Research Information System
Turkish Journal of Immunology, no.4, pp.70, 2016 (Scopus, TRDizin)
The etiology of most autoimmune diseases remains elusive. Multiple publications have reported a role for Helicobacter pylori infection in causing a variety of extra-intestinal manifestations such as systemic lupus erythematosus and rheumatoid arthritis. There are many proposed pathways by which H. pylori may cause loss of self-tolerance. Cytotoxin-associated gene A (cagA) positive H. pylori strains cause more severe inflammation. This study was conducted to determine relationship with active H. pylori infection rate and CagA-IgG positivity among autoimmune diseases. A total of 86 adult patients included the study with a diagnosis of various autoimmune diseases (35 Rheumatoid arthritis, Scleroderma 14, Systemic lupus erythematosus 10, Ankylosing spondylitis 9 and others 18) as patient group prospectively. A questionnaire (age, sex, occupation, living area, body mass index, blood group, systemic illnesses, gastrointestinal disease history, H. pylori eradication story, allergic diseases, education level, antidepressant usage, the number of households, CBC counts etc.) was applied. Age and sex-matched healthy subjects have included in the study as control group (not completed). Serum and fecal samples were collected from both study groups and stored at -80 °C. H. pylori stool antigens were detected by an immuno-chromatic commercial kit (HpSA, TOYO) according to manufacturer's directions and quantity of H. pylori IgG and Anti-CagA IgG was determined by EIA (Dia.Pro). Unfortunately, the analyses of control group are incomplete yet. The mean age of patient group was 51.4(±15.3), female 61 (70.9%) and male 25 (29.1%). HP Stool Ag test result which is marker of active H. pylori infection was 35.1% (27/77). The serological results of H. pylori infections were as H. pylori IgG 82.1% (69/84) and H. pylori CagA-IgG 47.7% (31/65). There was no significant difference between autoimmune diseases for anti-CagA-IgG positivity (p>0.05). Interestingly, the frequency of active infection (HP stool Ag, 35.1%) was significantly higher in autoimmune patients when compared with the data of our microbiology laboratory (15.5%) for 2015 (p=0.000). In our study, approximately half of the infected autoimmune patients were positive for anti-CagA IgG that it is similar to results obtained from the samples collected in Turkey. In spite of the fact that lacking control group, in a similar manner to the some literature our first findings suggest that active H. pylori infections rates are higher in patients with autoimmune diseases when compared with our laboratory data.