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Evolution of the Calcium Paradigm: The Relation between Vitamin D Serum Calcium and Calcium Absorption

机译:钙范例的演变:维生素D血清钙和钙吸收之间的关系

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摘要

Osteoporosis is the index disease for calcium deficiency, just as rickets/osteomalacia is the index disease for vitamin D deficiency, but there is considerable overlap between them. The common explanation for this overlap is that hypovitaminosis D causes malabsorption of calcium which then causes secondary hyperparathyroidism and is effectively the same thing as calcium deficiency. This paradigm is incorrect. Hypovitaminosis D causes secondary hyperparathyroidism at serum calcidiol levels lower than 60 nmol/L long before it causes malabsorption of calcium because serum calcitriol (which controls calcium absorption) is maintained until serum calcidiol falls below 20 nmol/L. This secondary hyperparathyroidism, probably due to loss of a “calcaemic” action of vitamin D on bone first described in 1957, destroys bone and explains why vitamin D insufficiency is a risk factor for osteoporosis. Vitamin D thus plays a central role in the maintenance of the serum (ionised) calcium, which is more important to the organism than the preservation of the skeleton. Bone is sacrificed when absorbed dietary calcium does not match excretion through the skin, kidneys and bowel which is why calcium deficiency causes osteoporosis in experimental animals and, by implication, in humans.
机译:骨质疏松症是钙缺乏症的指标疾病,病/骨软化症是维生素D缺乏症的指标疾病,但两者之间存在很大的重叠。对此重叠现象的常见解释是,维生素D缺乏引起钙吸收不良,继而引起继发性甲状旁腺功能亢进,实际上与钙缺乏症相同。这种范例是不正确的。低维生素D导致血清钙化二醇水平低于60 nmol / L时继发甲状旁腺功能亢进,很早就导致钙吸收不良,因为血清钙化三醇(控制钙吸收)一直维持到血清钙化二醇降至20 nmol / L以下。这种继发性甲状旁腺功能亢进症,可能是由于1957年首次描述的维生素D对骨骼的“钙化”作用丧失引起的,破坏了骨骼,并解释了维生素D功能不足是骨质疏松症的危险因素的原因。因此,维生素D在维持血清(离子化)钙中起着核心作用,这对生物体而言比骨骼的保存更为重要。当膳食中吸收的钙与皮肤,肾脏和肠内的排泄物不匹配时,就会牺牲骨骼,这就是钙缺乏会导致实验动物乃至人类骨质疏松的原因。

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