Aim: To evaluate the effectiveness of L-arginine in the prevention of endothelial dysfunction, which may be a predictor of anthracycline-induced myocardial injury, in patients with acute leukemia (AL) on the background of anthracycline antibiotics low cumulative doses from 100 to 200 mg/m2. Materials and Methods: A total of 81 adult AL patients (38 males and 43 females with the age of 16–59 years) were studied. The patients were divided into two groups: group I (n = 34), AL patients treated with chemotherapy (CT) and L-arginine hydrochloride; group II (n = 47) — AL patients treated with CT only. Cardiac evaluation and endothelial function assessment were performed at baseline and after second CT. Electrocardiography (ECG) parameters, lipid peroxidation activity, antioxidant protection and NO system state were evaluated. Results: The bioelectric activity abnormalities of the myocardium were observed in studied patients with low cardiac risk after induction CT. In case of L-arginine administration, only minimal daily ECG changes were recorded. A significant difference in the lipid peroxidation and antioxidant defense system activity in patients of groups I and II was determined. We noticed deepening of endothelial dysfunction on the background of cytostatic therapy with anthracycline antibiotics compared with baseline values in patients of group II. It was found that prophylactic L-arginine increases superoxide dismutase level and reduces the total NOS activity due to its inducible isoform. Conclusion: The leading factor of anthracycline-induced cardiotoxicity is the imbalance between free radical generation and their inactivation that leads to endothelial dysfunction development. L-arginine eliminates the prooxidant-antioxidant imbalance and improves the endothelial function.

The aim: To define clinical peculiarities of chronic active gastritis in patients with type 2 diabetes mellitus (T2DM) considering Helicobacter pylori (HP) status and small intestinal bacterial overgrowth (SIBO). Materials and methods: 172 patients with chronic active gastritis were enrolled in the study, 92 out of them had concomitant T2DM. Symptoms were collected with the questionnaire, HP infection was diagnosed with stool antigen test, SIBO was assessed with glucose hydrogen breath test. Results: 87.5% (n=70) patients with chronic gastritis without DM had epigastric pain, however those with T2DM reported pain only in 41.3% (n=38) cases. Other symptoms included: nausea, bloating, early satiety, postprandial fullness, heartburn, belching and vomiting. HP infection in patients with chronic gastritis and concomitant T2DM is significantly associated with symptoms of epigastric pain (OR=2.78, 95%CI 0.92-8.41), bloating (OR=3.92, 95%CI 1.40-10.99), nausea (OR=2.32, 95%CI 0.85-0.6.30), postprandial fullness (OR=1.45, 95%CI 0.54-3.87) and belching (OR=1.01, 95%CI 0.32-3.16), whereas SIBO – with bloating (OR=8.82, 95%CI 2.88-27.01), nausea (OR=5.15, 95%CI 1.88-14.10) and belching (OR=2.53, 95%CI 0.67-9.52). Conclusions: Patients with T2DM and chronic active gastritis report epigastric pain significantly less than non-diabetics. HP infection probably plays a prominent role in development of epigastric pain in patients with T2DM. Additionally, HP is linked to SIBO, which may lead to bloating, belching and nausea onset.

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The chemotherapy for chronic lymphoproliferative disorders is associated with the risk of chemotherapyinduced hepatotoxicity. The objective of this study is to assess the effectiveness of S-ademetionine in the prophylaxis of chemotherapy-induced liver injury in patients with chronic lymphoprolypherative disorders. Materials and methods. The study included twenty-five patients with chronic lymphoprolypherative disorders. The patients were examined before chemotherapy and after three courses of chemotherapy. We assessed the following biochemical markers: the activity of alanine and asparagine aminotransferases, gammaglutamyltranspeptidase, alkaline phosphatase, total bilirubin, total protein, creatinine, and urea. Patients were divided into three groups: І (n=14) included patients, who received chemotherapy only; ІІ (n=16) involved patients who received chemotherapy and S-ademetionine in a dose of 1000 mg/day intravenously for 10 days, and then orally 500 mg twice a day for 20 days; ІІІ (n=20) was a control group including 20 healthy individuals. Results and discussion. During the initial examination, abnormal biochemical liver markers were found in 38,5% (5/13) of the group I patients and in 25% (3/12) of group II patients that pointed out a cholestatic pattern of liver injury. On the second examination hepatotoxic reactions were determined in 76,9% (10/13) of group I patients, and 2 (16,6%) patients in the group II. Administration of S-ademetionine into the course of adjuvant therapy led to statistically significant reduction in the total risk of hepatotoxic reactions (RR=0,21: 95% CI 0,059-0,79; p<0,05) and the increase activity of gammaglutamyl transpeptidase in blood serum (RR=0,21: 95% CI 0,059-0,79; p<0,05). Conclusion. S-ademetionine as a component of adjuvant therapy for patients with chronic lymphoprolipherative disorders, who undergo chemotherapy, provides the effective prevention of hepatotoxic reactions.