Vitamin D receptor genotypes are not associated with rheumatoid arthritis or biochemical parameters of bone turnover in German RA patients
B. Goertz1, W.J. Fassbender3, J.C. Williams2, A.M. Marzeion2, R.G. Bretzel2, H. Stracke2, M.N. Berliner2
1Institute of Pathology and 2IIIrd Medical Department, Justus-Liebig-University of Giessen; 3 Ist Medical Department, Johann Wolfgang Goethe-University Frankfurt, Germany
ABSTRACT
Objective
Vitamin D is known to exert immunomodulatory effects. An overrepresentation of the b allele of the vitamin D receptor (VDR) has been detected in autoimmune diseases as type-1-diabetes and multiple sclerosis. VDR
polymorphisms have been shown to influence bone metabolism and bone density. The aim of the present study was to examine the distribution of VDR alleles in German rheumatoid arthritis (RA) patients and their relation to bone turnover parameters.
Methods
62 German RA patients were included and compared to 40 controls. Three VDR alleles were examined (Bsm I, Taq I and Fok I). In addition, serum intact osteocalcin (OC), parathyroid hormone, bone specific alkaline phosphatase (B-ALP), the carboxyterminal extension peptide of type I procollagen, 25-OH-vitamin D and urinary deoxypyridinoline (DPD) excretion were measured. Furthermore, C-reactive protein, erythrocyte sedimentation rate and rheumatoid factor were measured.
Results
We found a slightly higher frequency of the bB and tT-genotype in RA patients compared to controls, which was not statistically significant. OC and B-ALP were found to be significantly higher in RA patients with positive correlations between bone formation and resorption parameters indicating higher bone turnover in RA patients with maintained coupling. CRP in RA patients correlated with DPD and inversely with PTH. VDR genotype showed no association with bone turnover, family history or the presence of rheumatoid factor.
Conclusions
Our results suggest that VDR polymorphisms do not play a major role in RA predisposition in Germans.
Key words
Rheumatoid arthritis, genetics, vitamin D receptor, bone metabolism.
Please address correspondence and requests for reprints to: Dr. Birgit Goertz, Institute of Pathology, Langhansstrasse 10, D-35385 Giessen, Germany.
E-mail: Birgit.Goertz@patho.med.uni-giessen.de
Clin Exp Rheumatol 2003; 21: 333-339.
© Copyright Clinical and Experimental
Rheumatology 2003.