Research Information System
Turkish Journal of Gastroenterology, vol.14, no.4, pp.228-233, 2003 (SCI-Expanded)
Background/aims: The pathogenesis of non-alcoholic steatohepatitis (NASH) is poorly understood. Hepatic iron and copper overload can directly cause lipid peroxidation and eventually hepatic damage. The aim of this study was to investigate the role of hepatic iron and copper accumulation in the development of NASH. Methods: Fifty-three patients with NASH were studied. All patients underwent liver biopsy. Clinical and biochemical variables were examined. Serum iron, serum iron binding capacity (SIBC), transferrin saturation, ferritin, ceruloplasmin, and 24-hour urinary copper level were measured. The presence of stainable iron and copper on liver biopsy specimen was investigated. Results: Serum iron level in 14 (26%) patients, SIBC in 2 (3.7%), ferritin level in 1 (1.9%) and transferrin saturation in 2 (3.7%) patients were elevated. One male patient had abnormality in serum iron metabolism showing the possibility ofhemochromatosis. Slightly decreased serum ceruloplasmin level in 4 (7.5%) patients and slightly elevated 24-hour urinary copper amount in 6 (11%) patients were identified. No patients had the abnormality showing the possibility of Wilson disease. NASH was grade I in 25 (47%) patients, grade II in 20 (38%) and grade III in 8 (15%). Fourteen (26%) patients had no fibrosis, 31 (59%) patients had mild fibrosis. None of the patients had bridging or septal fibrosis or cirrhosis. No hepatic iron or copper staining was demonstrated in any patient. Conclusion: There was no correlation between hepatic iron and copper accumulation and the development of NASH.