Need Allan G, O'Loughlin Peter D, Morris Howard A, Coates Penelope S, Horowitz Michael, Nordin B E Christopher
Division of Clinical Biochemistry, Institute of Medical and Veterinary Science, University of Adelaide, Adelaide, South Australia.
J Bone Miner Res. 2008 Nov;23(11):1859-63. doi: 10.1359/jbmr.080607.
Contrary to frequent claims, vitamin D insufficiency does not generally cause malabsorption of calcium because serum 1,25(OH)(2)D, which is the major determinant of calcium absorption, is maintained by secondary hyperparathyroidism. Nevertheless, because malabsorption of calcium has been described in osteomalacia, there must be a 25(OH)D level below which the serum 1,25(OH)(2)D can no longer be sustained, although it has never been defined. This paper seeks to define it. We examined the records of 3661 patients and found 319 with a serum 25(OH)D < or = 40 nM, in whom calcium absorption, serum calcium, PTH, bone markers, and vitamin D metabolites had been measured. They were grouped according to their serum 25(OH)D into four categories, 0-10, 11-20, 21-30, and 31-40 nM, and differences between the groups were tested by ANOVA. Correlations between the variables were also examined. Serum calcium, 1,25(OH)(2)D, and calcium absorption were significantly decreased and serum PTH and alkaline phosphatase (ALP) and urine hydroxyproline were increased in those with 25(OH)D < or = 10 nM. Serum ALP and urine hydroxyproline were more strongly related, inversely, to calcium absorption than to the vitamin D metabolites. We conclude that vitamin D deficiency does not reduce serum 1,25(OH)(2)D, and therefore calcium absorption, until the serum 25(OH)D falls to approximately 10 nM. At this level, the substrate concentration seems to be insufficient to maintain the level of the dihydroxy metabolite despite secondary hyperparathyroidism. Further studies are needed to see how these changes correlate with the histological changes of osteomalacia.
与常见观点相反，维生素D不足一般不会导致钙吸收不良，因为作为钙吸收主要决定因素的血清1,25(OH)₂D会通过继发性甲状旁腺功能亢进得以维持。然而，由于在骨软化症中已描述有钙吸收不良的情况，所以必然存在一个25(OH)D水平，低于此水平血清1,25(OH)₂D便无法再维持，尽管这一水平从未被明确界定。本文旨在对其进行界定。我们检查了3661例患者的记录，发现319例血清25(OH)D≤40 nM的患者，这些患者均已测定钙吸收、血清钙、甲状旁腺激素（PTH）、骨标志物及维生素D代谢产物。根据血清25(OH)D水平将他们分为四组，即0 - 10、11 - 20、21 - 30及31 - 40 nM，通过方差分析检验组间差异。同时也检查了各变量之间的相关性。血清25(OH)D≤10 nM的患者血清钙、1,25(OH)₂D及钙吸收显著降低，血清PTH、碱性磷酸酶（ALP）及尿羟脯氨酸升高。血清ALP及尿羟脯氨酸与钙吸收的负相关性比与维生素D代谢产物的更强。我们得出结论，在血清25(OH)D降至约10 nM之前，维生素D缺乏不会降低血清1,25(OH)₂D，因此也不会影响钙吸收。在此水平，尽管存在继发性甲状旁腺功能亢进，但底物浓度似乎不足以维持二羟基代谢产物的水平。还需要进一步研究来观察这些变化与骨软化症组织学变化之间的相关性。
