The Rediscovery of H. pylori Bacteria in the Gastric Mucosa by Robin Warren, and Implications of this Finding for Human Biology and Disease

Moss, Steven F.

doi:10.1007/s10620-013-2863-y

Cited by 8 publications

(5 citation statements)

References 35 publications

(36 reference statements)

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“…10 Nobel Prize was awarded to the researchers in 2005 who isolated this bacterium and confirmed its association with gastric disorders. 11 This infection usually occurs in childhood and the risk of complications increase with the duration of infection. 12 A timely and accurate diagnosis can significantly reduce the morbidity and mortality associated with this infection and improves the quality of life of the people.…”

Section: Discussionmentioning

confidence: 99%

“…Although the gold standard test for diagnosis of H. pylori infection is the histopathological examination of gastric biopsy, yet it is performed in special situations like severe vomiting, epigastric pain, unexplained weight loss and anemia, inability to eradicate H.pylori infection despite treatment, patients above 45 years and in patients with a family history of gastric cancer. 11 Non-invasive tests like HPSA test and Urea breath test (UBT) are commonly used for detection and treatment purposes, patients with mild dyspeptic symptoms or any risk factors and patients with age less than 45 years. Several studies have been performed previously correlating results of HPSA with histological diagnosis which showed comparable results.…”

Section: Discussionmentioning

confidence: 99%

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Comparison of Stool Antigen Test with Histopathology of Endoscopic Gastric Biopsies for Detection for Helicobacter Pylori; A Hospital-Based Study

Zubair

Nawaid

Afridi

et al. 2022

PAFMJ

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Objective: The objective of this study is to evaluate the diagnostic accuracy of H. pylori Stool Antigen (HpSA) test keeping histopathology as gold standard. Study Design: This is a cross sectional observational study. Place and Duration: This study was performed from Jan 2015 to Mar 2020 at Najran Armed Forces Hospital, kingdom of Saudi Arabia. Methodology: Total 151 patients in whom HpSA was done were included in the study. They were followed for their results of histopathology on gastric biopsies. Results: Among 151 patients 85(56.3%) were females and 66 (43.7%) were males. Mean age was 40 years. Forty three (28.5%) patients were positive for both HpSA and on histology, Fifteen (9.9%) patients were positive on HpSA test but negative on histology. Twenty two (14.6%) patients were negative on HpSA but they were positive on histology. Seventy one (47%) patients were negative both on HpSA and histology. The sensitivity and specificity were 66.1% and 82.5% respectively. Positive predictive value (PPV) was 74.1% and negative predictive value (NPV) was 76.3% for HpSA. Diagnostic accuracy for this test was 75.5%. Conclusion: Keeping in view the low sensitivity and diagnostic accuracy HpSA test cannot be used as screening tool in all patients, however it can be used for clinical correlation in setups where other diagnostic tests are not available due to the simplicity of its use, low cost and easy repeatability

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Comparison of Stool Antigen Test with Histopathology of Endoscopic Gastric Biopsies for Detection for Helicobacter Pylori; A Hospital-Based Study

Zubair

Nawaid

Afridi

et al. 2022

PAFMJ

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“…He then recruited Marshall, a medical resident looking for a research project, to correlate the pathologic findings with the endoscopic features. 10 Together, they discovered that these bacteria (initially termed Campylobacter pyloridis , then C pylori , and, subsequently, H pylori ) were very common in peptic ulcer patients. Eventually, they successfully cultured these formerly elusive bacteria and showed that they caused gastritis and ulcer disease.…”

Section: The Inflammatory Origins Of Gastric Cancermentioning

confidence: 99%

The Clinical Evidence Linking Helicobacter pylori to Gastric Cancer

Moss

2017

Cellular and Molecular Gastroenterology and Hepatology

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Gastric cancer has long been recognized to be accompanied and preceded by chronic gastritis, lasting decades. Arguably, the most important development in our understanding of gastric cancer pathogenesis over the past 50 years has been the realization that, for most cases of gastric cancer, Helicobacter pylori is the cause of the underlying gastritis. Gastritis can promote gastric carcinogenesis, typically via the Correa cascade of atrophic gastritis, intestinal metaplasia, and dysplasia. Nested case-control studies have shown that H pylori infection increases the risk of gastric cancer significantly, both of the intestinal and diffuse subtypes, and that H pylori is responsible for approximately 90% of the world’s burden of noncardia gastric cancer. Based largely on randomized studies in high gastric cancer prevalence regions in East Asia, it appears that primary and tertiary intervention to eradicate H pylori can halve the risk of gastric cancer. Some public health authorities now are starting screening and treatment programs to reduce the burden of gastric cancer in these high-risk areas. However, there is currently much less enthusiasm for initiating similar attempts in the United States. This is partially because gastric cancer is a relatively less frequent cause of cancer in the United States, and in addition there are concerns about theoretical downsides of H pylori eradication, principally because of the consistent inverse relationship noted between H pylori and esophageal adenocarcinoma. Nevertheless, establishing a link between chronic H pylori infection and gastric cancer has led to novel insights into cancer biology, the gastrointestinal microbiome, and on individual and population-based gastric cancer prevention strategies.

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“…Nevertheless, there is still controversy as to whether the bacterium is a pathogen or a commensal [52], hence the concept of test and treat is not universally accepted [53]. The relationship of Hp infection to PUD and to gastric cancer created a paradigm shift in treatment of PUD [54], suggesting strongly that prophylactic eradication is justified. It is universally accepted that eradication is needed for symptomatic disease.…”

Section: Helicobacter Pylorimentioning

confidence: 99%