A Practical Approach to Vitamin D Deficiency and Rickets.

Endocrine development Pub Date : 2015-01-01 Epub Date: 2015-06-12 DOI:10.1159/000381000
Jeremy Allgrove, Nick J Shaw
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引用次数: 28

Abstract

Rickets is a condition in which there is failure of the normal mineralisation (osteomalacia) of growing bone. Whilst osteomalacia may be present in adults, rickets cannot occur. It is generally caused by a lack of mineral supply, which can either occur as a result of the deficiency of calcium (calciopaenic rickets, now known as parathyroid hormone-dependent rickets) or of phosphate (phosphopaenic rickets, now called FGF23-dependent rickets). Renal disorders may also interfere with the process of mineralisation and cause rickets. Only parathyroid hormone-dependent rickets and distal renal tubular disorders will be discussed in this chapter. The most common cause of rickets is still vitamin D deficiency, which is also responsible for other problems. Disorders of vitamin D metabolism or responsiveness may also cause similar issues. Distal renal tubular acidosis may also be caused by a variety of metabolic errors similar to those of osteoclasts. One form of distal renal tubular acidosis also causes a type of osteopetrosis. This chapter describes these conditions in detail and sets out a logical approach for treatment.

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维生素D缺乏和佝偻病的实用方法。
佝偻病是生长骨骼的正常矿化(骨软化)失败的一种情况。虽然骨软化症可能存在于成人,但不会发生佝偻病。它通常是由缺乏矿物质供应引起的,这可能是由于缺钙(钙缺乏性佝偻病,现在称为甲状旁腺激素依赖性佝偻病)或磷酸盐(磷缺乏性佝偻病,现在称为fgf23依赖性佝偻病)造成的。肾脏疾病也可能干扰矿化过程并引起佝偻病。本章只讨论甲状旁腺激素依赖性佝偻病和远端肾小管疾病。佝偻病最常见的原因仍然是维生素D缺乏,这也会导致其他问题。维生素D代谢或反应紊乱也可能导致类似的问题。远端肾小管酸中毒也可能由多种类似于破骨细胞的代谢错误引起。一种形式的远端肾小管酸中毒也会引起一种骨质疏松症。本章详细描述了这些情况,并提出了合理的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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