Belarusian State Medical University

About: Belarusian State Medical University is a education organization based out in Minsk, Belarus. It is known for research contribution in the topics: Population & Medicine. The organization has 536 authors who have published 513 publications receiving 4635 citations.

Thyroid cancer in persons as a result of the Chernobyl accident

Abstract: This study analyzed the sex and age characteristics of the incidence of thyroid cancer between residents of contaminated and not contaminated by the iodine-131 districts of Belarus in whom thyroid cancer was registered from 1986 to 2016. The analysis was carried out according to the data of the Belarusian Cancer Register and was focused on the age groups of 0-4, 5-9, 10-14, and 15-18 years old as of April 1986, i.e. at the time of the Chernobyl accident. The control group of patients was taken from the Lepel district of the Vitebsk region, which was not contaminated with iodine isotopes . The shortest latency period until the onset of the disease (16 years) was found for the 0-4 years old group. There are no significant gender differences in latency time and the age of diagnosis of thyroid cancer. In general, the incidence rates of thyroid cancer in the Brest region are higher than in the Vitebsk region, where there was practically no radioactive fallout of iodine-131. Comparison of the incidence in the Brest region with the nationwide one showed its decrease in 2006-2010, that can be explained by different latency periods of different age groups and the characteristics of radiation exposure. The data obtained supports the hypothesis of the radiation-induced nature of thyroid cancer due to the exposure of the population to radioactive iodine in April 1986. Cite this article as: Alexander N. Stojarov, Aleksey E. Okeanov, Vladislav V. Khrustalev, et al. 2021. Thyroid cancer in persons as a result of the Chernobyl accident. Int J Hematol Oncol. 4: 01-11. Copyright: This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Copyright © 2021; Alexander N. Stojarov Thyroid cancer in persons as a result of the Chernobyl accident DOI will be allocated in final stage IJHO: February-2021: Page No: 01-11

Sat0432 gouty arthritis and drug-induced liver injury after the treatment with nsaids

Abstract: Background: In order to relieve the pain during acute gout attacks, most patients take high doses of nonsteroidal anti-inflammatory drugs (NSAIDs), which can provoke the hepatotoxicity, or DILI (drug-induced liver injury). Objectives: To define the timing of DILI formation after the treatment with NSAIDs and its severity in patients with gouty arthritis (GA). Methods: 738 patients with GA from our database who meet the criteria of the ACR (1977) were included into the study. NSAIDs-induced liver damage is known to be mainly hepatocellular. The dynamic ALT concentration in blood before the start of NSAIDs and during the treatment has been assessed. Hepatocellular toxicity was determined according to the DILI classification criteria based on the blood ALT level increased > 2 times to the upper limit of norm (42 U/l for men and 35 U/l for women). Inclusion criteria for the study group (n = 88) were: normal ALT before the treatment with NSAIDs, its increase during the treatment and return to the norm after the treatment. Exclusion criterion was chronic hepatitis of any etiology. The comparison group (n = 650) consisted of patients with normal blood ALT level throughout the treatment. Results: Among 738 patients with GA, 11.9% (n = 88) developed the hepatotoxicity following the NSAIDs therapy. No significant differences in age (54 (44-59.5) and 57 (52-63) years; p> 0.05) and gender (men 93.3% and 87.6%; p > 0.5) between the study and comparison groups were found. In the study group, the duration of NSAIDs administration was 10 (6–14) days, which did not differ from that in the comparison group — 9.5 (7–12) days (p> 0.05). In patients with DILI, the elevated ALT was o, bserved as follows: 2-3 times in 74 patients (84.1%); 3 to 5 times in 10 (11.4%); more than 5 times in 4 patients (4.5%). So, minimal cytolysis was presented more frequently than more severe forms (p In the subgroup with the ALT concentration > 3-5 times (n = 10), 6 patients received Diclofenac in high doses, 2 patients were treated with Nimesulide, 1 patient with Etodolac and 1 with Dexalgin during the observation period. The elevation of ALT concentration > 5 times was observed in 3 patients taking Diclofenac i/m and Nimesulide per os, simultaneously, and in 1 patient taking Diclofenac in high doses. Patients with DILI were taking the following medications: Diclofenac 48.9% (n = 43); Nimesulide 18.2% (n = 16); Meloxicam 5.7% (n = 5), the combination of NSAIDs 20.5% (n = 18) without statistical differences (p > 0.05). The number of patients who abused alcohol in DILI and control groups did not differ significantly — 53.4% and 48.2%, respectively (p>0.05). Conclusion: In patients with GA, the hepatocellular DILI was observed in 11.9% cases after the treatment with NSAIDs during 10 days (from 6 to 14 days). Among patients with DILI, 84.1% (n = 74) had NSAIDs-induced hepatitis with minimal cytolysis. Mild cytolysis was seen in 10 (11.4%), moderate in 4 patients (4.5%). In our study, no severe or fatal DILI has been noted. No significant differences for particular drugs in the hepatotoxicity incidence have been found (p > 0.05). Disclosure of Interests: None declared

Association of the ace I/D gene polymorphism with DNA damage in hypertensive men.

Abstract: The aim of the study was to evaluate the association between the angiotensin-converting enzyme ACE I/D (rs 4340) polymorphism and DNA damage in patients with essential hypertension (EH). The I/D polymorphism of ACE was determined by polymerase chain reaction in 170 male hypertensive patients and 64 normotensive blood donors. We used flow cytometry to determine the levels of cell death, micronuclei and accumulation of peripheral blood leukocytes in G1/G0, S, G2/M phases of the cell cycle. Additionally, the whole blood samples were incubated in vitro at 4°C for 24 h to investigate the genotype effects on the susceptibility of cells to DNA damage. We found lower frequency of cells in DNA synthesis S phase and higher levels of micronuclei in the hypertensive compared to normotensive group (p 0.05) in the II genotype carriers too. However, hypertensive patients displayed different cellular response to incubation-induced DNA damages in the ACE I/D genotype groups; after incubation, the frequencies of micronuclei were significantly higher in the DD genotype carriers (p < 0.05). To conclude, the study suggests that the ACE I/D polymorphism may contribute to mechanisms and intensity of DNA damages in hypertensive and normotensive individuals.