[Association of hyperhomocysteinemia with liver steatosis in patients with chronic hepatitis C]

Med Clin (Barc). 2011 Jan 29;136(2):45-9. doi: 10.1016/j.medcli.2010.05.024. Epub 2010 Nov 3.
[Article in Spanish]

Abstract

Background and objectives: Liver steatosis in chronic hepatitis C (CHC) is related to viral and metabolic factors and likely to genetic factors. The aim of this study was to know if hyperhomocysteinemia and methylenetetrahydrofolate reductase (MTHFR)-C677T polymorphisms are associated with liver steatosis in nonalcoholic patients with CHC.

Patients and method: In 54 consecutive patients with CHC, alcohol consumption less than 40g/week, and no other causes of liver disease, a liver biopsy was performed. All variables were obtained at the time of biopsy. MTHFR-C677T was also performed in 128 healthy subjects, with age and gender similar to the patients.

Results: Liver steatosis was found in 33 patients (61%), 30 of them having a mild degree. Hyperhomocysteinemia was more prevalent in patients with steatosis (61% vs 24%; p=0.008) and overweight tended to be more prevalent in the same patients (61% vs 33%; p=0.05). All patients with virus C genotype 3 had steatosis. Viral load, liver inflammatory and fibrosis score were not different in patients with and without steatosis. MTHFR-C677T polymorphism was similar in controls and cases and in cases with and without steatosis. A multiple logistic regression showed that hyperhomocysteinemia was associated with liver steatosis after adjustment for age and sex (OR: 3.94; 95% CI: 1.09-14.29), and adjustment for overweight (OR: 4.43; 95% CI: 1.27-15.51).

Conclusions: In nonalcoholic patients with CHC mild liver steatosis is frequent, and is associated with hyperhomocysteinemia. An association between steatosis and MTHFR-C677T polymorphism was not found.

Publication types

  • English Abstract

MeSH terms

  • Adult
  • Fatty Liver / complications*
  • Fatty Liver / genetics
  • Female
  • Hepatitis C, Chronic / complications*
  • Hepatitis C, Chronic / genetics*
  • Humans
  • Hyperhomocysteinemia / complications*
  • Hyperhomocysteinemia / genetics*
  • Male
  • Methylenetetrahydrofolate Reductase (NADPH2) / genetics*
  • Mutation*
  • Polymorphism, Genetic*

Substances

  • Methylenetetrahydrofolate Reductase (NADPH2)