Introduction: Anti GAD (antibodies on glutamic acid decarboxylase) and anti-IA2 antibodies (against tyrosine phosphatase), today, have their place and importance in diagnosis and prognosis of Type 1 diabetes. Huge number of patients with diabetes mellitus type 1 have these antibodies. Insulin antibodies are of critical importance in diagnosis of diabetes mellitus type 1 for pediatric population. Materials and methods: During 2014, the samples of 80 patients from Clinical Center University Sarajevo (CCUS) Pediatrics clinic’s, Endocrinology department were analyzed on anti-GAD and IA2 antibodies. The samples of serums of all patients were analyzed with ELISA tests using Anti GAD ELISA (IgG) kites from EUROIMMUN company. These are quantitative in vitro tests for human antibodies against decarboxylase of glutamine acid (GAD) and IA2, in serum or EDTA plasm. Results: During the period of one year, in CCUS’s Organizational unit, Institute for Clinical Immunology, 80 samples of patients with anti GAD and IA2 antibodies were analyzed. Out of total number of samples, 41 were male patients, or 51% and 39 female, or 49%. The youngest patient was born in 2012, and the oldest in 1993. Age average was represented by the patients born in 2001. Share of positive results for IA2 antibodies and GAD antibodies was 37% for IA2 antibodies, and 63% for GAD antibodies. Discussion: During an autoimmune – mediated Diabetes mellitus type 1 leads to T-cell mediated destruction of beta cells of pancreatic islets, reduced production of insulin and glucose metabolism. Studies have shown that these bodies are the most intense single marker for identifying persons with increased risk for diabetes development.

Abstract Background. Helicobacter pylori infection is the main cause of gastric cancer. The disease progression is influenced by the host inflammatory responses, and cytokine single nucleotide polymorphisms (SNPs) may have a role in the course of the disease. The aim of our study was to investigate proinflammatory cytokine polymorphisms, previously associated with the development of gastric cancer, in a Slovenian population. Patients and methods. In total 318 patients and controls were selected for the study and divided into three groups: (i) patients with gastric cancer (n = 58), (ii) patients with chronic gastritis (n = 60) and (iii) healthy control group (n = 200). H. pylori infection in patient groups was determined by serology, histology and culture. Four proinflammatory gene polymorphisms were determined (IL-1β, IL-1rα, TNF-α, TLR-4) in all subjects. Results. We found a statistically significant difference between males and females for the groups (p = 0.025). Odds ratio (OR) for gastric cancer risk for females was 0.557 (95% confidence interval [CI]: 0.233―1.329) and for chronic gastritis 2.073 (95% CI: 1.005―4.277). IL-1B-511*T/T homozygous allele for cancer group had OR = 2.349 (95% CI: 0.583―9.462), heterozygous IL-1B-511*T had OR = 1.470 (95% CI: 0.583―3.709) and heterozygotes in TNF-A-308 genotype for chronic gastritis had OR = 1.402 (95% CI: 0.626―3.139). Other alleles had OR less than 1. Conclusions. We could not prove association between gastric cancer and chronic gastritis due to H. pylori in any cytokine SNPs studied in Slovenian population. Other SNPs might be responsible besides infection with H. pylori for the progression from atrophy to neoplastic transformation.

Introduction: Regulatory T cells (Treg) play a central role in the immunopathogenesis of psoriasis. Immunoregulatory T cells (Tregs) are involved in important homeostatic mechanism for maintaining tolerance and preventing autoimmunity, and autoimmune diseases. The aim of this study was to examine the role of Tregs cells in the pathogenesis of psoriasis, and determine the range value for Treg cells (CD4+ CD25+) in the peripheral blood of patients with psoriasis compared to the severity of disease. Material and methods: The study included 51 patients diagnosed with psoriasis and 25 healthy individuals. Phenotype profile of peripheral blood lymphocytes was determined by flow cytometry, and assessment of severity of disease was determined on the basis of PASI score (e.g. Psoriasis Area and Severity Index). Results: Proportion of CD4+CD25+T cells in the control group was significantly higher than in the patients with psoriasis [6,4% ±(5,4-7,6) vs. 4,1% (3,1 -5,8)–Mann–Whitney U test, p <0.001]. In the present study we did not find a statistically significant correlation between the levels of CD4+CD25+cells, in patients with psoriasis, compared to the severity of disease–PASI. (i.e. Pearson correlation, r = 0.197, p = 0.194). Conclusion: The stratification of patients, according to the severity of the clinical course was not possible on the basis of Treg cells’ level. ROC curve analysis of the optimal cutoff (PASI=10) and the CD4+CD25+, which distinguishes between patients and healthy individuals was 5% of CD4+CD25+ of the total number of CD4+ lymphocytes with specificity of 69% and sensitivity of 84%.