484 Paradoxical Effects of H. pylori Infection on Low-Dose Aspirin Induced Gastropathy Depending on the Gastric Acid Secretion Level

2012 ◽  
Vol 142 (5) ◽  
pp. S-103 ◽  
Author(s):  
Katsunori Iijima ◽  
Nobuyuki Ara ◽  
Yasuhiko Abe ◽  
Tomoyuki Koike ◽  
Toshimitsu Iwabuchi ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Low Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Paradoxical Effects ◽  
H Pylori

Biphasic effects of H. pylori infection on low-dose aspirin-induced gastropathy depending on the gastric acid secretion level

2012 ◽  
Vol 47 (12) ◽  
pp. 1290-1297 ◽  
Author(s):  
Katsunori Iijima ◽  
Nobuyuki Ara ◽  
Yasuhiko Abe ◽  
Tomoyuki Koike ◽  
Toshimitsu Iwabuchi ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Low Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
H Pylori

T1958 Recurrent Ulcer Bleeding with Use of Low-Dose Aspirin After Eradication of H. pylori: An 8-Year Prospective Cohort Study

2009 ◽  
Vol 136 (5) ◽  
pp. A-609
Author(s):  
Francis K.L. Chan ◽  
Jessica Ching ◽  
Bing Yee Suen ◽  
Justin Wu ◽  
Vincent W. Wong ◽  
...  
Keyword(s):  
Cohort Study ◽  
Prospective Cohort Study ◽  
Prospective Cohort ◽  
Low Dose ◽  
Ulcer Bleeding ◽  
Recurrent Ulcer ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
H Pylori

Study of Incidence of Gastric Cancer After H. pylori Eradication in Patients With Long-Term Administration of Low-Dose Aspirin

2018 ◽  
Vol 113 (Supplement) ◽  
pp. S1595
Author(s):  
Koji Takahashi ◽  
Takashi Kawai ◽  
Yuki Aoki ◽  
Akihiko Sugimoto ◽  
Shinʼichi Takahashi
Keyword(s):  
Gastric Cancer ◽  
Low Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Term Administration ◽  
H Pylori

Alteration of correlation between serum pepsinogen concentrations and gastric acid secretion after H. pylori eradication

2009 ◽  
Vol 44 (8) ◽  
pp. 819-825 ◽  
Author(s):  
Katsunori Iijima ◽  
Tomoyuki Koike ◽  
Yasuhiko Abe ◽  
Nobuyuki Ara ◽  
Kaname Uno ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Serum Pepsinogen ◽  
H Pylori

The Role of Gastric Acid in Preventing Foodborne Disease and How Bacteria Overcome Acid Conditions†

2003 ◽  
Vol 66 (7) ◽  
pp. 1292-1303 ◽  
Author(s):  
JAMES L. SMITH
Keyword(s):  
Peptic Ulcer ◽  
Acid Secretion ◽  
Peptic Ulcer Disease ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Fluid ◽  
The Body ◽  
Peptic Ulcers ◽  
Ulcer Disease ◽  
H Pylori

The secretion of hydrochloric acid by the stomach plays an important role in protecting the body against pathogens ingested with food or water. A gastric fluid pH of 1 to 2 is deleterious to many microbial pathogens; however, the neutralization of gastric acid by antacids or the inhibition of acid secretion by various drugs may increase the risk of food- or waterborne illnesses. Peptic ulcer disease is often treated by decreasing or eliminating gastric acid secretion, and such treatment blocks the protective antibacterial action of gastric fluid. The majority of peptic ulcer disease cases originate from Helicobacter pylori infections. Treatment of H. pylori–induced peptic ulcers with antibiotics reduces the need for drugs that inhibit gastric acid secretion and thereby diminishes the risk of food- and waterborne illness for peptic ulcer disease patients. Many bacterial pathogens, such as Escherichia coli, Salmonella Typhimurium, and H. pylori, can circumvent the acid conditions of the stomach by developing adaptive mechanisms that allow these bacteria to survive in acid environments. As a consequence, these bacteria can survive acidic stomach conditions and pass into the intestinal tract, where they can induce gastroenteritis.

scholarly journals Helicobacter pylori infection potentiates the inhibition of gastric acid secretion by omeprazole

Gut ◽  
1999 ◽  
Vol 44 (4) ◽  
pp. 468-475 ◽  
Author(s):  
D Gillen ◽  
A A Wirz ◽  
W D Neithercut ◽  
J E S Ardill ◽  
K E L McColl
Keyword(s):  
Helicobacter Pylori ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Intragastric Ph ◽  
Ammonia Production ◽  
Intragastric Acid ◽  
H Pylori

