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Michael F Holick, The D-lemma: To Screen or Not to Screen for 25-Hydroxyvitamin D Concentrations, Clinical Chemistry, Volume 56, Issue 5, 1 May 2010, Pages 729–731, https://doi.org/10.1373/clinchem.2009.139253
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Until recently, there has been little interest in the medical and pediatric communities regarding the vitamin D status of their patients. It had been assumed that everyone was vitamin D sufficient and that only those patients with fat-malabsorption syndromes were at risk(1). African Americans were at risk because of their sunscreening skin pigment, but little attention was placed on their vitamin D status because African Americans were at less risk of fracture than Caucasians. The introduction of drugs to treat osteoporosis made physicians aware that vitamin D deficiency was a contributing factor for osteoporosis.
Vitamin D made in the skin or ingested from the diet is converted in the liver to 25-hydroxyvitamin D [25(OH)D]1 (1)(2), the major circulating form of vitamin D used for evaluating the vitamin D status of patients. 25(OH)D is hydroxylated in the kidneys to form the biologically active metabolite 1,25-dihydroxyvitamin D [1,25(OH)2D](1)(2). Because most children and adults were assumed to be vitamin D sufficient when reference intervals for 25(OH)D were determined, values ranged from 10 μg/L (ng/mL) to 55 μg/L. Studies of adults that evaluated parathyroid hormone (PTH) with 25(OH)D revealed, however, that PTH concentrations began to plateau at 30–40 μg/L(3). Healthy adults receiving vitamin D and calcium supplementation who had blood 25(OH)D concentrations between 11 μg/L and 19 μg/L demonstrated substantial decreases in their PTH concentrations, whereas adults with a 25(OH)D concentration between 20 μg/L and 25 μg/L had no significant change in PTH, suggesting that vitamin D deficiency should be defined as a 25(OH)D concentration <20 μg/L(4). Postmenopausal women whose 25(OH)D concentration increased from approximately 20 μg/L to approximately 32 μg/L had a 65% increase in intestinal calcium absorption(5). Thus, vitamin D deficiency was defined as a 25(OH)D concentration of <20 μg/L, but for maximizing the vitamin D effect on calcium metabolism, the recommendation was that a 25(OH)D concentration >30 μg/L was needed. The gap was bridged by defining vitamin D insufficiency as a 25(OH)D concentration of 21–29 μg/L(1)(5).
