Correspondence

Clinical Course of Acute Gastric Mucosal Lesions Caused by Acute Infection with Helicobacter pylori

N Engl J Med 1999; 341:456-457August 5, 1999

Article

To the Editor:

The clinical course of acute Helicobacter pylori infection in adults is not well known. Information on the clinical features and natural course of acute H. pylori infection is available from only a few voluntary-ingestion studies and scattered reports of postendoscopic acute gastric mucosal lesions caused by cross-infection. We report on the clinical course of postendoscopic acute gastric mucosal lesions caused by acute infection with H. pylori.

Five adults (ranging in age from 27 to 61 years) without previous gastroduodenal disease underwent endoscopic screening for gastric disease at another hospital and were found to be endoscopically normal. After five or six days, epigastric pain and nausea developed in all five. Repeated endoscopy at our hospital showed the presence of acute gastric mucosal lesions (mainly in the antrum) in all five patients. Mucosal-biopsy specimens were obtained from the gastric antrum and body for histologic examination, culture, and the rapid urease test. In all five cases, H. pylori was detected by culture and Giemsa staining, although the rapid urease test was negative. Since serum tests for anti–H. pylori IgG antibody were initially negative in all five cases, they were diagnosed as acute gastric mucosal lesions caused by acute H. pylori infection. All isolated strains possessed the CAGA gene, which is known to be an important factor in the development of severe damage to the gastric mucosa.

Three of the patients did not receive antimicrobial therapy, and their lesions healed within 14 days. In two of these three patients, H. pylori was not detected on repeated histologic examination and culture. In the other patient, a few H. pylori organisms were detected histologically. Severe gastritis developed in this patient after three months, without any trigger.

Marshall et al. reported on the initial oral-ingestion study of H. pylori infection.1 Acute, histologically confirmed gastritis developed, and the organism was eradicated without any specific therapy. Miyaji et al. reported a case of acute gastric mucosal lesions caused by endoscopic cross-infection, in which H. pylori was eliminated spontaneously.2 Several other studies of postendoscopic acute gastric mucosal lesions have had the same results. These studies suggest that host immunity can often eliminate the organism. However, Morris and Nicholson described a volunteer who ingested H. pylori and had chronic infection.3 These findings suggest that differences in the mode of acute infection do not influence susceptibility or resistance of the host to chronic infection. Boren et al. reported that the Lewis blood-group antigen Le^b is implicated in the attachment of H. pylori to the gastric mucosa and that the availability of the fucosylated receptor is reduced in persons with blood groups A and B.4 The patient with relapsing acute gastric mucosal lesions had blood group O and Le^b. These data suggest that host genetic factors influence the establishment of chronic infection.

Tetsuya Moriai, M.D., Ph.D.
Nobustune Hirahara, M.D.
Megumino Hospital, Hokkaido 061-1395, Japan

4 References

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   Miyaji H, Kohli Y, Azuma T, et al. Endoscopic cross-infection with Helicobacter pylori. Lancet 1995;345:464-464
   Web of Science | Medline

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   Morris A, Nicholson G. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol 1987;82:192-199
   Web of Science | Medline

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   Boren T, Falk P, Roth KA, Larson G, Normark S. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science 1993;262:1892-1895
   CrossRef | Web of Science | Medline

Citing Articles (5)

Citing Articles

1. 1

   Hiroyuki Hashimoto, Akiko Seno, Akiko Ishizaki, Shuichi Terasaki, Tatsuya Kimoto. (2008) Superior mesenteric artery syndrome resulting from acute massive gastric dilatation caused by Helicobacter pylori-induced acute antral gastritis. Clinical Journal of Gastroenterology 1:4, 153-156
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2. 2

   Zhannat Z. Nugalieva, Antone R. Opekun, David Y. Graham. (2006) Problem of Distinguishing False-Positive Tests from Acute or Transient Helicobacter pylori Infections. Helicobacter 11:2, 69-74
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3. 3

   David Y Graham. (2000) Community acquired acute Helicobacter pylori gastritis. Journal of Gastroenterology and Hepatology 15:12, 1353-1355
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4. 4

   Antone R. Opekun, Mark A. Gilger, Susan M. Denyes, Milton H. Nirken, Soman P. Philip, Michael S. Osato, Hoda M. Malaty, John Hicks, David Y. Graham. (2000) Helicobacter pylori Infection in Children of Texas. Journal of Pediatric Gastroenterology and Nutrition 31:4, 405-410
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5. 5

   Jagannatha V. Mysore, Thomas Wigginton, Paul M. Simon, David Zopf, Lillie M. Heman-Ackah, Andre Dubois. (1999) Treatment of Helicobacter pylori infection in rhesus monkeys using a novel antiadhesion compound. Gastroenterology 117:6, 1316-1325
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