Histological and histochemical alterations in liver of chronic hepatitis C patients with Helicobacter pylori infection
Zoology Department, Faculty of Science, Menoufia University, Menoufia, Egypt. Electronic address: .Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (Impact Factor: 2.02). 03/2013; 67(5). DOI: 10.1016/j.biopha.2013.03.004
Hepatitis C is an infectious disease affecting the liver. Chronic infection can progress fibrosis and cirrhosis, liver failure or liver cancer. Helicobacter pylori (H. pylori) is a spiral bacterium infects the stomach of more than 50% of the human population worldwide. H. pylori DNA has been identified in human livers and has been implicated in chronic liver disease and liver cancer. The present work was aimed to study the histological and histochemical alterations in liver of HCV patients with or without H. pylori infection. Immunohistochemical detection of H. pylori showed positive reactivity in 62 biopsies out of 100 biopsies (38% HCV patients and 62% HCV patients coinfected with H. pylori). Histological examination of liver of HCV patients showed microvesicular and macrovesicular steatosis, lymphocytic infiltrations, fibrosis and cirrhosis. Cirrhotic nodules and impairment of hepatic parenchyma were common in HCV patients coinfected with H. pylori. HCV patients coinfected with H. pylori recorded higher NIC score and pronounced fibrosis stages than HCV patients. Glycogen and total proteins decreased in hepatocytes and cirrhotic nodules in HCV patients. Such decrease was marked in liver of HCV patients coinfected with H. pylori. So it is recommended to perform a complete analysis for H. pylori in HCV patients suggesting that it will help in therapy of this disease.
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ABSTRACT: Helicobacter pylori (H. pylori) and hepatitis C virus (HCV) infect millions of people and can induce cancer. We investigated if H. pylori infection promoted HCV-associated liver cancer. Helicobacter-free C3B6F1 wild-type (WT) and C3B6F1-Tg(Alb1-HCVN)35Sml (HT) male and female mice were orally inoculated with H. pylori SS1 or sterile media. Mice were euthanized at ~12 mo postinoculation and samples were collected for analyses. There were no significant differences in hepatocellular tumor promotion between WT and HT mice; however, HT female mice developed significantly larger livers with more hepatic steatosis than WT female mice. H. pylori did not colonize the liver nor promote hepatocellular tumors in WT or HT mice. In the stomach, H. pylori induced more corpus lesions in WT and HT female mice than in WT and HT male mice, respectively. The increased corpus pathology in WT and HT female mice was associated with decreased gastric H. pylori colonization, increased gastric and hepatic interferon gamma expression, and increased serum Th1 immune responses against H. pylori. HT male mice appeared to be protected from H. pylori-induced corpus lesions. Furthermore, during gastric H. pylori infection, HT male mice were protected from gastric antral lesions and hepatic steatosis relative to WT male mice and these effects were associated with increased serum TNF-α. Our findings indicate that H. pylori is a gastric pathogen that does not promote hepatocellular cancer and suggest that the HCV transgene is associated with amelioration of specific liver and gastric lesions observed during concurrent H. pylori infection in mice.Gut Microbes 08/2013; 4(6). DOI:10.4161/gmic.26042
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ABSTRACT: The discovery of Helicobacter pylori infection in the stomach could be considered as one of the most important events of modern gastroenterology. Understanding of the natural history of many disorders of the upper gastrointestinal tract, including chronic gastritis, peptic ulcer disease, gastric cancer and MALT lymphoma, was altered by this discovery. Interestingly, epidemiological studies have also revealed a correlation between H. pylori infection and some diseases localized outside the stomach, especially those characterized by persistent and low-grade systemic inflammation. Of note, H. pylori has an important role in iron deficiency anaemia, idiopathic thrombocytopenic purpura and vitamin B12 deficiency. Moreover, the association of this bacterial pathogen with many other diseases, including hepatobiliary, pancreatic, cardiovascular and neurodegenerative disorders is currently under investigation. In this Review, we summarize the results of the most important studies performed to date surrounding the association of H. pylori infection with extragastric diseases, as well as the strength of the evidence. We also provide information concerning bacterial-host interactions and the mechanisms implicated in the pathogenesis of each of these extragastric diseases.Nature Reviews Gastroenterology & Hepatology 12/2013; 11(4). DOI:10.1038/nrgastro.2013.243 · 12.61 Impact Factor
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ABSTRACT: This work to show the relation between Helicobacter Pylori infection and Hepatocellular Carcinoma in Egyptian patients. This study was completed at National liver institute in Egypt. Patients in this study were recognized cases of chronic Hepatitis C virus liver disease with and without hepatocellular carcinoma. Serum samples of patients of hepatocellular carcinoma with hepatitis C Virus (HCV) of 40 male and 30 female adults had been collected, Helicobacter pylori (H. pylori) was detected by enzyme linked immunosorbent assay with comparison with ten males and ten females patients as control groups with chronic Hepatitis C Virus (HCV) without HCC. All patients were free from hepatitis B virus (HBV) infection, without cigarette smoking and without alcohol drinking. Positive H. pylori was found more in male and female patients with hepatocellular carcinoma combined by chronic HCV than those with HCV without hepatocellular carcinoma and there was significant difference between both groups. There is a significant association between infection with H. pylori, elevated titers of H. pylori antibodies and the increased risk of hepatocellular carcinoma in males and females Egyptian patients.American Journal of Biochemistry and Biotechnology 06/2015; 11(2):110-113. DOI:10.3844/ajbbsp.2015.110.113
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