Pediatric Hepatitis C virus (HCV) chronic infection: A potential serum marker reflects liver apoptosis and degree of steatosis

VALVA, P.; DE MATTEO, E.; GISMONDI, M. I.; GALOPPO, C.; MARIA VICTORIA PRECIADO

Foz de Iguazú, Misiones

Congreso; III World Congress of Pediatric Gastroenterology, Hepatology and Nutrition.; 2008

European Society for Paediatric Gastroenterology Hepatology and Nutrition y North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition

In Hepatitis C virus chronic infection apoptosis may play a role in pathogenesis as well as steatosis may influence disease progression. Cytokeratins (CK) have been studied as serum markers of liver disease. Recent evidence suggests that CK-18 is cleaved by caspases and released from apoptotic cells. Our aim was to detect early apoptosis markers in liver biopsies and serum samples from pediatric HCV+ patients and to assess the usefulness of a serum marker of liver injury progression. Twenty patients [median age: 8.5 years (range 1-17 yrs)] were included. Fibrosis (F), hepatitis (H), steatosis, lymphoid follicles and bile duct damage were assessed in liver biopsies. HCV infected hepatocytes (NS3) and apoptosis markers (activated caspase-3 [casp-3a] and caspase-generated CK-18 fragment [M30]) were evaluated by immunohistochemistry. Results were expressed as nº positive hepatocytes/nº total hepatocytes in 20 high-power fields (1000). In a subgroup of 14 serum samples, at time of biopsy, M30 was quantified. A group of 8 controls was included. Forty percent of biopsies displayed F1, 50% F2 and 10% F3. Thirty five percent showed mild H and 65% moderate H. No patient displayed cirrhosis or severe H. Sixty percent of biopsies showed variable steatosis (