<i>Helicobacter pylori</i> infection is a protective factor for bleeding gastric ulcers but not for bleeding duodenal ulcers in NSAID users

Santolaria, Santos; Lanas, Ángel; Benito, Rafael; Pérez-Aisa, M f; Montoro, Miguel; Sainz, Ricardo Calle

doi:10.1046/j.1365-2036.1999.00631.x

Cited by 101 publications

(80 citation statements)

References 27 publications

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“…6). The presence of H. pylori and coexisting gastritis has been shown to increase (37), have no effect (38), and even decrease (39), the risk of ulcer bleeding among patients ingesting aspirin or NSAIDs. In the present study, we found that despite long-term exposure to these two risk factors in groups 4 and 5, there was no increase in gastric inflammation or mucosal destruction compared with groups 1 and 2, which were exposed to a single risk factor.…”

Section: Discussionmentioning

confidence: 99%

The Selective Cyclooxygenase-2 Inhibitor Nimesulide Prevents Helicobacter pylori -Associated Gastric Cancer Development in a Mouse Model

Nam

Hahm

et al. 2004

Clinical Cancer Research

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Purpose: Helicobacter pylori infection can lead to gastric cancer, and cyclooxygenase-2 (COX-2) is overexpressed in the stomach during H. pylori infection. Therefore, we investigated whether nonsteroidal anti-inflammatory drugs might protect against this form of cancer. Specifically, we examined the chemopreventive effect of the COX-2 inhibitor nimesulide on H. pylori-associated gastric carcinogenesis in mice.Experimental Design: C57BL/6 mice were treated with the carcinogen N-methyl-N-nitrosourea (MNU) and/or H. pylori. To determine the effect of COX-2 inhibition, nimesulide was mixed with feed pellets and administered for the duration of the experiment. All of the mice were sacrificed 50 weeks after the start of the experiment. Histopathology, immunohistochemistry, and Western blotting for COX-2, Bax and Bcl-2 were performed in stomach tissues. In vitro experiments with the human gastric cancer cell line AGS were also performed to identify mechanisms underlying cancer chemoprevention by nimesulide.Results: Gastric tumors developed in 68.8% of mice that were given both MNU and H. pylori, whereas less than 10% developed gastric tumors when given either MNU or H. pylori alone. These findings indicate that H. pylori promotes carcinogen-induced gastric tumorigenesis. In mice treated with both MNU and H. pylori, nimesulide administration substantially reduced H. pylori-associated gastric tumorigenesis, whereas substantial inductions of apoptosis were observed. In vitro studies demonstrated that nimesulide and H. pylori when combined acted synergistically to induce more apoptosis than either alone.Conclusions: Our data show that nimesulide prevents H. pylori-associated gastric carcinogenesis, and suggest that COX-2 may be a target for chemoprevention of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

The Selective Cyclooxygenase-2 Inhibitor Nimesulide Prevents Helicobacter pylori -Associated Gastric Cancer Development in a Mouse Model

Nam

Hahm

et al. 2004

Clinical Cancer Research

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“…[9][10][11][12] It has been suggested that the presence of H. pylori may confer protection against ulcer bleeding, especially gastric ulcer bleeding. [10][11][12] The most direct evidence of an interaction between H. pylori and NSAIDs comes from studies investigating the effects of H. pylori eradication on the development of ulcers in NSAID users. The eradication of H. pylori has been shown to be beneficial in patients without previous NSAID exposure and no history of ulcers.…”

Section: Discussionmentioning

confidence: 99%

“…In the intention-to-treat analysis, five patients (7.1%; 95% CI, 2-16) in the treatment group developed peptic ulcers (all gastric ulcers) at the end of 12 weeks, compared with six patients (8.6%; 95% CI, [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] in the placebo group (four gastric ulcers and two duodenal ulcers) (P ¼ 1.00). The ulcer size ranged from 5 to 12 mm.…”

