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Logo of arthrestherBioMed Centralbiomed central web sitesearchsubmit a manuscriptregisterthis articleArthritis Research & Therapy
 
Arthritis Res Ther. 2006; 8(2): R48.
Published online Feb 20, 2006. doi:  10.1186/ar1910
PMCID: PMC1526606
Vitamin D receptor gene BsmI polymorphisms in Thai patients with systemic lupus erythematosus
Wilaiporn Sakulpipatsin,1 Oravan Verasertniyom,2 Kanokrat Nantiruj,1 Kitti Totemchokchyakarn,1 Porntawee Lertsrisatit,1 and Suchela Janwityanujitcorresponding author1
1Division of Allergy, Immunology and Rheumatology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Rama 6 Road, Bangkok10400, Thailand
2Research Center, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Rama 6 Road, Bangkok 10400, Thailand
corresponding authorCorresponding author.
Wilaiporn Sakulpipatsin: wilaiporn_ws/at/hotmail.com; Oravan Verasertniyom: raovr/at/mahidol.ac.th; Kanokrat Nantiruj: raknt/at/mahidol.ac.th; Kitti Totemchokchyakarn: rakty/at/mahidol.ac.th; Porntawee Lertsrisatit: teplt/at/mahidol.ac.th; Suchela Janwityanujit: rasjw/at/mahidol.ac.th
Received September 15, 2005; Revisions requested October 13, 2005; Revised January 31, 2006; Accepted January 31, 2006.
Abstract
The immunomodulatory role of 1,25-dihydroxyvitamin D3 is well known. An association between vitamin D receptor (VDR) gene BsmI polymorphisms and systemic lupus erythematosus (SLE) has been reported. To examine the characteristics of VDR gene BsmI polymorphisms in patients with SLE and the relationship of polymorphisms to the susceptibility and clinical manifestations of SLE, VDR genotypings of 101 Thai patients with SLE and 194 healthy controls were performed based on polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The relationship between VDR gene BsmI polymorphisms and clinical manifestations of SLE was evaluated. The distribution of VDR genotyping in patients with SLE was 1.9% for BB (non-excisable allele homozygote), 21.78% for Bb (heterozygote), and 76.23% for bb (excisable allele homozygote). The distribution of VDR genotyping in the control group was 1.03% for BB, 15.98% for Bb, and 82.99% for bb. There was no statistically significant difference between the two groups (p = 0.357). The allelic distribution of B and b was similar within the groups (p = 0.173). The relationship between VDR genotype and clinical manifestation or laboratory profiles of SLE also cannot be statistically demonstrated. In conclusion, we cannot verify any association between VDR gene BsmI polymorphism and SLE. A larger study examining other VDR gene polymorphisms is proposed.
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