Secondary Hyperparathyroidism in the Elderly: Means to Defining Hypovitaminosis D
1998
Since the advent of assays for serum 25(OH)D many studies have reported a high prevalence of hypovitaminosis D in the elderly [1,2]. The rationale for defining hypovitaminosis D is the need to establish means of preventing hypovitaminosis D and its consequences, most notably hip fracture. Definition of hypovitaminosis D as judged by assay of serum 25-hydroxyvitamin D (25(OH)D), its major circulating metabolite, poses many questions. Should the reference range for the elderly be seasonally adjusted and similar to values found in young adults in countries of similar latitude? Should the cut-off point be the lowest value seen in young or elderly healthy adults in summertime? Should the duration of exposure to the lowest level of serum 25(OH)D be taken into consideration? Should the cut-off point be the serum 25(OH)D concentration which is associated with secondary hyperparathyroidism? Should the capacity to produce 1,25-dihydroxyvitamin D (1,25(OH)2D) be the judge of deficiency? Should the cut-off point be tempered by different levels of calcium intake, both from basal diet and calcium-supplemented intake? Finally, should the cut-off be that which is associated with evidence of diminished fracture rate or with the improvement in bone remodeling balance in groups following vitamin D supplementation? It is customary for the term hypovitaminosis D to denote a diminution in the serum 25(OH)D concentration and for the term vitamin D deficiency to imply an associated clinical, biochemical, radiologic or histologic abnormality [3]. Preece et al. [4] in England in 1973 suggested a level of 8–10 nmol/l. An expert group in the USA in 1982 proposed a level of 25 nmol/l [3], which remains the standard despite growing evidence to the contrary. Peacock et al. [5] in 1985 introduced the term insufficiency for serum 25(OH)D concentration between 25 and 50 nmol/l based on changes in serum 1,25(OH)2D. Heaney in 1986 [6] hypothesized a threshold level of 75–80 nmol/l. On the basis of studies in different countries, we proposed a minimum level of 50 nmol/l as the concentration that would restore serum parathyroid hormone (PTH) values in the elderly to levels found in healthy young adults [7]. The Decalyos study by Meunier and colleagues [8] demonstrated efficacy of vitamin D and calcium supplementation in hip fracture prevention by achieving a serum 25(OH)D level of 105 nmol/l. Dawson-Hughes et al. [9] suggested a threshold level of 110 nmol/l based on PTH status in North American elderly. On the basis of a comparison of reports in the elderly of baseline vitamin D and PTH status and the response to vitamin D therapy, we suggested a threshold level of greater than 100 nmol/l [10]. In this short review, we will focus on secondary hyperparathyroidism in the elderly as an approach to defining hypovitaminosis D.
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