Clinical Significance of Vitamin D Deficiency in Primary Hyperparathyroidism, and Safety of Vitamin D Therapy

Nasser Mikhail, MD, MSc

Disclosures

South Med J. 2011;104(1):29-33. 

In This Article

Prevalence of Vitamin D Deficiency in Primary Hyperparathyroidism

The majority of prevalence studies of vitamin D deficiency in patients with PHPT are limited by lack of adequate control subjects, and by failure to report serum 25-OHD levels as a function of the season of the year (a factor that can significantly alter serum concentrations of 25-OHD).[5,6] Despite these limitations, available data worldwide suggest that the prevalence of vitamin D deficiency among patients with PHPT is higher than in the general population. In one of the few controlled studies, Moosgaard et al[5] from Denmark reported that 81% of 289 patients with PHPT had vitamin D deficiency (defined as 25-OHD serum levels <25 ng/mL) compared with 60% of age-, sex-, and season-matched subjects referred for osteoporosis evaluation, and 35% of healthy blood donors. In France, Boudou et al[7] found that 93% of 72 patients with PHPT had serum 25-OHD values <20 ng/dL, compared with the 38% prevalence previously reported among French postmenopausal women.[6] In the United States (US), the frequencies of patients with PHPT having serum 25-OHD levels <20 ng/mL and <25 ng/mL were 53% and 61%, respectively.[8,9] The previous proportions are higher than the most recent statistics released by the National Health and Nutrition Examination Survey (NHANES, 2001–2004) suggesting that 36% of the US population have serum 25-OHD levels <20 ng/mL.[10] The causes of low circulating levels of 25-OHD in patients with PHPT are not totally understood. Proposed mechanisms include accelerated conversion of 25-OHD to 1,25-dihydroxy vitamin D (1,25-(OH)2D) by PTH, and the increased catabolism of 25-OHD by the high levels of 1,25-(OH)2D that prevail in PHPT.[11,12] In addition, the increased adiposity described in patients with PHPT might be a contributing factor, due in part to sequestration of vitamin D in fatty tissue.[13,14]

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