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Liver steatosis correlates with iron overload but not with HFE gene mutations in chronic hepatitis C

Hepatobiliary & Pancreatic Diseases International 2013年第4期12卷 377-384页

作者： Katarzyna Sikorska Piotr Stalke Tomasz Romanowski robert rzepko Krzysztof Piotr Bielawski Department of Infectious Diseases Medical University of GdanskSmoluchowskiego 18 80-214 Gdansk Poland Department of Biotechnology Intercollegiate Faculty of Biotechnology University of Gdansk and Medical University of GdanskKladki 24 80-822 Gdansk Poland Department of Pathology Medical University of GdanskDebinki 7 80-952 Gdansk Poland

BACKGROUND: Liver steatosis and iron overload, which are frequently observed in chronic hepatitis C (CHC), may contribute to the progression of liver injury. This study aimed to evaluate the correlation between liver steatosis and iron overload in Polish patients with CHC compared to non- alcoholic fatty liver disease (NAFLD) and HFE-hereditary hemochromatosis (HH) patients. METHODS: A total of 191 CHC patients were compared with 67 NAFLD and 21 HH patients. Liver function tests, serum markers of iron metabolism, cholesterol and triglycerides were assayed. The inflammatory activity, fibrosis, iron deposits and steatosis stages were assessed in liver specimens. HFE gene polymorphisms were investigated by PCR-RFLP. RESULTS: Liver steatosis was associated with obesity and diabetes mellitus. This disease was confirmed in 76/174 (44%) CHC patients, most of whom were infected with genotype 1. The average grade of steatosis was higher in NAFLD patients. CHC patients had significantly higher iron concentrations and transferrin saturations than NAFLD patients. Compared with CHC patients, HH patients had higher values of serum iron parameters and more intensive hepatocyte iron deposits without differences in the prevalence and intensity of liver steatosis. In the CHC group, lipids accumulation in hepatocytes was significantly associated with the presence of serummarkers of iron overload. No correlation between the HFE gene polymorphism and liver steatosis in CHC patients was found. CONCLUSIONS: Liver steatosis was diagnosed in nearly half of CHC patients, most of whom were infected with genotype 1. The intensity of steatosis was lower in CHC patients than that in NAFLD patients because of a less frequent diagnosis of metabolic syndrome. Only in CHC patients were biochemical markers of iron accumulation positively correlated with liver steatosis; these findings were independent of HFE gene mutations.

关键词： hepatitis C virus iron overload fatty liver hemochromatosis metabolic syndrome X

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Neutrophil engagement and septic challenge in acute experimental pancreatitis in rats

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World Journal of Gastroenterology 2005年第41期11卷 6459-6465页

作者： Stanisiaw Ha Marek Dobosz Jan J Kaczor robert rzepko Ewa Aleksandrowicz-Wrona Zdzislaw Wajda Zbigniew ledzi■ski Jacek Krajewski Department of General Endocrine and Transplant Surgery Medical University of Gdask Poland Department of General and Gastroenterological Surgery St. Vincent a' Paulo Hospital of Gdynia Poland Department of Bioenergetics J. niadecki University School of Physical Education in Gdask Poland Department of Pathomorphology Medical University of Gdask Poland Department of Clinical Nutrition Medical University of Gdask Poland Ⅱ Department of General Gastroenterological and Endocrinological Surgery Medical University of Gdask Poland

AIM： To investigate the influence of neutrophil adhesion molecule blockade with rnonoclonal antibody （MoAb CD11b） and E. coli lipopolysaccharide （LPS） administration on experimental acute pancreatitis （AP）. METHODS： AP was induced by four ip injections of cerulein （Cn） at 1-h intervals. MoAb CD 11b and LPS were administered at the beginning of the experiment. RESULTS： The neutrophil count and chemiluminescence were diminished at the beginning of AP. The oxidative stress parameters were found within the pancreatic gland. MoAb CD 11b used for AP resulted in a significant reduction of pancreatic infiltration and pancreatitis oxidative stress parameters. Serum interleukin-6 （IL-6） was not detected in AP animals, whereas high serum IL-6 concentration was noted only in animals receiving LPS. CONCLUSION： Neutrophils are involved in pancreatic damage in the early stage of AP. Neutrophil infiltration reduction protects the pancreatic gland from destruction during AP. LPS does not change the early course of Cn pancreatitis in rats.

关键词： Acute pancreatitis Polymorphonuclear cells Immunomodulation Septic shock

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