Community-acquired pneumonia is remaining one of the most common diseases in the world. The high morbidity and mortality rates establish the necessity for further in-depth research into the mechanisms of the development and progression of the disease, finding ways to optimize diagnosis and treatment. The purpose of this study is to investigate indicators of the oxidative metabolism of erythrocytes in patients with community-acquired pneumonia and to evaluate its significance in the pathogenesis of the disease. Participants and methods: the study involved 20 adult patients suffering from community-acquired pneumonia, who took the course of treatment at the therapeutic department of the City Clinical Hospital No. 25, Kharkiv. The diagnosis of community-acquired pneumonia was established on the basis of epidemiological, clinical, laboratory, and radiological findings. All indicators were compared with the findings in the group of healthy individuals. A comparative analysis of the content of carbonyl derivatives, the level of malondialdehyde, and membrane-bound haemoglobin was carried out. We revealed the presence of intracellular oxidative stress in erythrocytes of the patients with community-acquired pneumonia that leads to damage to their membranes and the release of hemoglobin into the blood plasma. Conclusion. Oxidative metabolism provokes an impairment of redox reactions in the blood plasma and contributes to the progression of the disease. Hypoxia, which develops during community-acquired pneumonia, aggravates the course of the disease and worsens the prognosis for recovery. The obtained results allow us to recommend the addition of antihypoxic agents to the traditional antibacterial therapy of community-acquired pneumonia.
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