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Z Gastroenterol 2000; 38(7): 559-564
DOI: 10.1055/s-2000-7449
Originalarbeit
© Karl Demeter Verlag im Georg Thieme Verlag

Helicobacter pylori vacA genotypes and cagA gene in a series of 383 H. pylori-positive patients

J. Rudi1 , D. Kuck1 , A. Rudy1 , A. Sieg 2 , M. Maiwald3 , W. Stremmel1
  • Medizinische Klinik IV (Abteilung für Gastroenterologie) der Ruprecht-Karls-Universität, Heidelberg
  • Praxis für Gastroenterologie, Östringen
  • Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, USA
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Publication History

6.8.1999

4.4.2000

Publication Date:
31 December 2000 (online)

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Summary

Background: Only 10-15 % of all patients infected with Helicobacter pylori develop peptic ulcer disease (PUD) or gastric cancer. Apart from immunological factors in the host, virulence determinants of H. pylori such as the vacuolating cytotoxin (VacA) or the cytotoxin-associated protein A (CagA) might represent a predisposition for the development of PUD.

Methods: We studied antral biopsies of 383 H. pylori-positive patients with peptic ulcer disease (PUD) or other H. pylori-related diseases for H. pylori vacA genotypes and the presence of the cagA gene by PCR.

Results: VacA genotypes and cagA status could be completely determined in 357 (93.2 %) of the patients. In 91 (93.8 %) of 97 patients with PUD, the vacA s1 genotype (s1m1, 45; s1m2, 46 patients) was present. The vacA s2m2 genotype was found in only 6 (6.2 %) of 97 patients with PUD. In contrast, 180 (75.3 %) of 239 patients (s1m1, 89; s1m2, 91 patients) without PUD and without gastric malignancies harbored strains with the vacA s1 genotype. The vacA genotype s2m2 was found in 59 (24.7 %) of these patients. The presence of the cagA gene was closely associated with the vacA genotype s1 and found in 124 (88.6 %) and in 113 (80.7 %) of patients with the s1m1 or s1m2 genotypes, respectively, whereas strains with the genotype s2m2 were almost exclusively cagA negative.

Conclusion: Most H. pylori strains found in patients with PUD possess the vacA s1 genotype and the cagA gene. Patients with this type of H. pylori strain but without PUD might be at higher risk of developing PUD. In contrast, the risk for PUD might be significantly decreased in those patients who are infected by H. pylori strains with the vacA s2 genotype lacking the cagA gene.

(Helicobacter-pylori-vacA-Genotypen und cagA-Gen in einer Serie von 383 H. pylori-positiven Patienten)

Hintergrund: Lediglich 10-15 % aller mit Helicobacter pylori infizierten Patienten entwickeln in der Folge ein peptisches Ulkus (PU) oder ein Magenkarzinom. Neben immunologischen Faktoren können Virulenzfaktoren von H. pylori, wie z. B. das vakuolisierende Zytotoxin (VacA) oder das Zytotoxinassozi­ierte Protein A (CagA), bei der Entwicklung eines peptischen Ulkus prädisponierend sein.

Methoden: In Antrumbiopsien von 383 H. pylori-positiven Patienten mit peptischem Ulkus (PU) oder anderen H. pylori-assoziierten Erkrankungen wurden die H. pylori-vacA-Genotypen und die Präsenz des cagA-Gens mit PCR untersucht.

Ergebnisse: Die H. pylori-vacA-Genotypen und der cagA-Status konnten bei 357 (93,2 %) Patienten vollständig bestimmt werden. Bei 91 (93,8 %) von 97 Patienten mit einem PU lagen H. pylori-Stämme mit dem vacA-Genotyp s1 (s1m1: 45; s1m2: 46 Patienten) vor. Der vacA-Genotyp s2m2 war nur bei 6 (6,2 %) von 97 Patienten mit PU vorhanden. Dagegen hatten 180 (75,3 %) von 239 Patienten ohne PU und ohne ein Magenmalignom Stämme mit dem vacA-Genotyp s1 (s1m1: 89; s1m2: 91 Patienten). Der vacA-s2m2-Genotyp wurde bei 59 (24,7 %) dieser Patienten nachgewiesen. Der Nachweis des cagA-Gens war eng mit dem vacA-s1-Genotyp assoziiert und wurde bei 124 (88,6 %) bzw. 113 (80,7 %) der Patienten mit den vacA-Genotypen s1m1 oder s1m2 gefunden, während Stämme mit dem vacA-Genotyp s2m2 fast ausschließlich cagA-negativ waren.

Schlussfolgerung: Bei nahezu allen H. pylori-positiven Pa­tienten mit peptischem Ulkus liegen H. pylori-Stämme mit dem vacA-Genotyp s1 und mit cagA-Gen vor. Patienten ohne PU mit H. pylori-Stämmen dieses Genotyps haben vermutlich ein höheres Risiko, ein peptisches Ulkus zu entwickeln. Dagegen erscheint das Risiko für ein Ulkus bei Patienten mit H. pylori-Stämmen des vacA-Genotyps s2 und ohne cagA-Gen signifikant verringert zu sein.

Key words

Helicobacter Pylori - Gastric Biopsies - Polymerase Chain Reaction - Peptic Ulcer Disease

Schlüsselwörter

Helicobacter-pylori - Magenbiopsien - Polymerasekettenreaktion - peptisches Ulkus

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Address for correspondence:

Priv.-Doz. Dr. med. Jochen Rudi

Medizinische Klinik IV (Abteilung für Gastroenterologie) Ruprecht-Karls-Universität Heidelberg

Bergheimerstraße 58

69115 Heidelberg

Email: jochen_rudi@med.uni-heidelberg.de

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