Intragastric bacterial activity and nitrosation before, during, and after treatment with omeprazole.

Sharma, Bhawna; Santana, Isabelle; Wood, Elizabeth; Walt, R P; Pereira, Marina Alessandra; Noone, Paul; Smith, Penny; Walters, C. L.; Pounder, R. E.

doi:10.1136/bmj.289.6447.717

Cited by 192 publications

(91 citation statements)

References 16 publications

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“…Our data demonstrate that suppression of gastric acid would permit the survival of germinated C. difficile cells. This finding is consistent with the results of other studies correlating reduced acidity (pH Ͼ 3) and increased bacterial growth in gastric contents from people taking PPIs (10,23,25,26). Because conditions in the stomach are not as anaerobic or reduced as in the colon, the ability of vegetative C. difficile to survive under aerobic conditions could also facilitate the survival of germinated spores in the stomach.…”

Section: Discussionsupporting

confidence: 82%

Vegetative Clostridium difficile Survives in Room Air on Moist Surfaces and in Gastric Contents with Reduced Acidity: a Potential Mechanism To Explain the Association between Proton Pump Inhibitors and C. difficile -Associated Diarrhea?

Jump

Pultz

Donskey

2007

Antimicrob Agents Chemother

210

145

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Proton pump inhibitors (PPIs) have been identified as a risk factor for Clostridium difficile-associated diarrhea (CDAD), though the mechanism is unclear because gastric acid does not kill C. difficile spores. We hypothesized that the vegetative form of C. difficile, which is killed by acid, could contribute to disease pathogenesis if it survives in room air and in gastric contents with elevated pH. We compared the numbers of C. difficile spores and vegetative cells in stools of patients prior to and during the treatment of CDAD. We assessed the survival of vegetative cells on moist or dry surfaces in room air versus anaerobic conditions and in human gastric contents, in pH-adjusted gastric contents, and in gastric contents from individuals receiving PPI therapy. Stool samples obtained from patients prior to the initiation of antibiotic treatment for C. difficile contained ϳ10-fold more vegetative cells than spores. On dry surfaces, vegetative C. difficile cells died rapidly, whereas they remained viable for up to 6 h on moist surfaces in room air. Vegetative C. difficile cells had only marginal survival in gastric contents at low pH; adjustment to a pH of >5 resulted in survival similar to that in the phosphate-buffered saline control. The survival of vegetative C. difficile in gastric contents obtained from patients receiving PPIs was also increased at a pH of >5. The ability of the vegetative form of C. difficile to survive on moist surfaces and in gastric contents with an elevated pH suggests a potential mechanism by which PPI therapy could increase the risk of acquiring C. difficile.

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Section: Discussionsupporting

confidence: 82%

Vegetative Clostridium difficile Survives in Room Air on Moist Surfaces and in Gastric Contents with Reduced Acidity: a Potential Mechanism To Explain the Association between Proton Pump Inhibitors and C. difficile -Associated Diarrhea?

Jump

Pultz

Donskey

2007

Antimicrob Agents Chemother

210

145

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“…The fact that patients with pernicious anemia, invariably associated with gastric atrophy and hypochlorhydria, have an increased risk of developing stomach cancer [52,53] has raised the question of whether therapeutic hypochlorhydria is carcinogenic to the stomach. Pharmacologically induced hypochlorhydria has been shown to be associated with increased gastric bacterial growth, reduction of nitrate to nitrite, and increased concentration of carcinogenic N-nitroso compounds in the gastric juice [54,55]. Some studies have indicated that long-term treatment with PPIs may accelerate the development of atrophic changes of the gastric mucosa in individuals infected with H. pylori [56 -58].…”

Section: Medical Therapy For Peptic Ulcer and Its Relation To Stomachmentioning

confidence: 99%

Risk of Stomach Cancer in Patients with Peptic Ulcer Disease

Hansson

2000

World j. surg.

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Abstract. The relation between peptic ulcer and stomach cancer has long been disputed, but there is accumulating evidence that gastric ulcer disease is positively associated and duodenal ulcerations negatively associated with the risk of developing stomach cancer. As Helicobacter pylori infection is associated with both types of ulceration and stomach cancer, the varying outcomes of the infection indicate that factors other than the infection must be of importance. At present, there is no convincing evidence that pharmacologic inhibition of acid secretion for treatment of peptic ulcer increases the risk of stomach cancer. However, some recent studies indicate that prolonged treatment with proton pump inhibitors may accelerate the development of atrophic gastritis, a risk factor for stomach cancer, in individuals infected with H. pylori. It has repeatedly been shown that there is an at least twofold increased risk of stomach cancer 15 years after gastric resection for peptic ulcer disease, and that the risk increases with the passage of time. Whether vagotomy has the same risk-increasing effect is still unclear.

