I thank Trevor Marshall for paying such close attention to our article,1 and I wish I had done the same in my proofreading. The normal range for the 1,25-(OH)2D, or calcitriol, assay published in our paper was incorrect and was that for the earlier INCSTAR (later to become Diasorin) assay kit for calcitriol. This assay was in use at the Foothills Medical Centre when I submitted my grant proposal for this project. However, the current Diasorin calcitriol assay kit is currently used, in both my laboratory and the Calgary Health Region clinical laboratory, and the normal range (2 standard deviations above and below the mean for a group of healthy hospital workers) is 55–190 pmol/L. This is the range we should have included in Table 2, and our reported 1,25-(OH)2D levels were within it.
Our 1,25-(OH)2D assay still provided results consistent with known vitamin D physiology. The 2 seasons with the highest mean levels of 1,25-(OH)2D were associated with the highest mean levels of parathyroid hormone and the lowest mean levels of serum inorganic phosphate, both known stimuli to conversion of 25(OH)D to 1,25-(OH)2D by renal 1α-hydroxylase.
Although 1,25-(OH)2D is the most biologically active form of vitamin D, it is generally accepted that, when assessing patients' vitamin D stores, measurement of 25(OH)D in blood is much more clinically useful than that of 1,25-(OH)2D.2,3 Serum 25(OH)D levels are consistently low in malabsorption syndromes and clinical osteomalacia, although 1,25-(OH)2D levels may be normal or high.4 In osteomalacia due to vitamin D deficiency, the serum 25(OH)D level, not the 1,25-(OH)2D level, correlates with the mineralization status of bone.5 Recent identification of 1α-hydroxylase activity in nonrenal tissue provides a plausible explanation of how 25(OH)D may mediate vitamin D action at a cellular level,6,7 and evidence also exists of direct effects of 25(OH)D on calcium absorption.8
David A. Hanley Professor and Head Division of Endocrinology and Metabolism Department of Medicine University of Calgary Calgary, Alta.
References
- 1.Rucker D, Allan JA, Fick GH, Hanley DA. Vitamin D insufficiency in a population of healthy western Canadians. CMAJ 2002;166(12):1517-24. [PMC free article] [PubMed]
- 2.Holick MF. The use and interpretation of assays for vitamin D and its metabolites. J Nutr 1990; 120 (Suppl 11):1464-9. [DOI] [PubMed]
- 3.Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 1999;69(5):842-56. [DOI] [PubMed]
- 4.Corazza GR, Di Sario A, Cecchetti L, Tarozzi C, Corrao G, Bernardi M, et al. Bone mass and metabolism in patients with celiac disease. Gastroenterology 1995;109(1):122-8. [DOI] [PubMed]
- 5.Demiaux B, Arlot ME, Chapuy MC, Meunier PJ, Delmas PD. Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings. J Clin Endocrinol Metab 1992;74(5):1146-51. [DOI] [PubMed]
- 6.Zehnder D, Bland R, Williams MC, McNinch RW, Howie AJ, Stewart PM, et al. Extrarenal expression of 25-hydroxyvitamin D3-1 α-hydroxylase. J Clin Endocrinol Metab 2001;86(2):888-94. [DOI] [PubMed]
- 7.Segersten U, Correa P, Hewison M, Hellman P, Dralle H, Carling T, et al. 25-hydroxyvitamin D3-1α-hydroxylase expression in normal and pathological parathyroid glands. J Clin Endocrinol Metab 2002;87(6):2967-72. [DOI] [PubMed]
- 8.Heaney RP, Barger-Lux MJ, Dowell MS, Chen TC, Holick MF. Calcium absorptive effects of vitamin D and its major metabolites. J Clin Endocrinol Metab 1997;82(12):4111-6. [DOI] [PubMed]