The aim of this study was to evaluate the prevalence of Helicobacter pylori genotypes (vacA and cagPAI) directly in gastric biopsy specimens in patients with gastric diseases in Belarus. Gastric biopsies were collected from 461 patients with different gastrointestinal disorders: superficial gastritis (287 subjects), atrophy gastritis (59 subjects), erosive gastritis (47 subjects), duodenal ulcer disease (54 subjects), and stomach ulcer (14 subjects). PCR-based genotyping was used to detect s1a, s1b, s2, m1a, m1b, m2, cagM, cagA, and cagT genes. Overall prevalence of vacA s1a allele was 60.5% followed by m2 (47.1%) and m1a (37.5%). The analysis of data showed that genotype s1a/m1a was significantly more prevalent in patients with duodenal ulcer (21.4% vs. 45.1%, OR = 3.0, 95% CI = 1.5-6.1). The cagA gene was found with a high incidence in most patients with inflammatory diseases of stomach and duodenum. There was a significant increase in the frequency of cagT in patients with duodenal ulcer as compared to superficial gastritis. A high cagM prevalence was found in patients with atrophy gastritis and duodenal ulcer disease. All three island genes of pathogenicity of cagPAI are more often detected in patients with duodenal ulcer, which increases the risk of developing duodenal ulcer by 4.5 times.

A B S T R A C TObjectives: Tuberculosis (TB) still remains an important medical problem due to high levels of morbidity and mortality worldwide. Tuberculous pleurisy is the most common form of extrapulmonary TB. Since tuberculous pleural effusion usually contains a low number of mycobacteria, the diagnostic sensitivity of both direct microscopy and pleural fluid cultures is relatively low.Adenosine deaminase (ADA) is an essential enzyme in the metabolism of purine nucleosides. For an adequate interpretation of ADA, it is important to highlight the fact that ADA is represented by two isoenzymes: ADA1 and ADA2. The ADA1 isoenzymes are found in all cells, with the highest activity in lymphocytes, whereas ADA2 isoenzymes appear to be found only in antigen-presenting cells.The aim of this study is to evaluate the ADA and ADA1 and ADA2 isoenzyme activity in patients with pulmonary TB and tuberculous pleurisy.Methods: This study included 25 patients with pleural effusions (11 with pleural TB and 14 with nontuberculous etiologies), 35 patients with pulmonary tuberculosis (PTB) and 42 healthy subjects.Total ADA activity level in pleural fluid and blood plasma was measured by the ''ADA-test kit'' developed in the Republican Scientific and Practical Center for Epidemiology & Microbiology (Minsk, Belarus). The principle ''ADA-test'' is a colorimetric method in which adenosine is deaminated by ADA and the free ammonia is estimated. Estimated ADA2 activity was calculated from the ADA and 2 0 -deoxyadenosine deaminase activities using the affinity of ADA2 for the two substrates. Results:The mean plasma ADA level in patients with PTB was 19.2 ± 3.3 U/L that was significantly higher than the control group (10.4 ± 0.6 U/L). The difference between patients with pleural TB and the controls is also significant (18.2 ± 2.5 U/L versus 10.4 ± 0.6 U/L, p < 0.05). A significantly higher activity of ADA1 and ADA2 in the blood plasma was observed in patients with PTB and pleural TB than those of the corresponding controls (p < 0.05). I n t e r n a t i o n a l J o u r n a l o f M y c o b a c t e r i o l o g y 4 ( 2 0 1 5 ) 9 3 -9 4 H O S T E D BY A v ai l abl e a t w w w . s c i e n c e d i r e c t. c o m ScienceDirect j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / I J M Y C O

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