Genetic predisposition alongside with environmental factors play a major role in the pathogenesis of coronary heart disease, causing the deregulation of various biochemical processes leading to the disease onset. Antioxidant system deregulation, marked mainly by lipid peroxidation products and a number of enzymes, is known to be one of the risk factors for coronary heart disease. A genetic defect might lead to a change in enzyme activity and inhibition of antioxidant protection. However, the pathogenic factors and antioxidant system deregulation mechanisms in different clinical courses of coronary heart disease are not studied enough as phenotypic expression of genetic polymorphism is largely dependent on the gene pool and the living conditions of a particular population, explaining the controversial data on the association of polymorphisms candidate genes with the risk of coronary heart disease. Currently, the role of genes encoding antioxidant system enzymes in predisposition to coronary heart disease development is not sufficiently studied, and research results are contradictory. The review summarizes the current data on the antioxidant system genes (superoxide dismutase enzymes, glutathione peroxidase and catalase) genetic polymorphisms association with the risk of coronary heart disease (as an acute myocardial infarction, angina рectoris).

Aim. To study the factors worsening the course of chronic obstructive pulmonary disease and bronchial asthma.Methods. At the first stage, assessment of 1561 case histories of patients with internal diseases was performed, of whom 341 had lung diseases. A more detailed analysis with the assessment of the clinical characteristics of hospitalized patients was conducted at the second stage of our study, which included evaluation of 38 case histories of patients over a 6-month period in 2016.Results. In the structure of mortality from lung disease chronic obstructive pulmonary disease is the dominant cause (53.8%) predominating deaths from pneumonia (46.2%). Mean age of patients who died from chronic obstructive pulmonary disease was 67.2±5.97 years. Exacerbation of chronic obstructive pulmonary disease was the cause of hospitalization in 24 (63.2%) cases, bronchial asthma in 11 (28.9%) cases, chronic obstructive pulmonary disease and asthma overlap syndrome was observed in 3 (7.9%) cases. Exacerbation of chronic bronchoobstructive pathology was mostly caused by respiratory tract infections (84.2% of cases), which required administration of pluripotent antibacterial therapy. In 60.5% cases deterioration of concomitant diseases was observed with cardiovascular diseases prevailing (arterial hypertension, chronic heart failure decompensation).Conclusion. When organizing the strategy of urgent care for patients with chronic bronchoobstructive diseases, paying more attention to assessment of comorbidities is relevant; it is critical to raise awareness of practicing physicians of the criteria for the diagnosis of asthma and chronic obstructive pulmonary disease overlap syndrome.