Serum prolidase enzyme activity in Helicobacter pylori infection

Aim: There is still no ideal method in the diagnosis of Helicobacter Pylori infection which has high sensitivity and specificity, easy to apply, is cheap, gives immediate results and is minimally invasive. Therefore, noninvasive methods predicting Helicobacter pylori infection are being investigated. Studies have shown that the activity of prolidase enzyme increases when collagen turnover increases. In this study, we aimed to investigate the correlation between atrophy, metaplasia, chronic inflammation, Helicobacter pylori and prolidase enzyme activity in patients with a non-invasive method and whether there was any change in prolidase activity after Helicobacter pylori infection treatment. Materials and Methods: This study included 146 patients who underwent upper gastrointestinal endoscopy for dyspeptic complaints, had no ulcers detected and biopsies were taken from the antrum and corpus. The patients were divided into two groups as Helicobacter pylori negative and positive. Serum prolidase enzyme activity and other laboratory tests were compared between the groups. Prolidase enzyme activity of the patients with atrophy and intestinal metaplasia were compared with those without atrophy and intestinal metaplasia. Serum prolidase enzyme activity was measured after Helicobacter pylori was eradicated with bismuth-containing treatment in patients who had Helicobacter pylori at the beginns of the study. Results: Of the patients included in this study, 63 were negative and 83 were positive for Helicobacter pylori. There was no statistically significant difference between the two groups in terms of age, sex and laboratory values. Serum prolidase activity was significantly higher in the Helicobacter pylori positive group than the negative group (p=0,002) and was correlated with the severity of Helicobacter pylori infection (p <0,01). Prolidase levels increased after Helicobacter pylori eradication treatment but there was no statistically significant difference. Endoscopic biopsy showed that serum prolidase enzyme activity was significantly higher in patients with atrophy examination than those without atrophy (p<0,05). Conclusion: There was a relationship between Helicobacter pylori and serum prolidase enzyme activity. This relationship showed that prolidase could be involved in the pathogenesis of Helicobacter pylori. Prolidase could be a new target for Helicobacter pylori treatment, after proving its role in the pathogenesis of Helicobacter pylori infections. Furthermore, prolidase enzyme activity could be used as a noninvasive marker for predicting Helicobacter pylori infection and its complications. Our findings should be supported with further studies. Keywords: Helicobacter pylori, Atrophy, Prolidase, Non-invasive method, Intestinal metaplasia