Detection of identical Helicobacter DNA in the stomach and in the non-cirrhotic liver of patients with hepatocellular carcinoma

Verhoef, Cornelis; Pot, Raymond G.J.; Man, Rob A. de; Zondervan, Pieter E.; Kuipers, Ernst J.; IJzermans, Jan N.M.; Kusters, Johannes G.

doi:10.1097/00042737-200311000-00004

Cited by 45 publications

(39 citation statements)

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“…106(6): 748-754, September 2011 The hypothesis that Helicobacter spp might be a risk factor for human liver diseases has arisen after the discovery of Helicobacter hepaticus and its association with murine hepatitis and hepatocellular carcinoma (HCC). Subsequent studies in humans have shown the presence of Helicobacter DNA in hepatic tissue of patients with hepatobiliary diseases, mainly cirrhosis and/ or HCC secondary to hepatitis B virus (HBV) and hepatitis C virus (HCV) (Avenaud et al 2000, Dore et al 2002, Fan et al 2002, Verhoef et al 2003, Rocha et al 2005, Pellicano et al 2008. Although these studies have contributed to the debate on the participation of Helicobacter species in the severe human liver disease outcomes, no explanation that justifies the presence of the bacterium in the human liver has yet been proposed.…”

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confidence: 99%

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

Silva

Rocha

et al. 2011

Mem. Inst. Oswaldo Cruz

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The hypothesis that Helicobactermight be a risk factor for human liver diseases has arisen after the detection of Helicobacter DNA in hepatic tissue of patients with hepatobiliary diseases. Nevertheless, no explanation that justifies the presence of the bacterium in the human liver has been proposed. We evaluated the presence of Helicobacterin the liver of patients with hepatic diseases of different aetiologies. We prospectively evaluated 147 patients (106 with primary hepatic diseases and 41 with hepatic metastatic tumours) and 20 liver donors as controls. Helicobacter species were investigated in the liver by culture and specific 16S rDNA nested-polymerase chain reaction followed by sequencing. Serum and hepatic levels of representative cytokines of T regulatory cell, T helper (Th)1 and Th17 cell lineages were determined using enzyme linked immunosorbent assay. The data were evaluated using logistic models. Detection of Helicobacter pylori DNA in the liver was independently associated with hepatitis B virus/hepatitis C virus, pancreatic carcinoma and a cytokine pattern characterised by high interleukin (IL)-10, low/absent interferon-γ and decreased IL-17A concentrations (p < 10-3). The bacterial DNA was never detected in the liver of patients with alcoholic cirrhosis and autoimmune hepatitis that are associated with Th1/Th17 polarisation. H. pylori may be observed in the liver of patients with certain hepatic and pancreatic diseases, but this might depend on the patient cytokine profile

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confidence: 99%

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

Silva

Rocha

et al. 2011

Mem. Inst. Oswaldo Cruz

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“…Fourth, the lack of DNA from other gut organisms in HCC tissues, suggesting that helicobacter DNA detection does not represent non-specific DNA contamination from the portal circulation [13,15]. Finally, the absence or lower frequency of helicobacter in primary versus metastatic liver carcinomas suggests a more specific association with HCC [12,14,16]. Nevertheless, this link between HCC and Helicobacter is tempered by the observations of others that Helicobacter DNA was not detected in a group of 55 liver tissues [21].…”

Section: Discussionmentioning

confidence: 99%

“…To date, the possible association between HCC and helicobacter has been supported by a number of diverse observations which can be summarized as follows. First, based on serological studies as well as direct detection in liver tissues, Helicobacter is more common in those with cirrhosis than non-cirrhosis and, of those with cirrhosis, positive serology is found more frequently in those who have HCC [9][10][11][12][13][14][15][16]19]. Secondly, helicobacter DNA in HCC tissues has been reported from multiple geographic locations.…”

Section: Discussionmentioning

confidence: 99%

“…Environmental, genetic, or clinical management methods may explain the discrepancy between our findings and those from other geographical locations. It seems unlikely that this discrepancy is entirely explained by Helicobacter pylori prevalences in the general population alone, as studies from France [9,15], Sweden [12], and the Netherlands [16] have also identified a higher frequency of Helicobacter DNA in HCC tissues, despite have an overall low Helicobacter prevalence, similar to the United States. Further study of this question may reveal important information on the biology of helicobacter infection as well as HCC.…”

Section: Discussionmentioning

confidence: 99%

“…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%

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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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Long‐term risk of gastrointestinal cancers in persons with gastric or duodenal ulcers

et al. 2016

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Peptic ulcer predicts gastric cancer. It is controversial if peptic ulcers predict other gastrointestinal cancers, potentially related to Helicobacter pylori or shared lifestyle factors. We hypothesized that gastric and duodenal ulcers may have different impact on the risk of gastrointestinal cancers. In a nationwide cohort study using Danish medical databases 1994–2013, we quantified the risk of gastric and other gastrointestinal cancers among patients with duodenal ulcers (dominantly H. pylori‐related) and gastric ulcers (dominantly lifestyle‐related) compared with the general population. We started follow‐up 1‐year after ulcer diagnosis to avoid detection bias and calculated absolute risks of cancer and standardized incidence ratios (SIRs). We identified 54,565 patients with gastric ulcers and 38,576 patients with duodenal ulcers. Patient characteristics were similar in the two cohorts. The 1–5‐year risk of any gastrointestinal cancer was slightly higher for gastric ulcers patients (2.1%) than for duodenal ulcers patients (2.0%), and SIRs were 1.38 (95% CI: 1.31–1.44) and 1.30 (95% CI: 1.23–1.37), respectively. The SIR of gastric cancer was higher among patients with gastric ulcer than duodenal ulcer (1.92 vs. 1.38), while the SIRs for other gastrointestinal cancers were similar (1.33 vs. 1.29). Compared with gastric ulcer patients, duodenal ulcer patients were at lower risk of smoking‐ and alcohol‐related gastrointestinal cancers. The risk of nongastric gastrointestinal cancers is increased both for patients with gastric ulcers and with duodenal ulcers, but absolute risks are low. H. pylori may be less important for the development of nongastric gastrointestinal cancer than hypothesized.

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Detection of identical Helicobacter DNA in the stomach and in the non-cirrhotic liver of patients with hepatocellular carcinoma

Abstract: These data suggest that gastric colonization with a specific subset of Helicobacter strains is associated with the induction of HCC, either directly via colonization of the liver or indirectly, e.g. via secretion of specific toxins by Helicobacter residing in the stomach.

Cited by 45 publications

References 20 publications

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

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

Long‐term risk of gastrointestinal cancers in persons with gastric or duodenal ulcers

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