / 306
页数:6
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