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Helicobacter pylori, Peptic Ulcer, and Cimetidine: The authors reply

      We appreciate the comments of Kaya and colleagues; however, more information about the inoculum size used, the adequacy of the broth, the response in controls, and the use of any quantitative determination of inhibitor activity is necessary to interpret the data they cite.
      The issue remains whether Helicobacter pylori is a pathogen or a commensal. At least in the stomach, overwhelming evidence is available in support of a causative role for H. pylori in chronic gastritis, and Koch's postulates have been fulfilled.
      • Talley NJ
      Chronic (nonerosive) gastritis: pathogenesis and management.
      • Ormand JE
      • Talley NJ
      Helicobacter pylori: controversies and an approach to management.

      Ormand JE, Talley NJ, Shorter RG, Carpenter HA, Rouse M, Wilson W, Phillips SF: Prevalence of Helicobacter pylori in specific forms of gastritis. Dig Dis Sci (in press)

      The clinical significance of H. pylori gastritis, however, remains controversial; clearly, H. pylori gastritis is common in totally asymptomatic persons.
      • Dooley CP
      • Cohen H
      • Fitzgibbons PL
      • Bauer M
      • Appleman MD
      • Perez-Perez GI
      • Blaser MJ
      Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons.
      A very strong association has been noted between H. pylori gastritis and chronic duodenal ulcer disease.
      • Talley NJ
      Chronic (nonerosive) gastritis: pathogenesis and management.
      • Ormand JE
      • Talley NJ
      Helicobacter pylori: controversies and an approach to management.
      In their letter, Kaya and co-workers report that cimetidine, which effectively promotes healing of ulcers, did not have antibacterial or phagocytosispromoting effects. Other investigators have shown that the 90% minimal inhibitory concentration of the H2 antagonists is more than 1,000 mg/liter.
      • Andreasen JJ
      • Andersen LP
      In vitro susceptibility of Campylobacter pyloridis to cimetidine, sucralfate, bismuth and sixteen antibiotics.
      The lack of effect of cimetidine on phagocytic function of macrophages is of interest; although little information has been published on the role of macrophages in H. pylori gastritis, they are usually considerably increased in this condition. One study suggested that, in vitro, the speed of ingestion of H. pylori by mouse peritoneal macrophages varied with different bacterial strains, but the importance of this finding in vivo is unknown.

      Gavinet AM, Megraud F: In vitro phagocytosis of Campylobacter pylori by macrophages obtained from Biozzi's mice. Proceedings of the first meeting of the European Campylobacter pylori Study Group. Bordeaux, France, October 1988, Abstract No. 119

      Clearly, ulcers heal with H2-receptor blockers despite the continued presence of H. pylori.
      • Hui W-M
      • Lam S-K
      • Chau P-Y
      • Ho J
      • Lui I
      • Lai C-L
      • Lok AS
      • Ng M-T
      Persistence of Campylobacter pyloridis despite healing of duodenal ulcer and improvement of accompanying duodenitis and gastritis.
      This result implies that a decrease in gastric acid is sufficient to allow healing of ulcers, and H. pylori is not independently capable of inhibiting this process. This finding does not, however, negate a possibly important role of H. pylori in duodenal ulcer disease. Indeed, relapse rates for chronic duodenal ulcer disease seem to be substantially less at 1 year in those patients who have had H. pylori infection eradicated in comparison with those who have not,
      • Marshall BJ
      • Goodwin CS
      • Warren JR
      • Murray R
      • Blincow ED
      • Blackbourn SJ
      • Phillips M
      • Waters TE
      • Sanderson CR
      Prospective double-blind trial of duodenal ulcer relapse after eradication of Campylobacter pylori.
      • Coghlan JG
      • Gilligan D
      • Humphries H
      • McKenna D
      • Dooley C
      • Sweeney E
      • Keane C
      • O'Morain C
      Campylobacter pylori and recurrence of duodenal ulcers—a 12-month follow-up study.
      although further data are needed.

      REFERENCES

        • Talley NJ
        Chronic (nonerosive) gastritis: pathogenesis and management.
        Dig Dis. 1989; 7: 61-75
        • Ormand JE
        • Talley NJ
        Helicobacter pylori: controversies and an approach to management.
        Mayo Clin Proc. 1990; 65: 414-426
      1. Ormand JE, Talley NJ, Shorter RG, Carpenter HA, Rouse M, Wilson W, Phillips SF: Prevalence of Helicobacter pylori in specific forms of gastritis. Dig Dis Sci (in press)

        • Dooley CP
        • Cohen H
        • Fitzgibbons PL
        • Bauer M
        • Appleman MD
        • Perez-Perez GI
        • Blaser MJ
        Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons.
        N Engl J Med. 1989; 321: 1562-1566
        • Andreasen JJ
        • Andersen LP
        In vitro susceptibility of Campylobacter pyloridis to cimetidine, sucralfate, bismuth and sixteen antibiotics.
        Acta Pathol Microbiol Immunol Scand [B]. 1987; 95: 147-149
      2. Gavinet AM, Megraud F: In vitro phagocytosis of Campylobacter pylori by macrophages obtained from Biozzi's mice. Proceedings of the first meeting of the European Campylobacter pylori Study Group. Bordeaux, France, October 1988, Abstract No. 119

        • Hui W-M
        • Lam S-K
        • Chau P-Y
        • Ho J
        • Lui I
        • Lai C-L
        • Lok AS
        • Ng M-T
        Persistence of Campylobacter pyloridis despite healing of duodenal ulcer and improvement of accompanying duodenitis and gastritis.
        Dig Dis Sci. 1987; 32: 1255-1260
        • Marshall BJ
        • Goodwin CS
        • Warren JR
        • Murray R
        • Blincow ED
        • Blackbourn SJ
        • Phillips M
        • Waters TE
        • Sanderson CR
        Prospective double-blind trial of duodenal ulcer relapse after eradication of Campylobacter pylori.
        Lancet. 1988; 2: 1437-1442
        • Coghlan JG
        • Gilligan D
        • Humphries H
        • McKenna D
        • Dooley C
        • Sweeney E
        • Keane C
        • O'Morain C
        Campylobacter pylori and recurrence of duodenal ulcers—a 12-month follow-up study.
        Lancet. 1987; 2: 1109-1111

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      • Helicobacter pylori, Peptic Ulcer, and Cimetidine
        Mayo Clinic ProceedingsVol. 65Issue 9
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          We read with interest the article by Fich and associates in the February 1990 issue of the Proceedings (pages 187 to 191). An interesting association between Helicobacter pylori (formerly called Campylobacter pylori) and gastritis or peptic ulcer diseases has been claimed by many authors.1–6 Although we agree with Dooley and colleagues7 that H. pylori infection may be of potential importance in the asymptomatic population, suggesting that the bacterium is a commensal of the stomach, we would like to ask Fich and colleagues whether H.
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