Abstract

Objective — to investigate the functional state of endothelium and methods of correction of endothelial dysfunction in patients with gastric and duodenal peptic ulcers (GPU and DPU) in combination with hypertension (AH) and type 2 diabetes mellitus (DM2).
 Materials and methods. The investigation involved 100 patients, who were divided into the groups: group 1 consisted of 20 apparently healthy individuals (AHI), group 2 included 40 patients with GPU (n = 23) and DPU (n = 17) without signs of AH and DM2, group 3 involved 40 patients with GPU (n = 15) and DPU (n = 25) in combination with hypertension and DM2. The groups were sub‑divided into subgroups A and B depending on the H. pylori strains’ toxigenicity: group A included patients with CagA+ VacA+ strains’ combination, groups B — infected with H. pylori with a combination of strains of CagA+ or VacA+. All patients were administered the traditional antihelicobacter therapy (AHBT) (esomeprazole 20 mg twice daily + amoxicillin 1.0 g twice daily + clarithromycin 500 mg twice daily for 10 days). To increase the effectiveness of eradication therapy, 40 patients in addition to AHBT, received a combined probiotic (Bifidobacterium bifidum, B. lactis, Enterococcusus acidophilus, L. paracasei, L. plantarum, L. rhamnosus, L. salivarius) 1 sachet twice a day for 1 month. Eradication control was monitored 4 weeks after completion of treatment.
 Results. The increased expression of the vascular cell adhesion molecule‑1 (VCAM‑1) and the number of desquamated endothelial cells (DEK) and improvement of the oxidant‑antioxidant system have been established. Before the treatment, in comparison with the levels in AHI, levels of sVCAM exceeded in 5.88 times (р < 0.05), of erythrocytic malondialdehyde in 1.92 times (р < 0.05), and levels of the reduced glutathione was lower by 46.39 % (р < 0.05). The use of triple therapy improved the endothelial condition and the state of the oxidative‑antioxidant system, and additional application of probiotic promoted more effective correction of the indices of endothelial state and oxidative‑antioxidant system by means of maximal decrease of the levels of sVCAM and erythrocytic malondialdehyde and increase of the reduced glutathione levels.
 Conclusions. The presence of H. pylori, in particular its toxigenic strains, results in the development of endothelial disfunction in patients with GPU and DPU, combined with arterial hypertension and DM 2. When combined with hypertension and DM2, the course of GPU and DPU is accompanied with «mutual burden» syndrome resulting in the exhaustion of the antioxidant defense system and increased indexes of the glutathione system.

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