Cimetidine Is Unlikely to Increase Formation of Intragastric N-Nitroso-Compounds in Patients Taking a Normal Diet

Muscroft, T. J.; Burdon, D. W.; Youngs, Denise; Keighley, MichaelR.B.

doi:10.1016/s0140-6736(81)91791-8

Cited by 45 publications

(10 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Patients acterial flora of the were treated with omeprazole for short periods, .ated with omepra-and few reported side effects; however, the c intubation of the development of clinically significant manifestarial overgrowth in tions of bacterial overgrowth syndromes treated with 20-40 depends on the presence of anaerobic bacteria in Lr to eight weeks, a the upper small intestine over prolonged applied in everyday periods.34 Anaerobic colonisation can be associated with the development of vitamin B12 ie stomach and the deficiency and malabsorption syndromes with Is on the degree of steatorrhea,34 and recently, omeprazole has been id secretion. '891 [12][13][14][15][16][17][18][19] shown to decrease cobalamine absorption.33 The acid secretionfor risk of bacterial overgrowth syndromes during I antral resectiontreatment with omeprazole should therefore be nal'9 bacterial over-evaluated in prospective controlled studies sabove 4-0. Recent especially in risk patients with long term prazole diminishes omeprazole treatment.…”

Section: Discussionmentioning

confidence: 99%

Duodenal bacterial overgrowth during treatment in outpatients with omeprazole.

Fried

Siegrist

Frei

et al. 1994

Gut

179

106

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Duodenal bacterial overgrowth during treatment in outpatients with omeprazole.

Fried

Siegrist

Frei

et al. 1994

Gut

179

106

View full text Add to dashboard Cite

show abstract

“…Elder et al [40] proposed that cimetidine is converted to its nitroso analog which structurally resembles other known gastric carcinogens, but Muscroft et al [41] contended that cimetidine is unlikely to cause gastric cancer, as a result of their finding low concentrations of gastric juice nitrite in patients taking the drug.…”

Section: Frequencies Of Duodenal Ulcer and Gastric Cancermentioning

confidence: 99%

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

View full text Add to dashboard Cite

The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1-1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.

show abstract

“…One paper (16) on peptic ulcer patients reported an increase in enterococci and nitrate-reducing organisms (among others) in gastric aspirates; however, there was no attempt to standardize specimens as to relation to food intake, a factor known to influence gastric flora (2). The other two reports (14,15) were both from the same investigators. One (15) found no increase in gastric bacterial titers in six volunteers in either the fasting or postprandial state; the other (14) reported a marked increase in bacterial titers in fasting gastric aspirates from patients receiving cimetidine (the postprandial state was not studied).…”

mentioning

confidence: 99%

“…The other two reports (14,15) were both from the same investigators. One (15) found no increase in gastric bacterial titers in six volunteers in either the fasting or postprandial state; the other (14) reported a marked increase in bacterial titers in fasting gastric aspirates from patients receiving cimetidine (the postprandial state was not studied). In all three studies (after excluding lactobacilli), enterococci were the bacteria most commonly isolated.…”

mentioning

confidence: 99%

Effect of cimetidine and antacid on gastric microbial flora

Snepar¹,

Poporad²,

Romano³

et al. 1982

Infect Immun

View full text Add to dashboard Cite

The effect of a standard regimen of cimetidine on the gastric flora of 20 male volunteers was studied in a double-blind manner and compared with the effects of a standard antacid regimen. Postprandial microbial titers in gastric aspirates were significantly higher at 4, 8, and 16 weeks of therapy in subjects taking antacids and at 4 weeks in subjects taking cimetidine when compared with their pretreatment titers. Although not significant, there was a tendency for fasting microbial titers to be higher in subjects receiving cimetidine as compared with pretreatment titers. The higher titers were primarily related to increases in survival of mouth flora (viridans streptococci and Neisseria spp.); Enterobacteriaceae and other nitratereducing organisms were unusual isolates. There was no significant difference in the total titers or types of organisms isolated when subjects taking cimetidine were compared with those taking antacid. In 1939 Garrod demonstrated the bactericidal activity of hydrochloric acid and gastric juice (6). Others have subsequently reported that the type and numbers of microbial flora present in the stomach are affected by gastric pH (3, 8, 9). Drasar et al. (3) and Giannella et al. (7) showed that, unlike normal stomachs, which contain few bacteria, stomachs of patients with hypochlorhydria or achlorhydria maintain high bacterial counts. Bacterial overgrowth in the stomach increases the risk of wound sepsis after gastric surgery (14).

show abstract

Cimetidine Is Unlikely to Increase Formation of Intragastric N-Nitroso-Compounds in Patients Taking a Normal Diet

Cited by 45 publications

References 13 publications

Duodenal bacterial overgrowth during treatment in outpatients with omeprazole.

Duodenal bacterial overgrowth during treatment in outpatients with omeprazole.

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

Effect of cimetidine and antacid on gastric microbial flora

Contact Info

Product

Resources

About