Section: Development Of Gastroduodenal Ulcers and Erosionsmentioning

confidence: 99%

Effect of treatment of Helicobacter pylori on the prevention of gastroduodenal ulcers in patients receiving long‐term NSAIDs: a double‐blind, placebo‐controlled trial

Lai¹,

Lau²,

et al. 2003

Aliment Pharmacol Ther

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SUMMARYBackground: There is controversy as to whether Helicobacter pylori and non-steroidal anti-inflammatory drugs interact to cause peptic ulcers. Aim: To study whether the eradication of H. pylori in patients on long-term non-steroidal anti-inflammatory drug therapy prevents the development of ulcers. Methods: Patients infected with H. pylori whilst receiving long-term non-steroidal anti-inflammatory drug therapy, but with no ulcers at baseline endoscopy, were randomized to receive either triple antibiotic therapy (metronidazole 300 mg, clarithromycin 250 mg and amoxicillin 500 mg, given four times daily; n ¼ 70) or placebo (n ¼ 70) for 2 weeks. Non-steroidal antiinflammatory drugs were continued throughout the study period. Endoscopy was repeated 12 weeks after

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“…Of the total 142 GC patients, 32 (22.5%) were classified as cardia or gastroesophageal junction cancers and 110 (77.5%) as non-cardia or distal GC cases. According to Lauren's criteria, 55 56,57 NSAIDs use The use of NSAIDs at the time of the diagnosis of PU was determined by structured data collection. A patient was considered positive if the drug had been taken within the week before the hospital admission of the endoscopic diagnosis of DU or GU.…”

Section: Study Populationmentioning

confidence: 99%

TGFB1 gene polymorphisms: their relevance in the susceptibility to Helicobacter pylori-related diseases

et al. 2006

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Recent studies have revealed elevated expression of transforming growth factor b1 (TGF-b1) in gastric mucosa of patients with gastric cancer (GC) and those undergoing ulcer repair. As production of TGF-b1 is genetically regulated, we aimed to assess whether functional polymorphisms of the TGFB1 gene are involved in susceptibility to and clinical characteristics of Helicobacter pylori-related diseases. DNA from 142 unrelated Spanish patients with GC, 200 with peptic ulcer and 342 healthy controls was typed for the MspA1I T þ 869C, and the Sau96I G þ 915C polymorphisms of the TGFB1 gene using polymerase chain reaction and RFLP analysis. H. pylori infection and CagA/VacA antibody status were determined by Western blot in patients and controls. H. pylori infection (odds ratio (OR): 11.44; 95% confidence interval (CI): 4.45-29.42; Po0.001) and nonsteroidal anti-inflammatory drugs (OR: 5.07; 95% CI: 2.53-10.16; Po0.001) were identified as independent risks factors for duodenal ulcer (DU), whereas the TGFB1 þ 869*C/C genotype was associated with reduced risk of developing the disease (OR: 0.32; 95% CI ¼ 0.15-0.68; P ¼ 0.003). Our results show that the TGFB1 T þ 869C gene polymorphism is involved in the susceptibility to DU and provide further evidence that host genetic factors play a key role in the pathogenesis of H. pylorirelated diseases.

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Helicobacter pylori infection is a protective factor for bleeding gastric ulcers but not for bleeding duodenal ulcers in NSAID users

Abstract: Interaction of both H. pylori infection and NSAID use decreases the risk of bleeding due to gastric ulcers, but not that due to duodenal ulcers.

Cited by 101 publications

References 27 publications

The Selective Cyclooxygenase-2 Inhibitor Nimesulide Prevents Helicobacter pylori -Associated Gastric Cancer Development in a Mouse Model

The Selective Cyclooxygenase-2 Inhibitor Nimesulide Prevents Helicobacter pylori -Associated Gastric Cancer Development in a Mouse Model

Effect of treatment of Helicobacter pylori on the prevention of gastroduodenal ulcers in patients receiving long‐term NSAIDs: a double‐blind, placebo‐controlled trial

TGFB1 gene polymorphisms: their relevance in the susceptibility to Helicobacter pylori-related diseases

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