Association between polymorphisms in the vitamin D receptor and susceptibility to multiple sclerosis.

Abstract:

OBJECTIVES:Multiple sclerosis (MS) is a neurodegenerative chronic inflammatory. Mutations in the vitamin D receptor (VDR) gene can substantially affect serum vitamin D levels or alter its functionality, and can consequently increase susceptibility to developing MS. The objective of this study was to evaluate the association between polymorphisms in the VDR gene and risk of MS in a (Spanish) Caucasian population. PATIENTS AND METHODS:We conducted a retrospective case-control study comprising 209 patients with relapsing-remitting multiple sclerosis (RRMS) and 836 controls of Caucasian origin from southern Spain. The ApaI (rs7975232), BsmI (rs1544410), Cdx2 (rs11568820), FokI (rs2228570), and TaqI (rs731236) gene polymorphisms were determined by allelic discrimination real-time PCR using TaqMan probes. RESULTS:The recessive logical regression model, adjusted for age and sex, revealed that the TT genotype for VDR FokI (rs2228570) polymorphism was associated with higher risk of MS (P = 0.0150; OR = 1.82; 95% CI = 1.12-2.94; TT vs. CT + CC). No association between the other polymorphisms and development of MS was found in any of the models analyzed. The haplotype analysis, adjusted for age, smoking, and sex, did not find any statistically significant association between the haplotypes analyzed and risk of MS. CONCLUSIONS:The VDR FokI (rs2228570) polymorphism was significantly associated with developing MS. We found no influence of the ApaI (rs7975232), BsmI (rs1544410), Cdx2 (rs11568820), FokI (rs2228570), and TaqI (rs731236) gene polymorphisms on the risk of developing MS in our patients.

journal_name

Pharmacogenet Genomics

authors

Cancela Díez B,Pérez-Ramírez C,Maldonado-Montoro MDM,Carrasco-Campos MI,Sánchez Martín A,Pineda Lancheros LE,Martínez-Martínez F,Calleja-Hernández MÁ,Ramírez-Tortosa MC,Jiménez-Morales A

doi

10.1097/FPC.0000000000000420

subject

Has Abstract

pub_date

2021-02-01 00:00:00

pages

40-47

issue

2

eissn

1744-6872

issn

1744-6880

pii

01213011-202102000-00002

journal_volume

31

pub_type

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