Detection Of Vitamin D Receptor Gene Polymorphisms In Rheumatoid Arthritis Patients And Their Clinical Relevance

Rheumatoid arthritis (RA) is a long-term autoimmune disease with complex genetic causes. Vitamin D, working through its receptor (VDR), helps control immune function and may affect RA risk and severity. Objective of this paper is to study how VDR gene variations (FokI, BsmI, TaqI, ApaI) relate to RA risk and disease symptoms. We studied 50 RA patients who met standard diagnosis criteria and 10 healthy controls. We extracted DNA and analyzed VDR gene variations using laboratory techniques. We measured disease activity scores, blood inflammation markers, vitamin D levels, rheumatoid factor (RF), and anti-CCP antibodies. The FokI ff gene type was much more common in RA patients (30%) than healthy controls (10%) with significantly higher risk (OR = 4.50, 95% CI: 1.24-16.32, p = 0.032). RA patients with the ff gene type had higher disease activity scores (6.1 ± 1.2 vs. 4.8 ± 1.3, p = 0.003), higher inflammation levels (ESR: 52.4 ± 20.1 vs. 42.3 ± 16.8 mm/hr, p = 0.034; CRP: 16.2 ± 9.8 vs. 11.2 ± 7.2 mg/L, p = 0.025), and lower vitamin D levels (15.2 ± 4.8 vs. 20.1 ± 6.4 ng/mL, p = 0.002). The other gene variations showed no significant differences. VDR FokI gene variation is linked to both RA risk and disease severity. These findings suggest that testing for VDR gene types could help identify high-risk patients and guide personalized treatment.