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Influence of the BsmI Polymorphism of the Vitamin D Receptor Gene on Rheumatoid Arthritis Clinical Activity

CARMEN GÓMEZ-VAQUERO, JORDI FITER, ANA ENJUANES, XAVIER NOGUÉS, ADOLFO DÍEZ-PÉREZ, and JOAN M. NOLLA

ABSTRACT.

Objective. The etiopathogenesis of rheumatoid arthritis (RA) is not fully known; vitamin D has been shown to have immunomodulatory effects and could be implicated in it. BsmI polymorphism of vitamin D receptor (VDR) gene is involved in the pathogenesis of osteoporosis in RA. We analyzed the effect of this polymorphism on clinical activity in 123 Spanish postmenopausal women with RA.

Methods. Patients with RA were enrolled consecutively during outpatient clinic visits. RA severity and activity measures were recorded and a blood sample was extracted. Genetic analysis was made by DNA extraction techniques, amplification by polymerase chain reaction, and restriction using endonuclease BsmI.

Results. Mean age of the patients was 62.9 ± 8.4 years. The mean time of the evolution of RA was 12.5 ± 7.3 years and mean time since menopause was 15.2 ± 9.4 years. Seventy-six percent of the patients were rheumatoid factor-positive; mean Health Assessment Questionnaire (HAQ) score was 1.3 ± 0.7; 92% of the patients had been treated with low-dose glucocorticoids. Twenty-eight patients (23%) had genotype BB, 48 (39%) Bb, and 47 (38%) bb. Patients with BB or Bb genotype had statistically significantly higher HAQ scores, erythrocyte sedimentation rate, current and accumulated dose of glucocorticoids, and number of disease modifying antirheumatic drugs taken, and lower serum hemoglobin and albumin than patients with bb genotype (p < 0.05).

Conclusion. Among patients with RA, the bb genotype of the BsmI polymorphism of the VDR gene is associated with less severe disease. (First Release July 15 2007; J Rheumatol 2007;34:1823-6)

Key Indexing Terms:

RHEUMATOID ARTHRITIS
CLINICAL ACTIVITY
VITAMIN D RECEPTOR GENE POLYMORPHISM

From the Rheumatology Department, IDIBELL – Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat; and URFOA-IMIM, Internal Medicine Department, Hospital del Mar, Barcelona, Spain.

Supported by a grant from the FIS of the Instituto Carlos III, Red de centros RCMN (C03/08), Madrid, Spain.

C. Gómez-Vaquero, MD, PhD, Senior Registrar; J. Fiter, MD, Senior Registrar; J.M. Nolla, MD, PhD, Chief of Section, Associate Professor, Rheumatology Department, IDIBELL – Hospital Universitari de Bellvitge; A. Enjuanes, PhD, Senior Researcher; X. Nogués, MD, PhD, Senior Registrar, Associate Professor; A. Díez-Pérez, MD, PhD, Chief of Department, Senior Professor, URFOA-IMIM, Internal Medicine Department.

Address reprint requests to Dr. J.M. Nolla, Rheumatology Department (Pl. 10-2), Hospital Universitari de Bellvitge, Feixa Llarga s/n, 08907 L'Hospitalet de Llobregat, Barcelona, Spain. E-mail: jm.nolla@csub.scs.es

Accepted for publication May 24, 2007.