The effect of CagA status on response to helicobacter pylori eradication therapy Helicobacter pylori eradikasyonunda sus farkliligi basariyi etkileyen bir faktor mudur?


Saruc M. , Goksel G., Ozkaya S., Guclu F., Ozbakkaloglu B., Yuceyar H.

Turkish Journal of Gastroenterology, vol.11, no.2, pp.146-149, 2000 (Journal Indexed in SCI Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 11 Issue: 2
  • Publication Date: 2000
  • Title of Journal : Turkish Journal of Gastroenterology
  • Page Numbers: pp.146-149

Abstract

Background/aims: Despite a multitude of clinical trials during recent years, no one therapeutic regimen has clearly emerged as the optimal treatment for H. pylori infection. If CagA status affects the response rates of therapy, then it may be possible to predict eradication rates and choose appropriate regimens for each patient according to H. pylori strain either CagA positive or negative. We aimed to evaluate the response to eradication treatment of H. pylori infection in CagA positive and CagA negative patients. Methods: One hundred and eighty four patients (93 male, 91 female, mean age: 42.6±12.8 years) with chronic gastritis were included in the study all of whom had H. pylori infection. H. pylori positivity was determined by rapid urease test, serology and histological examination. Subjects underwent an upper gastrointestinal endoscopy and biopsy specimens were taken from the gastric antrum, body and fundus. Prior to commencement of eradication therapy, all patients were tested for CagA, TNF-a and gastrin levels. They were then prescribed lansoprazole (30 mg bid), clarithromycin (500 mg bid), and amoxycillin (1 g bid) for a week. On the eighth week, a second endoscopy was performed and further biopsy specimens were obtained from the same sites as initial endoscopy. Results: One hundred and twentyseven patients (69%) were found to have CagA positivity and 57 patients (30.9%) were CagA negative. The total eradication rate was 84.7%. In the CagA positive group, this rate was 87.4% and in the CagA negative group it was 78.9% (p=0.01). TNF-a levels were higher in the CagA positive than negative group (p=0.001) but no difference in gastrin levels was found between the groups (p=0.421). Conclusions: Our findings revealed that CagA negative status may be a risk factor for failure of H. pylori triple therapies. The Cag pathogenicity island gives a growth advantage to H. pylori strains and has been associated with an increase in the inflammatory response at the gastric mucosal level. These properties could make CagA positive H. pylori strains more susceptible to antibiotics.