Clinical

Liver steatosis highly prevalent in children with HCV

Last Updated: 2006-12-28 16:30:13 -0400 (Reuters Health)

NEW YORK (Reuters Health) - As many as half of children with chronic hepatitis C virus (HCV) infection are likely to develop liver steatosis, according to a study conducted by Italian and Spanish researchers and published in the current issue of the American Journal of Gastroenterology.

Principal investigator Dr. Maria Guido of the University of Padova, Italy, and colleagues studied the prevalence and severity of liver steatosis in 21 Italian and 45 Spanish children with HCV.

They found that 18 of 66 children, or 27%, had liver steatosis. Ten of the 21 Italian children and 7 of the 45 Spanish children had the HCV-related lesion. All but two of the 18 children with steatosis were infected with HCV genotype 1.

Fibrosis was present in 60 of the 66 children with chronic HCV and liver steatosis.

BMI was associated with both the presence and the severity of liver steatosis. BMI and serum triglycerides were also higher in children with the complication.

Mean BMI for age among children without steatosis was slightly above the 60th percentile, was at the 88th percentile for children with any degree of steatosis, and was above the 97th percentile for the seven children with severe steatosis.

Steatosis negatively affects antiviral response in adults, and Dr. Guido's team concludes that "adjuvant treatments for steatosis should be considered for children with HCV-related chronic hepatitis and high BMI."

Editorialists Drs. Nizar N. Zein of the Cleveland Clinic Foundation and John H. Poterucha of the Mayo Clinic in Rochester, Minnesota, posit that steatosis may be the missing link to metabolic abnormalities in HCV.

Strategies to minimize liver damage and treatment of hepatic inflammation associated with HCV infection are already being employed, the editorialists note. The study indicates that weight loss, insulin sensitization and tumor necrosis factor-alpha neutralization may also correct HCV-related metabolic abnormalities and affect liver disease progression.

Am J Gastroenterol 2006;101:2611-2615, 2616-2617.