Impact of vitamin D receptor and binding protein gene polymorphisms in clinical and laboratory data of HCV patients
2018
Potential relationship of vitamin D, vitamin D receptor (VDR), and vitamin D binding protein (DBP) have been suggested in the
pathophysiology of hepatitis C virus (HCV) infection. The aim of this observational study is to determine vitamin D levels, and VDR and
DBP genetic polymorphism according demographic and laboratory data in chronic HCV patients (CHC).
A total of 148 CHC patients gave serum samples for testing 25-hydroxyvitamin D (25 (OH)D) level by immunochemiluminometric
assay (<20ng/mL defined as deficient) and donated blood samples to allelic discrimination analysis using TaqMan assays. Analyzed
single nucleotide polymorphisms (SNPs) were: VDR-rs7975232 (ApaI) C>A, rs731236 A>G (TaqI), rs1544410 C>T (BsmI),
rs10735810 T>C (FokI) and carrier globulin/binding protein (GC)-rs4588 and rs7041 and the haplotype bAt [CCA]. Hepatic fibrosis
was assessed using Fib-4 and Forns index.
Eighty-two (54.40%) patients demonstrated deficiency of vitamin D and this was associated to AST (P=.019 [CI: 1.003–1.034]),
total cholesterol (P=.038 [CI: 1.004–1.164]), fibrosis grade (P<.001 [CI: 0.000–0.844]), and FokI (P=.028) allele T presence.
Association was found between VDR polymorphism and fibrosis (BsmI andTaqI), triglycerides (TaqI), and HDL (FokI). DBP
polymorphism was associated to HCV genotype (GC rs7041), previous HCV treatment, and GGT (GC rs4588).
In conclusion, lowfrequency of vitamin D deficiencywas found, but VDR polymorphisms were frequently associated to fibrosis grade
suggesting that they could be used as disease evaluation markers to understand the mechanisms underlying the virus–host interaction.
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