BACKGROUNDOmeprazole has a greater intragastric pH elevating effect in Helicobacter pylori positive than negative subjects. Ammonia production byH pylori has been suggested as a probable mechanism.AIMSTo assess the effect ofH pylori status on gastric acid secretion during omeprazole treatment, and to examine the possible role of ammonia neutralisation of intragastric acid in increased omeprazole efficacy in infected subjects.METHODSTwentyH pylori positive and 12H pylori negative healthy volunteers were examined before and six to eight weeks after commencing omeprazole 40 mg/day. On both occasions plasma gastrin and acid output were measured basally and in response to increasing doses of gastrin 17 (G-17). Gastric juice ammonium concentrations were also measured.RESULTSPrior to omeprazole, measurements were similar in the H pyloripositive and negative subjects. During omeprazole, median basal intragastric pH was higher in the H pyloripositive (7.95) versus negative (3.75) subjects (p<0.002). During omeprazole basal, submaximal (180 pmol/kg/h G-17), and maximal acid outputs (800 pmol/kg/h G-17) were lower in H pylori positive subjects (0.0, 3.6, 6.0 mmol/h respectively) versus negative subjects (0.3, 14.2, 18.6 mmol/h) (p<0.03 for each). This effect was not explained by neutralisation by ammonia.CONCLUSIONThe presence ofH pylori infection leads to a more profound suppression of acid secretion during omeprazole treatment. The effect cannot be explained by neutralisation of intragastric acid by bacterial ammonia production and its precise mechanism has to be explained.

scholarly journals AGT A-20C (rs5050) gene polymorphism and ulcer occurrence in patients treated with low-dose aspirin: a case-control study / Polimorfismul AGT A-20C și ulcerele gastro-duodenale la pacienții sub tratament cu aspirină în doze antiagregante: studiu caz-control

2015 ◽  
Vol 23 (2) ◽  
Author(s):  
Anca Negovan ◽  
Septimiu Voidăzan ◽  
Monica Pantea ◽  
Valeriu Moldovan ◽  
Simona Bataga ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Gene Polymorphism ◽  
Low Dose ◽  
Dose Aspirin ◽  
Concurrent Use ◽  
Increased Risk ◽  
Low Dose Aspirin ◽  
Gastrointestinal Side Effects ◽  
H Pylori ◽  
Bleeding Ulcers

AbstractGenetic factors may play a role in prediction of gastrointestinal side effects of aspirin, one of the most used drugs worldwide. We aim to determine a possible correlation between AGT A-20C (rs5050) gene polymorphism and gastro-duodenal ulcer in patients taking low-dose aspirin, adjusted for clinical and histological characteristics.Results. We enrolled 211 patients stratified according to AGT A-20C genotype: 122 AA, 83 AC and 6 CC patients. There were no significant differences regarding demographical and clinical parameters, except for the frequency of ulcers (4%, 8.4% respective 50%, p=0.03), endoscopic bleeding signs (12.3%, 14.5% respective 50%, p=0.0001) and the frequency of gastritis in biopsy (63.9%, 54.2% respective 16.7%, p=0.03) in genotype groups. When we compared ulcer and non-ulcer group, variant homozygous CC genotype carried an increased risk for ulcer (OR:9.66, 95% CI: 1.46-63.7, p=0.04) than AA group, as well as variant C allele compared with normal A allele (OR: 2.12, 95% CI: 1.07-4.63, p=0.04). On multivariate analysis, variant homozygous CC genotype AGT A-20C showed an OR: 12.32 (95% CI:1.40 -108.13, p=0.02) for ulcer, while H. pylori infection (OR:2.40, 95% CI:1.18 -6.54, p=0.04) and concurrent use of non-steroidal anti-inflammatory drugs (NSAIDs) (OR:1.31, 95% CI:1.07 - 2.27, p=0.05) remained predictors for ulcer in aspirin consumers.Conclusions. Variant C allele and variant homozygous CC genotype AGT A-20C, infection with H. pylori and NSAIDs co-treatment are risk factors for gastro-duodenal ulcer in low-dose aspirin consumers. The variant homozygous CC genotype AGT A-20C patients treated with LDA are more prone to have reactive gastropathy and bleeding ulcers in a population with a high prevalence of H. pylori infection

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