Species of Campylobacter genus participate in the etiology of enterocolitis at 3.86%. According to numerous parameters the infection in our population coincides with the infection in the population of European countries. Frequent findings of C. coli in our region are in discrepancy with the results of numerous studies conducted in the developed countries.
BACKGROUND: Helicobacter pylori (H. pylori) is classified as a Group 1 carcinogen, because H. pylori infection considerably increases the risk of gastric cancer development. METHODS: The study involved a total of 191 patients divided into two groups. The first group comprised 117 patients who underwent endoscopy. A total of 203 biopsy specimens of the gastric mucosa were taken and analyzed using microbiological and histopathological methods. The second group comprised 74 patients with gastric cancer, who were examined for the gastric cancer type, the presence of H. pylori infection and the cancer localization. The presence of H. pylori infection in the tissue was confirmed by staining pathohistological sections according to the method of Warthin-Starry. The microbilogical diagnosis involved the staining of direct tissue smears according to the method of Gram, as well as the cultivation of the specimens. To test the hypothesis for possible differences in H. pylori positive findings between the treatment groups, x2 test with Yates correction or Fisher exact test were used. RESULTS: The first treatment group comprised 117 patients with various clinical diagnoses. Gastric cancer was diagnosed in 8 patients, and of these 87.50% were found to have H. pylori. No statistically significant difference in H. pylori positive tests was detected between the patients with gastric ulcer and the patients with gastric cancer (Fisher exact test: p=1.00; p>0.05) nor was it established between the patients with duodenal ulcer and those with gastric cancer (Fisher exact test: p= 1.00; p>0.05). The second treatment group comprised 74 patients, of whom 52 (70.27%) had intestinal-type gastric cancer and 22 (29.72%) had diffuse-type gastric cancer. No statistically significant difference in the positive tests for H. pylori was registered between the patients with intestinal-type and those with diffuse-type gastric cancer (x2=0.07; p=0.798; p>0.05). The most frequent localization of the cancer was the antrum. CONCLUSION: The results are supportive of the hypothesis on a correlation between H. pylori infection and gastric adenocarcinoma development, but no differences between the intestinal and diffuse type of adenocarcinoma have been revealed with respect to the malignant process
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