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“…H. pylori survives in the human stomach at low pH (pH Ͻ 3) by creating an alkaline microenvironment with urease production (21). Although Acinetobacter has variable urease activity, this bacterial species has been reported previously to colonize the hypochlorhydric stomach of patients (32,39). In addition, the mouse stomach, which has a gastric acidic range of approximately 3 to 5 eq, provides an environment permissive for colonization by non-H. pylori organisms (42).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, these animals were clearly colonized with Since it has recently been shown that Toll-like receptor 9 (TLR-9) mediates a Th1 inflammatory response from bacterial DNA (10), it is highly possible that the presence of Acinetobacter DNA in the gut was sufficient to induce gastritis, but this requires further analysis. Acinetobacter has been previously isolated from the gastric contents of patients treated with proton pump inhibitors and is clinically relevant in humans (32). Both A. baumannii and A. lwoffii are known to cause nosocomial infections in ventilated patients (8).…”

Section: Discussionmentioning

confidence: 99%

Gastritis and Hypergastrinemia Due toAcinetobacter lwoffiiin Mice

Zavros

Rieder²,

Ferguson

et al. 2002

Infect Immun

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In mouse models and humans, Helicobacter pylori is associated with an increase in serum gastrin and gastrin-expressing (G) cells with a concomitant decrease in somatostatin-expressing D cells. Inflammation of the gastric mucosa can progress to metaplastic changes in the stomach and to decreased colonization by H. pylori and increased colonization by non-H. pylori organisms. In addition, about 20% of individuals with chronic gastritis are H. pylori negative, suggesting that other organisms may induce gastritis. Consistent with this hypothesis, we report here that Acinetobacter lwoffii causes the same histologic changes as does H. pylori. Gastric epithelial cells were isolated from the entire stomach by an enzymatic method for quantitation by both flow cytometry and morphometric analysis. Two months after mice were inoculated with H. pylori or A. lwoffii, the mucosal T-and B-cell numbers significantly increased. Helicobacter pylori causes chronic atrophic gastritis, and its presence is correlated with the development of peptic ulcer disease and gastric adenocarcinoma (19,25,27). However, there is also an association between colonization of the stomach by non-Helicobacter organisms and chronic atrophic gastritis (7,9,30). Approximately 25% of gastric cancer patients have no evidence of previous or current H. pylori infection based on serology (12). In addition, during long-term acid suppression, the presence of H. pylori and that of non -H. pylori bacteria are independent risk factors for the development of atrophic gastritis (29). Studies of several animal models and humans have clearly shown that bacteria are important in triggering mucosal damage and inflammation in the stomach (15,20,42). In addition, under hypochlorhydric conditions it is known that bacterial overgrowth by non-Helicobacter organisms triggers perturbations in the neuroendocrine and epithelial cell populations (42). The implications are that the pathology observed may not be specific for H. pylori but instead is the general response of the gastric mucosa to colonization by bacteria.H. pylori is characterized by its ability to survive in the low-pH milieu of the stomach by generating an alkaline microenvironment. With reduced levels of acid (hypochlorhydria or achlorhydria), the competitive niche established by H. pylori dissipates and the human stomach becomes susceptible to colonization by other organisms (9, 18). Gastric colonization by gram-negative bacteria other than H. pylori is common in intensive care unit patients, who often have an alkaline gastric pH due to routine treatment with antacids, proton pump inhibitors, and histamine 2 receptor antagonists. Antiulcer medications are known to increase the gastric pH and permit colonization of the stomach by opportunistic pathogens, such as Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas spp., believed to contribute to the development of nosocomial pneumonia (8,36). Patients with pernicious anemia are colonized by organisms other than H. pylori and develop atrophic gastritis an...

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Intragastric bacterial activity and nitrosation before, during, and after treatment with omeprazole.

Abstract: Ten healthy volunteers were studied before, during, and after treatment with omeprazole 30 mg daily for two weeks. On the 14th night mean nocturnal (2100-0700) intragastric acidity was significantly decreased by 75%

Cited by 192 publications

References 16 publications

Vegetative Clostridium difficile Survives in Room Air on Moist Surfaces and in Gastric Contents with Reduced Acidity: a Potential Mechanism To Explain the Association between Proton Pump Inhibitors and C. difficile -Associated Diarrhea?

Vegetative Clostridium difficile Survives in Room Air on Moist Surfaces and in Gastric Contents with Reduced Acidity: a Potential Mechanism To Explain the Association between Proton Pump Inhibitors and C. difficile -Associated Diarrhea?

Risk of Stomach Cancer in Patients with Peptic Ulcer Disease

Gastritis and Hypergastrinemia Due toAcinetobacter lwoffiiin Mice

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