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CONNECTION OF PNEUMOPATHY IN ANCA-ASSOCIATED SYSTEMIC VASCULITIS WITH THE ECOLOGY OF THE ATMOSPHERE OF THE REGIONS OF LIVING PATIENTS (CLINICAL AND EXPERIMENTAL RESEARCH)
Summary. Relevance. Lung damage is one of the main signs of systemic vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA-SV) — microscopic polyangiitis (MPA), Wegener granulomatosis with polyangiitis (GPA) and Churg-Strauss eosinophilic granulomatous vasculitis (EGV). The purpose and objectives of the study: on the basis of clinical and experimental studies to prove the role of air pollution by xenobiotics in lung pathology in patients with MPA, GPA and EGPA, to determine the commonality and differences of individual structural and functional signs of pneumopathy. Material and methods. 150 patients with ANCA-SV were under observation, among which MPA was diagnosed in 58% of cases, GPA — in 21%, EGV — in 21%. The experimental part of the study with the morphological study of lung tissue was carried out on white outbred rats with the ANCA-SV model. Antibodies to myeloperoxidase (AMP) and proteinase-3 (AP3) were detected in the serum of 65% of rats with a vasculitis model. Results. The development of ANCA-SV in general and pulmonary pathology in them in particular is closely related to the ecology of the atmosphere of the patient’s regions, the severity of pneumopathy in patients suffering from MPA is determined by the level of emissions from the metallurgical industry, the airborne content of 3,4-benzpyrene and dioxide S, GPA — inhaled phenol. Waste of the metallurgical industry in cases of MPA, coal mining industry, railway and automobile transport in GPA, chemical industry and dioxide S in EGV contribute to the formation of AMP. Disorders of pulmonary hemodynamics and diffusion capacity of the lungs primarily depend on the power of energy and engineering, the parameters of inhaled ammonia and dioxide N. The presence of xenobiotics in inhaled air in animals with experimental ANCA-CB is accompanied by inhibition of the synthesis of pulmonary surfactant, by an increase in the frequency of macrophages in the lumen of the alveoli, labrocytes , peribronchial and perivascular infiltration, alveolar, peribronchial and perivascular sclerosis.
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