Apoptosis markers related to pathogenesis of pediatric chronic Hepatitis C virus infection. M30 mirrors the severity of steatosis

VALVA P; DE MATTEO E; GALOPPO MC; GISMONDI MI; PRECIADO MV

JOURNAL OF MEDICAL VIROLOGY

WILEY-LISS, DIV JOHN WILEY & SONS INC

Lugar: Nueva York; Año: 2010 p. 949 - 957

0146-6615

Apoptosis involvement in liver damage related to Hepatitis C virus (HCV) chronic infection has been suggested. Although liver biopsy represents the gold standard for evaluating disease severity, non-invasive tests are a growing medical need. The aim of this study was to detect apoptosis markers in liver and serum from pediatric HCV infected patients and to assess its utility to predict liver damage progression. Twenty three patients were included. Liver biopsies were used for histological analysis as well as for immunodetection of a viral protein (NS3) and apoptosis markers (activated caspase-3 [casp-3a], caspase-generated CK-18 fragment [M30] and TUNEL). M30 was quantified in paired serum and biopsy samples. NS3 correlated both with casp-3a (r =0.83, p <0.0001) and TUNEL (r =0.61, p <0.0017). Casp-3a and TUNEL also displayed a correlation (r = 0.56, p = 0.005). Both NS3 and casp-3a were associated with fibrosis stage (p = 0.03). Serum M30 [median: 122.15 UL-1 (86.68-794.58)] was higher in patients than in controls [median: 81.44 UL-1 (41.17-129.30)], (p<0.0001). M30 showed a correlation with steatosis, and indeed it was linked to severe grade (p= 0.004). In children, HCV would be involved in liver damage through apoptosis induction. The apoptosis markers detected reflect liver injury. Serum M30 might be useful as a marker to detect the extent of liver steatosis.