COMPARATIVE EVALUATION OF AUTOANTIBODIES LEVELS, REFLECTING THE CONDITION OF THE CARDIOVASCULAR SYSTEM IN PATIENTS WITH VIBRATION DISEASE DUE TO LOCAL AND COMBINED VIBRATION

Abstract

Introduction. Vibration disease occupies one of the leading places in the structure of occupational pathology and is caused by exposure to both local and general vibration. Since the mechanism of local and general vibration effects on the body differs, it can be assumed that their effect on the cardiovascular system will have distinctive features. The aim of the work was to study the content of specific autoantibodies, which characterize the state of the cardiovascular system, in patients with vibration disease caused by exposure to local and combined vibration. Material and methods. The relative levels of specific autoantibodies to antigens, reflecting the state of the heart and the vascular bed, were determined in the blood of persons with vibration disease caused by exposure to local and combined vibration (29 and 36 cases, respectively). Results. 18 to 26% of persons with the vibratory disease caused by the effect of combined vibration were found to have elevated levels of autoantibodies to components of the membrane and cytoplasm of myocardial cells, components of the cytoplasm of neutrophils and endothelial cells, β1-adrenoreceptors, PAPP-A, and cardiomyosin protein. In the group of individuals exposed to local vibration, the frequency of occurrence of elevated levels of antibodies by more than 20% was detected only for β1-adrenoreceptors and PAPP-A protein. Elevated levels of other indices were observed in 10-14% of individuals in this group. The levels of antibodies to components of the membrane of myocardial cells and platelets were higher in patients with the vibratory disease caused by exposure to a combined vibration than in individuals with vibratory syndrome caused by the action of local vibration. conclusion. Elevated levels of auto-AT to platelet membrane structures may be due to changes in their membranes caused by the accumulation of highly toxic lipid peroxidation metabolites.