Gastroenterology

Gastroenterology

Volume 115, Issue 1, July 1998, Pages 58-66
Gastroenterology

Alimentary Tract
Clinical relevance of the cagA, vacA, and iceA status of Helicobacter pylori,☆☆

https://doi.org/10.1016/S0016-5085(98)70365-8Get rights and content

Abstract

Background & Aims: Clinical outcome of Helicobacter pylori infection may be associated with specific virulence-associated bacterial genotypes. The aim of this study was to assess the relationships between H. pylori cagA, vacA, and iceA status and severity of disease. Methods: Gastric biopsy specimens from 94 patients in The Netherlands were analyzed by polymerase chain reaction and reverse hybridization. Results: cagA was present in 63 (67%) of 94 cases and was associated with peptic ulcer disease (P = 0.0019). vacA genotypes s1a/m1, s1a/m2, s1b/m1, s1b/m2, and s2/m2 were found in 36.2%, 23.4%, 2.1%, 5.3%, and 20.2%, respectively. Ten isolates (10.6%) contained multiple vacA genotypes. The presence of peptic ulcers was associated with type s1 strains (P = 0.0006) but not with the m type (P = 0.2035). cagA and vacA s1 were strongly associated (P < 10−5). iceA1 was found in 53 (56.4%) and iceA2 in 25 (26.6%) of the 94 cases. In 14 isolates (14.9%), both iceA alleles were found, and 2 (2.1%) were negative for both iceA1 and iceA2. iceA1 was also associated with peptic ulcer disease (P = 0.0042). The iceA allelic type was independent of the cagA and vacA status. Conclusions: vacA s1, cagA, and iceA1 are markers of H. pylori strains that are more likely to lead to ulcer disease.

GASTROENTEROLOGY 1998;115:58-66

Section snippets

Patients

A total of 94 patients (57 male and 37 female; age, 53.3 ± 16.1 years; range, 22–85 years) with culture-proven H. pylori infection were recruited in a community hospital in Oss, The Netherlands, and underwent endoscopy before receiving anti-Helicobacter treatment. These patients were in need of anti-Helicobacter therapy, and because we normally do not treat all H. pylori–infected individuals, ulcer patients are relatively common in this patient group. The presence of ulcers was based on visual

Results

vacA, iceA, and cagA genotypes of H. pylori were analyzed in 94 patients living in The Netherlands. Thirty-four (36.2%) of these 94 patients had gastritis only and were classified as nonulcer cases. Sixty (63.8%) patients had proven peptic ulcer disease: 46 (48.9%) first or chronic duodenal ulcer disease, and 14 (14.9%) first or recurrent gastric ulcer. There was no significant difference between the mean age of patients with and without ulcers (52.9 ± 17.3 and 54.1 ± 14.1 years, respectively).

Discussion

The presence of H. pylori in the gastric mucosa leads to chronic gastritis and eventually atrophic gastritis and is associated with diseases such as peptic ulcers, gastric carcinoma, and MALT lymphoma.2, 23 However, there is a clear discrepancy between the number of infected individuals and patients with clinical symptoms. Although host and environmental factors are considered important,24, 25, 26 there is also evidence for a role of specific H. pylori genotypes. Infection with certain H. pylori

Acknowledgements

The authors thank Dr. G. J. J. M. Borsboom for his helpful suggestions and C. L. A. M. van Hoek for preparation of the LiPA strips.

References (51)

  • HL Mobley

    Defining Helicobacter pylori as a pathogen: strain heterogeneity and virulence

    Am J Med

    (1997)
  • JC Atherton

    The clinical relevance of strain types of Helicobacter pylori

    Gut

    (1997)
  • RD Leunk et al.

    Cytotoxic activity in broth culture filtrates of Campylobacter pylori

    J Med Microbiol

    (1988)
  • JL Telford et al.

    Gene structure of the Helicobacter pylori cytotoxin and evidence of its key role in gastric disease

    J Exp Med

    (1994)
  • TL Cover

    The vacuolating cytotoxin of Helicobacter pylori

    Mol Microbiol

    (1996)
  • LJ van Doorn et al.

    Expanding allelic diversity of Helicobacter pylori vacA

    (1998)
  • S Censini et al.

    cag, a pathogenicity island of Helicobacter pylori, encodes type I–specific and disease-associated virulence factors

    Proc Natl Acad Sci USA

    (1996)
  • MK Tummuru et al.

    Helicobacter pylori picB, a homologue of the Bordetella pertussis toxin secretion protein, is required for induction of IL-8 in gastric epithelial cells

    Mol Microbiol

    (1995)
  • T Shimoyama et al.

    Mucosal chemokines in Helicobacter pylori infection

    J Physiol Pharmacol

    (1997)
  • F. Megraud

    Pathogenic diversity of Helicobacter pylori

    J Gastroenterol

    (1997)
  • RMJ Peek et al.

    Expression of a novel ulcer-associated H. pylori gene, iceA , following adherence to gastric epithelial cells

    Gastroenterology

    (1996)
  • J Sambrook et al.

    Molecular cloning, a laboratory manual

    (1989)
  • L Stuyver et al.

    Typing of HCV isolates and characterization of new (sub)types using a line probe assay

    J Gen Virol

    (1993)
  • AC Wotherspoon

    Gastric MALT lymphoma and Helicobacter pylori

    Yale J Biol Med

    (1997)
  • DY Graham et al.

    Are there susceptible hosts to Helicobacter pylori infection?

    Scand J Gastroenterol Suppl

    (1994)
  • Cited by (0)

    Address requests for reprints to: Leen-Jan van Doorn, Ph.D., Delft Diagnostic Laboratory, R. de Graafweg 7, 2625 AD, Delft, The Netherlands. e-mail: [email protected]; fax: (31) 15-2604550.

    ☆☆

    Supported by PRAXIS XXI (to C.F.).

    View full text