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导致机构收容的残疾儿童在接受抗惊厥治疗时患佝偻病的因素。

Factors causing rickets in institutionalised handicapped children on anticonvulsant therapy.

作者信息

Morijiri Y, Sato T

出版信息

Arch Dis Child. 1981 Jun;56(6):446-9. doi: 10.1136/adc.56.6.446.

Abstract

An epidemiological study on vitamin D-dependent rickets was carried out in severely handicapped institutionalised children on long-term anticonvulsant therapy. Nine (10%) of 94 patients had overt rickets on the basis of roentgenological bone changes and biochemical indices, but 46 patients in hospital without medication, and 50 epileptic patients attending an outpatient clinic and taking anticonvulsants had no sign of rickets. Causative factors for the development of rickets were evaluated. Administration of anticonvulsive drugs depressed the serum 25-hydroxyvitamin D (25-OHD) level, but this was not the major factor in the development of rickets. Vitamin D intake seemed to be about average in these patients and its supplementation increased their serum 25-OHD level. This serum 25-OHD level was not maintained by supplemental vitamin D, unless the children were exposed to sunlight. These results indicate that although several factors--such as anticonvulsants, low vitamin D intake, and inactivity--are concerned in the development of rickets, the main cause is lack of sun in institutionalised handicapped children.

摘要

对长期接受抗惊厥治疗的重度残疾住院儿童进行了一项关于维生素D依赖性佝偻病的流行病学研究。94名患者中有9名(10%)根据X线骨改变和生化指标诊断为明显的佝偻病,但46名未用药的住院患者以及50名在门诊接受抗惊厥治疗的癫痫患者没有佝偻病迹象。对佝偻病发病的相关因素进行了评估。抗惊厥药物的使用会降低血清25-羟维生素D(25-OHD)水平,但这并非佝偻病发病的主要因素。这些患者的维生素D摄入量似乎处于平均水平,补充维生素D可提高他们的血清25-OHD水平。除非儿童接受阳光照射,否则补充维生素D并不能维持这种血清25-OHD水平。这些结果表明,尽管佝偻病的发病涉及多种因素,如抗惊厥药物、维生素D摄入不足和活动量少等,但主要原因是住院残疾儿童缺乏阳光照射。

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本文引用的文献

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Anticonvulsant osteomalacia.抗惊厥药所致骨软化症
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