<i>Helicobacter pylori</i> and pathogenesis of gallbladder cancer

Mishra, Ritusha; Tewari, Mallika; Shukla, H. S.

doi:10.1111/j.1440-1746.2010.06435.x

Cited by 36 publications

(37 citation statements)

References 43 publications

(57 reference statements)

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“…The accuracy of the 26KDa primer is 9.3 % compared to that of 11.6 % using the Ure A gene on the same samples. Mishra and others [2] recently reported that 42.5 % of gallbladder carcinoma tissues were positive for the HSP60 gene. Bansal et al [12] based the PCR on the UreA gene of H. pylori.…”

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confidence: 94%

“…BostanoAylu et al [1] could not culture Helicobacter in any of their 47 patients with gallstone disease and 30 controls. However, Mishra et al [2] recently demonstrated positive culture in 30 % patients of gallstone disease and 44 % gallbladder cancer specimens.…”

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confidence: 99%

“…Indirect evidence of H. pylori in gallbladder by demonstration of DNA of different components of bacillus is found in 7 % to 61.5 % tissue examined [2][3][4][5][6][7][8][9][10].…”

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confidence: 99%

“…Demonstration of Helicobacter in gallbladder tissue histology varies 40 from 0 % to 28 % [1][2][3][4][5][6]. BostanoAylu et al [1] could not culture Helicobacter in any of their 47 patients with gallstone disease and 30 controls.…”

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confidence: 99%

“…Antibodies to Helicobacter have been reported in 18 % to 80 % of patients with gallstone disease [2,[11][12][13], 32 % to 38.8 % of cancer gallbladder [2,11] and 13.1 % to 47.5 % of controls [11,13]. However, serology is not specific for Helicobacter infection of the gallbladder.…”

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confidence: 99%

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Discovery of Helicobacter pylori in gallbladder

Shukla

Tewari

2012

Indian J Gastroenterol

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Helicobacter pylori, a gramnegative and microaerophilic organism, is transmitted from person-to-person through the feco-oral route and colonizes the stomach. The organism persists in the healthy host in equilibrium, which is disturbed at times, leading to formation of peptic ulcer and gastric cancer. Presence of H. pylori in the biliary tree of a small proportion of individuals has led to the conjecture that it is a potential cause of gallbladder disease. The exact pathway of how the organism reaches the gallbladder is unclear. It could reach the gallbladder directly from the stomach or through the portal blood circulation. In contrast to the stomach, colonization of the gallbladder is unlikely due to the alkaline pH of bile, H. pylori being known to thrive at the low pH of gastric juice.There are several tests to confirm presence of H. pylori in the stomach. These include rapid urease test, and demonstration of the bacterium on histology and culture of gastric biopsy, and positive urea breath ( 13 C or 14 C) test. Molecular tests identify the genes of H. pylori in the tissue. Immunological evidence of H. pylori infection is provided by presence of H. pylori-specific IgG and IgM antibodies in the blood. Similar tests can be used to demonstrate H. pylori in gallbladder and bile.Demonstration of H. pylori in gallbladder has been attempted directly by culture of gallbladder, bile or gallbladder mucosal scrappings or demonstration of the bacillus on histology of gallbladder. Indirect evidence of H. pylori in gallbladder by demonstration of DNA of different components of bacillus is found in 7 % to 61.5 % tissue examined [2][3][4][5][6][7][8][9][10].Evidence of immunological response to Helicobacter is often positive in patients with gallbladder disease. Antibodies to Helicobacter have been reported in 18 % to 80 % of patients with gallstone disease [2,[11][12][13], 32 % to 38.8 % of cancer gallbladder [2, 11] and 13.1 % to 47.5 % of controls [11,13]. However, serology is not specific for Helicobacter infection of the gallbladder. It is a systemic effect of Helicobacter infection anywhere in the body.In this issue of the Journal, Bansal et al.[12] demonstrate the presence of H. pylori DNA in 32.6 % of 49 gallbladders surgically removed for benign biliary disease. None of these gallbladders showed H. pylori organisms on histology, even when special stains were used. DNA detection by PCR is very sensitive. Helicobacter genus (total 32 species) in general and H. pylori specifically are detected by an array of PCR tests using 26KDA, HSP60, Flagellin gene and other primers with varying sensitivities. The accuracy of the 26KDa primer is 9.3 % compared to that of 11.6 % using the Ure A gene on the same samples. Mishra and others [2] recently reported that 42.5 % of gallbladder carcinoma tissues were positive for the HSP60 gene. Bansal et al. [12] based the PCR on the UreA gene of H. pylori. However, it has been shown that this gene shares homology

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confidence: 94%

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confidence: 99%

“…Indirect evidence of H. pylori in gallbladder by demonstration of DNA of different components of bacillus is found in 7 % to 61.5 % tissue examined [2][3][4][5][6][7][8][9][10].…”

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Discovery of Helicobacter pylori in gallbladder

Shukla

Tewari

2012

Indian J Gastroenterol

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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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Cholangiocyte derived carcinomas and local microbiota

Arteta

Milanes‐Yearsley

Cardona‐Castro

2020

J Hepato Biliary Pancreat

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Trillions of bacteria are present in the gastrointestinal tract as part of the local microbiota. Bacteria have been associated with a wide range of gastrointestinal diseases including malignant neoplasms. The association of bacteria in gastrointestinal and biliary tract carcinogenesis is supported in the paradigm of Helicobacter pylori and intestinal‐type gastric cancer. However, the association of bacterial species to a specific carcinoma, different from intestinal‐type gastric cancer is unresolved. The relationship of bacteria to a specific malignant neoplasm can drive clinical interventions. We review the classic bacteria risk factors identified using cultures and PCR (polymerase chain reaction) with new research regarding a microbiota approach through 16S rRNA (16S ribosomal ribonucleic acid gene) or metagenomic analysis for selected carcinomas in the biliary tract.

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Helicobacter pylori and pathogenesis of gallbladder cancer

Abstract: The results revealed that H. pylori was present in a large population, including both GBC and GSD patients, which indicates its endemic presence in the Varanasi region. Thus, it appears H. pylori might not have a significant role in the etiopathogenesis of GBC in our region.

Cited by 36 publications

References 43 publications

Discovery of Helicobacter pylori in gallbladder

Discovery of Helicobacter pylori in gallbladder

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

Cholangiocyte derived carcinomas and local microbiota

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