CHANGES IN THE INTENSITY OF FREE RADICAL LIPID OXIDATION IN PATIENTS WITH BRONCHIAL ASTHMA WITH CONCOMITANT CHRONIC NON-CALCULOUS CHOLECYSTITIS
Keywords:Chronic non-calculous cholecystitis, bronchial asthma, free radical lipid oxidation
INTRODUCTION: The incidence rate of chronic non-calculous cholecystitis (CNCC) in the population is 35-38%, and in elderly patients it reaches to 65-72%. Free radical lipid oxidation (FRLO) plays a significant role in the development and progression of bronchial asthma (BA). The initiators of FRLO excessive activation can be the following: hypoxia, inflammation, immune damage to membranes and the imperfection of the antioxidant defense.
OBJECTIVE: To compare the intensity of FRLO processes in patients with BA and comorbid CNCC, and patients with BA and CNCC each without any comorbidities..
METHODS: The study was performed on 92 patients: 30 patients with BA (group 1), 30 patients with BA and comorbid CNCC (group 2), and 32 patients with CNCC (group 3). The control group consisted of 30 practically healthy persons (PHP). The number of compounds with isolated double bonds (IDB), diene conjugates (DC), ketodienes and conjugated trienes (K/CT), and malonic aldehyde (MA) in erythrocytes and blood plasma were determined.
RESULTS: In groups 1, 2, and 3, the content of IDB was higher in comparison with PHP by 1.4, 1.7, and 1.6 times respectively. In group 1, plasma K/CT was 12.0% higher, and DC was 1.5 times higher compared to the PHP group. In group 2, DC and K/CT were higher by 1.7 times and by 21.7% as compared with PHP. In group 1, plasma MA and red blood cell MA were higher by 18.0% and 29.8%. The highest content of plasma MA and red blood cell MA in group 2 of patients was 69.8% and 54.3% respectively. In group 3, plasma MA was 34.7% higher, and red blood cell MA was 44.4% higher compared to the normal values.
CONCLUSIONS: Intensification of FRLO processes leads to disruption of microcirculation and metabolic processes in the bronchial epithelium, supports local inflammatory process in the gallbladder and bronchi and promotes inhibition of tissue respiration with increased tissue hypoxia, which, in turn, leads to the progression of broncho-obstruction.
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