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维生素D缺乏所致骨软化症。第一部分:发病机制(作者译)

[Osteomalacia due to vitamin D deficiency. Part One: mechanisms (author's transl)].

作者信息

Kaplan G, Prost A, Vinceneux P

出版信息

Nouv Presse Med. 1980 Jun 21;9(27):1889-91.

PMID:6250130
Abstract

Vitamin D deficiency is in most cases subclinical and can only be detected by blood vitamin assays or biochemical changes in phosphorus and calcium metabolism. Clinical and radiological osteomalacia is much less common. It is due to prolonged and profound hypovitaminaemia, which in turn depends upon a variety of factors, the main one being defective photosynthesis. Low vitamin D dietary intake apparently does not result in osteomalacia unless it is accompanied by insufficient exposure to sun. Malabsorption of cholecalciferol results from steatorrhoea of various origina. Disorders in hepatic 25-hydroxylation are due to drug enzymatic induction and seem to be unrelated to the state of the renal function. Disorders in renal 1,25-hydroxylation may be consecutive to reduced renal tissue, impaired stimulation, or inhibiton or even congenital lack of 1-alpha hydroxylase.

摘要

维生素D缺乏在大多数情况下是亚临床的,只能通过血液维生素检测或磷和钙代谢的生化变化来检测。临床和放射性骨软化症则要少见得多。它是由于长期和严重的维生素血症不足,而这又取决于多种因素,主要因素是光合作用缺陷。维生素D膳食摄入量低显然不会导致骨软化症,除非同时伴有日照不足。各种原因引起的脂肪泻会导致胆钙化醇吸收不良。肝脏25-羟化紊乱是由药物酶诱导引起的,似乎与肾功能状态无关。肾脏1,25-羟化紊乱可能继发于肾组织减少、刺激受损、抑制,甚至先天性缺乏1-α羟化酶。

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