Cannabinoid receptor 2-63 QQ variant is associated with persistently normal aminotransferase serum levels in chronic hepatitis C

PLoS One. 2014 Jun 18;9(6):e99450. doi: 10.1371/journal.pone.0099450. eCollection 2014.

Abstract

Background and aim: To evaluate in anti-HCV-positive patients the clinical impact of the rs35761398 variant of the CNR2 gene leading to the substitution of Gln (Q) of codon 63 of the cannabinoid receptor 2 (CB2) with Arg (R).

Patients and methods: 253 consecutive anti-HCV-/HCV-RNA-positive patients were enrolled, of whom 53 were HCV carriers with persistently normal ALT (PNALT group) and 200 had a history of steadily abnormal serum ALT values (abnormal ALT group). All patients were naive for antiviral therapy and were screened for the CNR2 rs35761398 polymorphism by a TaqMan assay.

Results: Subjects in the PNALT group, compared with those in the abnormal ALT group were older (58.5±12 vs. 50.7±12.4 years, p = 0.001), more frequently female (66% vs. 42%, p = 0.003), with lower body mass index (BMI) (24.5±3.1 vs. 26.6±4.6, p = 0.003), and more frequently with HCV genotype 2 (43.1% vs 17.7%, p = 0.0002) and CB2-63 QQ variant (34% vs. 11%, p = 0.0001). Considering all 253 patients, no difference in the demographic, biochemical, or virological data was observed between patients in the different CB2-63 variants. The logistic regression analysis identified CB2-63 QQ, HCV genotype 2, older age and lower BMI as independent predictors of PNALT (p<0.00001).

Discussion: The CB2-63 QQ variant in HCV patients was independently associated with the PNALT status.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alanine Transaminase / blood*
  • Female
  • Genetic Association Studies
  • Hepatitis C, Chronic / blood
  • Hepatitis C, Chronic / genetics*
  • Humans
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide
  • Receptor, Cannabinoid, CB2 / genetics*

Substances

  • CNR2 protein, human
  • Receptor, Cannabinoid, CB2
  • Alanine Transaminase

Grants and funding

This study was supported by a grant from PRIN 2008, M.I.U.R., Rome, Italy “OTTIMIZZAZIONE DELLA DIAGNOSI EZIOLOGICA DELL’EPATITE ACUTA C E STUDIO DEI FATTORI VIRO-IMMUNOLOGICI DI GUARIGIONE, DI CRONICIZZAZIONE E DI RISPOSTA ALLA TERAPIA CON INTERFERONE” and in part by a grant from Regione Campania “Progetti per il miglioramento della qualità dell’assistenza, diagnosi e terapia del paziente affetto da AIDS nei settori: immunologia, coinfezioni, informazione e prevenzione”, 2008. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.