Epidemiology ofHelicobacter PyloriInfection, Peptic Ulcer Disease and Gastric Cancer

2014 ◽  
pp. 135-157
Author(s):  
Grigorios I. Leontiadis ◽  
Olof Nyrén
2021 ◽  
Author(s):  
Aaron Oh ◽  
Han Truong ◽  
Judith Kim ◽  
Sheila D. Rustgi ◽  
Julian A. Abrams ◽  
...  

Abstract Background: Helicobacter pylori is a major risk factor for gastric cancer. Screening and treatment of H. pylori may reduce the risk of gastric cancer and peptic ulcer disease. Polymerase chain reaction (PCR) of gastric biopsies provides superior sensitivity and specificity for the detection of H. pylori. This study explores whether population-based H. pylori screening with PCR is cost-effective in the US.Methods: A Markov cohort state-transition model was developed to compare three strategies: no screening with opportunistic eradication, 13C-UBT population screening and treating of H. pylori, and PCR population screening and treating of H. pylori. Estimates of risks and costs were obtained from published literature. Since the efficacy of H. pylori therapy in gastric cancer prevention is not certain, we broadly varied the benefit 30-100% in sensitivity analysis.Results: PCR screening was cost-effective and had an incremental-cost effectiveness ratio per quality adjusted life-year (QALY) of $38,591.89 when compared to 13C-UBT strategy with an ICER of $2373.43 per QALY. When compared to no screening, PCR population screening reduced cumulative gastric cancer incidence from 0.84% to 0.74% and reduced peptic ulcer disease risk from 14.8% to 6.0%. The cost-effectiveness of PCR screening was robust to most parameters in the model.Conclusion: Our modeling study finds PCR screening and treating of H. pylori to be cost-effective in the prevention of gastric cancer and peptic ulcer disease. However, the potential negative consequences of H. pylori eradication such as antibiotic resistance could change the balance of benefits of population screening.


2008 ◽  
Vol 43 (6) ◽  
pp. 669-674 ◽  
Author(s):  
Ashish Saxena ◽  
Kashi Nath Prasad ◽  
Uday Chand Ghoshal ◽  
Narendra Krishnani ◽  
Monty Roshan Bhagat ◽  
...  

2005 ◽  
Vol 100 (5) ◽  
pp. 1037-1042 ◽  
Author(s):  
Susumu Take ◽  
Motowo Mizuno ◽  
Kuniharu Ishiki ◽  
Yasuhiro Nagahara ◽  
Tomowo Yoshida ◽  
...  

Ulcers ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-23 ◽  
Author(s):  
Bianca Bauer ◽  
Thomas F. Meyer

With the momentous discovery in the 1980's that a bacterium, Helicobacter pylori, can cause peptic ulcer disease and gastric cancer, antibiotic therapies and prophylactic measures have been successful, only in part, in reducing the global burden of these diseases. To date, ~700,000 deaths worldwide are still attributable annually to gastric cancer alone. Here, we review H. pylori's contribution to the epidemiology and histopathology of both gastric cancer and peptic ulcer disease. Furthermore, we examine the host-pathogen relationship and H. pylori biology in context of these diseases, focusing on strain differences, virulence factors (CagA and VacA), immune activation and the challenges posed by resistance to existing therapies. We consider also the important role of host-genetic variants, for example, in inflammatory response genes, in determining infection outcome and the role of H. pylori in other pathologies—some accepted, for example, MALT lymphoma, and others more controversial, for example, idiopathic thrombocytic purpura. More recently, intriguing suggestions that H. pylori has protective effects in GERD and autoimmune diseases, such as asthma, have gained momentum. Therefore, we consider the basis for these suggestions and discuss the potential impact for future therapeutic rationales.


2013 ◽  
Vol 68 (2) ◽  
pp. 39-43 ◽  
Author(s):  
Thomas G. Blanchard ◽  
Steven J. Czinn ◽  
Pelayo Correa ◽  
Teruko Nakazawa ◽  
Monika Keelan ◽  
...  

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