Turkish Journal of Gastroenterology, vol.12, no.1, pp.27-31, 2001 (SCI-Expanded)
Background/aims: Early experimental and epidemiological studies suggested that the presence of CagA gene was a virulence factor for Helicobacter pylori. The aim of this study was to investigate the clinical significance of tissue CagA status in Helicobacter pylori infection and to assess its association with histological changes in gastric mucosa. Methods: Sixty-nine patients with Helicobacter pylori infection established by both urease test and histological examination were included in the study. Patient symptoms were recorded according to Glasgow dyspepsia scale and biopsies (cardia, corpus, angulus and antrum) were evaluated histologically according to Sidney system. CagA status was determined by polymerase chain reaction. Serum levels of tumor necrosis factor-a (TNF-α), and gastrin were also determined. All patients were prescribed lansoprazole (30 mg bid), cla-rithromycin (500 mg bid), and amoxycillin (1 g bid) for a week. At the 8th week a second endoscopy was performed and further biopsy specimens were obtained from same sites to evaluate Helicobacter pylori eradication. Results: Forty-seven patients (68.1%) were infected with CagA positive strains of Helicobacter pylori and the other 22 patients (31.8%) were infected with CagA negative strains. Helicobacter pylori density was greater in the CagA positive group 1.9±0.9 than the cagA negative group (1.2±0.7) (p=0.01). Helicobacter pylori activity and chronic inflammation were also significantly higher in the cagA positive group 1.4±0.8 and 2.1±1.1 than in the cagA negative group 0.7±0.2 and 1.3±0.5 respectively (p=0.001, p=0.002). There was no difference in the presence of atrophy and lymphoid aggregate between the two groups, but intestinal metaplasia was found to be significantly more frequent in patients infected with cagA positive Helicobacter pylori strains (p=0.001). The serum TNF-α level was 11.3±7.0 pg/ml in the cagA positive group and 4.9±2.7 pg/l in the cagA negative group (p=0.001). Gastrin levels also showed a significant difference between the two groups at 66.8±31.1 pg/ml and 37.2±19.2 pg/ml in cagA positive and negative groups respectively (p=0.001). Peptic ulcer was found in 17% of patients in the cagA positive group and 9% of those in cagA negative group (p=0.608). Despite these differences in the degree of inflammation, clinical spectrum and biochemical parameters, there was no significant difference in the severity of patient's symptoms according to Glasgow dyspepsia severity score (p=0.20). Conclusions: These results confirm that CagA positive strains of Helicobacter pylori cause greater histological changes. However, this virulence is not associated with more severe symptoms. The histological changes can be predicted by determining the tissue cagA status.