Abstract

Aneurysm and microorganism relationship, which is urged to be a cause of atherosclerotic and non atherosclerotic pathogenesis, is a subject that has been discussed for years. In addition to many known microorganisms about this relationship, in recent years Chlamydophila pneumoniae, anaerobic bacteria and Helicobacter pylori are the most emphasized microorganisms suggested as a possible factors influencing the development and expansion especially of abdominal aortic aneurysm. In this study, we aimed to evaluate the potential etiopathogenetic relationship between abdominal and ascending aneurysm and H. pylori. The study was conducted between January 2010 and December 2010 as a cross-sectional, case-control study with 50 cases admitted to TR Ministry of Health, Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, Department of Cardiovascular Surgery and diagnosed with abdominal aortic aneurysm (AAA) and ascendıng aortıc aneurysm (AsAA) according to their clinical findings and their radiodiagnostic data. Laboratory studies of the research were performed in Serology-enzyme linked immunosorbent assay (ELISA) and Molecular Biology laboratories of the Depatment of Medical Microbiology in Istanbul University, Cerrahpasa Faculty of Medicine and in private Burc Molecular Diagnostic Center. The study was performed in three groups. The first group was the patient group (PG) including 50 patients with aneurysm (40 ascending, 10 abdominal), the second group was the patient control group (PCG) including 30 patients with post-stenotic aneurysm (PSAG) and the third group was the healthy control group (HCG) with 47 healthy individuals selected among the people admitted to Computed Tomography (CT) laboratory of the department of radiodiagnostics of Istanbul University (IU) Cerrahpasa Faculty of Medicine (CFM) according to their particular complaint, but not having abdominal or cardiovascular complaints resembling the AAA and AsAA. H. pylori IgG test was applied to the serum samples taken from all people of the three groups by enzyme immunoassay method. Additionaly, DNA extraction was applied using a commercial tissue extraction kit in the tissue specimens of the patient group and in the tissue specimens of patients with post-stenotic aneurysm. H. pylori DNA was determined by real-time PCR method using a commercial kit (WAY2GENE^® Helicobacter pylori, Genmar, Turkey) according to the manufacturer’s protocol. H. pylori IgG positivity was detected in PG, PSAG and HCG as 76, 57 and 57%, respectively. H. pylori DNA was detected only in one male patient with atherosclerotic abdominal aneurysm and could not be detected in other 49 cases. While these strain’s genotype was identified as VagA s1b/m1, it was found to be negative for all other genes. In conclusion, however, VagA s1b1 type H. pylori was detected in vascular tissue of a case with atherosclerotic abdominal aneurysm and not detected in PCG with post-stenotic aneurysm, these data are not enough to support an etiopathogenetic relationship between aneurysm and H. pylori. The presence of H. pylori DNA in only one case suggests that H. pylori is not a primer agent and probably has an affinity to the vascular tissues.

Key words: Helicobacter pylori, aneurysm, PCR.