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Vitamin D Receptor Polymorphisms Correlate to Parathyroid Cell Function in Primary Hyperparathyroidism¹

Department of Surgery, Uppsala University Hospital, 751 85 Uppsala, Sweden

Address all correspondence and requests for reprints to: Tobias Carling, M.B., Department of Surgery, Uppsala University Hospital, S-751 85 Uppsala, Sweden. E-mail: Tobias.Carling{at}kirurgi.uu.se

Calcitriol acts via its receptor (VDR) and inhibits PTH secretion and parathyroid cell proliferation. Increased prevalence of the polymorphic VDR alleles b, a, and T has been demonstrated in sporadic primary hyperparathyroidism. Sixty-two patients with primary hyperparathyroidism due to parathyroid adenoma (mean age, 69.5 ± 1.4 yr) were genotyped for these VDR polymorphisms. Dispersed cells of the adenomas were exposed to increasing concentrations of extracellular Ca²⁺ and analyzed for PTH release and cytoplasmic Ca²⁺ concentrations. Ca²⁺-mediated PTH inhibition exhibited higher ED₅₀ and less suppression in the cells of patients who were homozygous for the b, a, and T alleles (P < 0.05–0.10). When analyzing haplotypes, the patients with baT demonstrated a ED₅₀ of 1.81 ± 0.15 vs. 1.29 ± 0.10 for BAt (P < 0.05). As VDR alleles were unrelated to parathyroid intracellular Ca²⁺, influences of polymorphic VDR alleles on PTH secretion seem to involve mechanisms other than the Ca²⁺-sensing protein of the parathyroid cell surface.

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