This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Correa, P. Articles by Carling, T. Search for Related Content PubMed PubMed Citation Articles by Correa, P. Articles by Carling, T.

The Vitamin D Receptor (VDR) Start Codon Polymorphism in Primary Hyperparathyroidism and Parathyroid VDR Messenger Ribonucleic Acid Levels¹

Endocrine Surgery Unit, Department of Surgery (P.C., J.R., G.W., E.L., G.Å., T.C.), and Department of Internal Medicine (A.K.), Uppsala University Hospital, S-751 85 Uppsala, Sweden; and the Department of Medicine (P.S.), Gentofte Hospital, University of Copenhagen, DK-2900 Hellerup, Denmark

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

Vitamin D regulates parathyroid cell proliferation and secretion of PTH. Increased prevalence of the polymorphic vitamin D receptor (VDR) alleles b, a, and T has been reported in sporadic primary hyperparathyroidism (PHPT), suggesting that these genetic variants may predispose to the disease. Recently, another polymorphism in the VDR gene was related to bone mineral density, and this VDR-FokI polymorphism causes different lengths of the VDR, implying possible functional consequences. The VDR-FokI polymorphism was studied in 182 postmenopausal women with sporadic PHPT and in matched controls. No significant differences in distribution of the VDR-FokI genotypes could be detected between the groups, although there was a tendency toward overrepresentation of the F allele in the PHPT patients (P = 0.05). There were no significant associations with age, serum calcium, serum PTH, bone mineral density, or parathyroid tumor weight. The VDR genotypes were unrelated to VDR and PTH messenger ribonucleic acid levels in the parathyroid adenomas of 42 PHPT patients. In 23 PHPT patients, the Ca²⁺-PTH set-points were determined in vivo and were unrelated to the VDR alleles. We suggest that the VDR-FokI polymorphism has at most a minor pathogenic importance in the development of PHPT.

This article has been cited by other articles:

				B.-W. Ogunkolade, B. J. Boucher, J. M. Prahl, S. A. Bustin, J. M. Burrin, K. Noonan, B. V. North, N. Mannan, M. F. McDermott, H. F. DeLuca, et al. Vitamin D Receptor (VDR) mRNA and VDR Protein Levels in Relation to Vitamin D Status, Insulin Secretory Capacity, and VDR Genotype in Bangladeshi Asians Diabetes, July 1, 2002; 51(7): 2294 - 2300. [Abstract] [Full Text] [PDF]

				T. Carling, J. Rastad, E. Szabó, G. Westin, and G. Åkerström Reduced Parathyroid Vitamin D Receptor Messenger Ribonucleic Acid Levels in Primary and Secondary Hyperparathyroidism J. Clin. Endocrinol. Metab., May 1, 2000; 85(5): 2000 - 2003. [Abstract] [Full Text]

				J. A. Eisman Genetics of Osteoporosis Endocr. Rev., December 1, 1999; 20(6): 788 - 804. [Abstract] [Full Text]