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[婴儿生理性低钙血症失代偿诱发维生素D缺乏性佝偻病]

[Decompensation of physiologic hypocalcemia in infants inducing vitamin D deficiency rickets].

作者信息

Sun B

出版信息

Zhonghua Yi Xue Za Zhi. 1990 May;70(5):265-7, 20.

PMID:2168795
Abstract

43 infants taking the same dosage of vitamin D and calcium were investigated. The results showed that vitamin D deficiency rickets (VDR) were still present in some infants when vitamin D was sufficient, because of deficiency of 1,25-dihydroxyvitamin D (1,25-(OH)2D3). Serum calcium, phosphorus, alkaline phosphatase, triiodothyronine (T3), thyroxine (T4), calcitonin (CT), immunoreactive parathyroid hormone (iPTH), and 25-hydroxyvitamin D (25 OHD3) concentrations were compared among infants with normal, VDR of the early and recovering stages. The decompensation of physiological hypocalcemia in infants is probably the real cause of VDR and the decompensation is correlated closely with the development of parathyroid gland. This new concept is raised both at home and abroad. More practical methods for the treatment and prevention of VDR are suggested.

摘要

对43名服用相同剂量维生素D和钙的婴儿进行了调查。结果显示,当维生素D充足时,仍有部分婴儿存在维生素D缺乏性佝偻病(VDR),原因是1,25-二羟维生素D(1,25-(OH)2D3)缺乏。比较了正常、早期和恢复期VDR婴儿的血清钙、磷、碱性磷酸酶、三碘甲状腺原氨酸(T3)、甲状腺素(T4)、降钙素(CT)、免疫反应性甲状旁腺激素(iPTH)和25-羟维生素D(25 OHD3)浓度。婴儿生理性低钙血症的失代偿可能是VDR的真正原因,且这种失代偿与甲状旁腺的发育密切相关。国内外均提出了这一新概念。还提出了更实用的VDR治疗和预防方法。

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