The relationship between cagA positivity and serum gastrin and TNF- alpha levels in patients with chronic active gastritis and duodenal ulcer associated with Helicobacter pylori [Helicobacter pylori (+) kronik aktif gastrit ve duodenal ulserli hastalarda, cagA pozitifligi ile serum gastrin ve TNF-alfa iliskisi]

Helicobacter pylori (H.pylori) infection, which is strongly associated with non-autoimmune chronic active gastritis and peptic ulcer disease, is also considered to be a co-factor in gastric adenocarcinoma and primer gastric B cell lymphoma. In order to examine the relationship between cag A (+) strain of H. pylori with gastrin and TNF-alpha, an inflammatory mediator, in both chronic active gastritis (CAG) and duodenal ulcer (DU) pathogenesis, 21 patients with CAG and 31 patients with DU disease were investigated in addition to 18 patients who had no pathological findings on either upper gastrointestinal endoscopy or histological examination. Prior to endoscopy, sera were collected from all of cases in order to evaluate gastrin and TNF- alpha and also for cag A antibody measurements. These three parameters were studied from the same blood sample. Cag A antibody was found in 33.3% (7/21) of patients with CAG and in 64.5% (20/31) of patients with DU disease (p < 0.05). When the cases with CAG (74.1 ± 26 pg/ml) and with DU (69.5 ± 22 pg/ml) were compared there was no significant difference between gastrin levels of the patient groups but both were significantly higher than the gastrin level (44.9 ± 5.7 pg/ml) of the control group (p < 0.001). The serum TNF-alpha level of cases with CAG (38 ± 34 pg/ml) was higher than control group (18 ± 9 pg/ml) (p < 0.05). There was no significant/difference between the serum gastrin and TNF-alpha levels of cag A(+) and cagA(-) cases. According to these results, there seems to be a positive relationship between cag A positive H. pylori strains and DU. Serum gastrin levels are high in H. pylori infection. This finding does not depend on the presence of cagA antibody of H. pylori and is also not related with CAG and DU, which are caused by H. pylori. As there is no correlation between the serum TNF-alpha level, gastrin level and presence of cagA antibody, we conclude that both the secretion of gastrin and the inflammatory cytokin response are free from the effect of cag A antibody.