Abstract
Background/AimsGenetic variants of MHC class I polypeptide-related chain A (MICA) at rs2596542 have been associated with hepatocellular carcinoma. The linkage between serum MICA (sMICA) and liver fibrosis in chronic hepatitis C is elusive.ResultsLinear regression analysis revealed that sMICA were independently correlated to α-fetoprotein (β: 0.149; 95% confidence interval [CI]: 0.001, 0.003; P = 0.007)and MICA rs2596542 GG genotype (β: 0.209; 95% CI: 0.153, 0.483; P < 0.001). While patients were stratified by MICA genetic variants, advanced fibrosis was the only factor independently correlated to sMICA among A allele carriers (β: 0.234; 95% CI: 0.107, 0.543; P = 0.004) but not among non-A allele carriers. Logistic regression analysis revealed that factors associated with advanced liver fibrosis was sMICA (OR/CI: 2.996/1.428–6.287, P = 0.004) and platelet counts (OR/CI: 0.988/0.982–0.994, P < 0.001) in MICA rs2596542 A allele carriers. sMICA > 50 pg/mL provided a positive predictive value of 72 % in predicting advanced liver fibrosis (F3-4) and of 90% in significant fibrosis (> F2) in MICA rs2596542 A allele carriers.Materials and MethodsSerum level and single nucleotide polymorphism at rs2596542 of MICA were tested for the association with liver fibrosis in 319 biopsy proven chronic hepatitis C patients.ConclusionsLevels of sMICA were highly correlated to liver disease severity in chronic hepatitis C patients who carried the MICA rs738409 A allele. Patients possessing the genetic predisposition had a higher likelihood of progressed liver fibrosis if they expressed higher sMICA levels.
Highlights
Chronic hepatitis C (CHC) infection is one of the leading causes of end sage liver diseases including hepatocellular carcinoma (HCC) [1]
Linear regression analysis revealed that soluble MICA (sMICA) were independently correlated to α-fetoprotein (β: 0.149; 95% confidence interval [CI]: 0.001, 0.003; P = 0.007)and MHC class I polypeptide-related chain A (MICA) rs2596542 GG genotype (β: 0.209; 95% CI: 0.153, 0.483; P < 0.001)
While patients were stratified by MICA genetic variants, advanced fibrosis was the only factor independently correlated to sMICA among A allele carriers (β: 0.234; 95% CI: 0.107, 0.543; P = 0.004) but not among non-A allele carriers
Summary
Chronic hepatitis C (CHC) infection is one of the leading causes of end sage liver diseases including hepatocellular carcinoma (HCC) [1]. Diabetic mellitus, age, age of infection, steatosis and host genetics [2,3,4,5]). When it comes to host genetics, a genome-wide association study (GWAS) has confirmed that the single nucleotide polymorphism (SNP) rs2596542 of MHC class I polypeptide-related chain A (MICA) was significantly associated with hepatitis C virus (HCV) related HCC [6]. High expression soluble MICA (sMICA) in the circulation might down-regulate NKG2D expression. We aimed to elucidate the association of sMICA with HCV-related liver fibrosis in patients with different genetic predispositions
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