Helicobacter pylori seroprevalence in patients with cirrhosis of the liver and hepatocellular carcinoma

Leone, Nicola; Pellicano, Rinaldo; Brunello, F.; Cutufia, Miguel Angel; Berrutti, M; Fagoonee, Sharmila; Rizzetto, Mario; Ponzetto, Antonio

doi:10.1016/j.cdp.2003.07.004

Cited by 48 publications

(36 citation statements)

References 24 publications

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“…As H. pylori infection increased hepatic AFP expression level and CCl 4 intoxication increased TGF-b1 levels, both in serum and tissues, H. pylori chronic infection might contribute to HCC progression from CCl 4 -induced fibrosis or cirrhosis. 17,56 Meanwhile, primary HSC was reported to differentiate into a hepatocyte-like cell that is round in structure and expresses AFP when treated with FGF4, HGF, bFGF, and IL-6. 54 H.pylori-induced inflammatory cytokines might lead hematopoietic progenitor cells as well as liver progenitor cells to differentiate into hepatocytes following liver damage, or abnormal proliferation of stem cells, which remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…13 Reportedly, H. pylori infection occurs with a high frequency in patients with cirrhosis and hepatocellular carcinoma (HCC), which may explain the frequent occurrence of gastroduodenal ulcer in cirrhotic patients. [14][15][16][17] Several studies have shown that H. pylori genomic sequences could be detected in the liver of patients with HCC. 18,19 H. hepaticus, a newly recognized Helicobacter sp., was experimentally proven to cause chronic hepatitis and HCC in mice.…”

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confidence: 99%

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Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

Goo

Park

et al. 2010

Laboratory Investigation

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Our earlier report has shown that Helicobacter pylori promoted hepatic fibrosis in a murine model. Herein, in order to elucidate the mechanism by which H. pylori accelerate liver fibrosis, the authors investigated the changes in expression levels of mitogen-activated protein kinases (MAPKs), p53-related proteins, antioxidants, and proinflammatory cytokines in liver samples. H. pylori infection enhanced CCl 4 -induced MAP kinase activation and p53 signaling pathway as well as Bax-and proliferating-cell nuclear antigen expressions, whereas H. pylori alone induced neither of these expressions nor hepatic fibrosis. Moreover, mRNA expressions of inflammatory cytokines, glutathione peroxidase expression, and the proliferative index were strongly augmented in livers of the H. pylori with CCl 4 treatment group compared with those of the CCl 4 -alone treatment group, whereas there was no difference in apoptotic index between the two groups. Interestingly, H. pylori treatment increased the number of a-fetoprotein-expressing hepatocytes independently of CCl 4 intoxication. In vitro analyses, using an immortalized rat hepatic stellate cell (HSC) line, revealed that H. pylori lysates increased the proliferation of HSCs, which was boosted by the addition of transforming growth factor-beta1 (TGF-b1). Furthermore, the treatment of H. pylori lysates promoted the translocation of nuclear factor kappa-light-chain enhancer of activated B cells (NF-kB) into the nucleus based on an increase in the degradation of NF-kB inhibitor alpha, in the presence of TGF-b1, as did H 2 O 2 treatment. In conclusion, H. pylori infection along with an elevated TGF-b1 may accelerate hepatic fibrosis through increased TGF-b1-induced pro-inflammatory signaling pathways in HSCs. Moreover, H. pylori infection might increase the risk of TGF-b1-mediated tumorigenesis by disturbing the balance between apoptosis and proliferation of hepatocytes.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

Goo

Park

et al. 2010

Laboratory Investigation

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“…There is large body evidence showing the association of HP and CLD (22)(23)(24)(25)(26). The prevalence of HP like DNA in the liver tissue samples of patients with CLD was significantly higher than the patients with metastatic adenocarcinoma (2).…”

Section: Discussion:-mentioning

confidence: 99%

Helicobacter Pylori Eradication Effect on Liver Fat Content in Patient With Non-Alcoholic Fatty Liver Disease.

Arnaout¹

2017

IJAR

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“…Since that time, a growing body of literature has suggested a role for Helicobacter in human HCC. Specifically, individuals with HCC are more likely to have serological evidence for past Helicobacter infection [5][6][7][8] and Helicobacter DNA can be found in HCC tissues more commonly than controls [9][10][11][12][13][14][15][16]. In addition to HCC, Helicobacter DNA has also been reported in intrahepatic cholangiocarcinomas [9,12].…”

Section: Introductionmentioning

confidence: 99%

Low frequency of Helicobacter DNA in benign and malignant liver tissues from Baltimore, United States

Vivekanandan

Torbenson

2008

Human Pathology

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Helicobacter DNA has been reported in hepatocellular carcinoma tissues in several studies from varying geographical locations, raising the possibility that helicobacter infection may contribute to the pathogenesis of hepatocellular carcinoma. Other known risk factors for hepatocellular carcinoma show significant geographical variability, but whether the same holds for helicobacter is unknown. We studied the prevalence of Helicobacter DNA in a United States cohort of HCC, where the prevalence of helicobacter infection is low in the general population. Liver tissues from 57 individuals were examined. Thirty-five individuals had paired tumor/non-tumor samples, including 21 cases of hepatocellular carcinoma, for a total of 92 samples studied. Both Helicobacter genus and Helicobacter pylori species specific PCR was performed. Helicobacter DNA was detected in 5/57 (9%) cases, all in non-neoplastic cirrhotic liver tissues from individuals with hepatitis C infection (N=4) or alcohol liver disease (N=1). Tissues from 22 hepatocellular carcinomas and 10 cholangiocarcinomas were all negative as were tissues from 8 benign primary hepatic tumors. In conclusion, Helicobacter DNA was detectable in 9% of liver tissues in this cohort, but was not found in primary benign or malignant liver tumors. These findings indicate that Helicobacter infection is unlikely to be etiologically associated with hepatocellular carcinoma in this cohort. If Helicobacter infection does contribute to the development of hepatocellular carcinoma in general, then significant regional variability must exist.

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Helicobacter pylori seroprevalence in patients with cirrhosis of the liver and hepatocellular carcinoma

Cited by 48 publications

References 24 publications

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

Helicobacter Pylori Eradication Effect on Liver Fat Content in Patient With Non-Alcoholic Fatty Liver Disease.

Low frequency of Helicobacter DNA in benign and malignant liver tissues from Baltimore, United States

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