Clinical and etiological characteristics and cytokine profile in school-age children with community-acquired pneumonia

The urgent task of modern pediatrics is the study of the etiology and pathophysiology of community-acquired pneumonia in school-aged children due to difficulties in diagnosis and treatment, as well as the high risk of life-threatening complications and death. Purpose. To investigate the activity of pro-inflammatory and anti-inflammatory responses as measured by cytokine levels in the peripheral blood of children with community-acquired pneumococcal and non-pneumococcal pneumonia. Material and methods. The etiology of community-acquired pneumonia was confirmed by comparing the results of rapid testing of pneumococcus in urine and data from traditional bacteriological methods. The study included 118 children (57 boys and 61 girls) aged 7 to 16 years with various morphological variants of community-acquired pneumonia, which were divided into 2 groups. The first group included 28 children with pneumococcal etiology of community-acquired pneumonia, and the second group included 90 patients with non-pneumococcal community-acquired pneumonia. Levels of interleukins IL-1, IL-4, IL-8 and TNF-α were determined in all children by enzyme immunoassays. Results. In the etiology of community-acquired pneumonia in school-age children, atypical pathogens are responsible for more than 50% of cases. The clinical effectiveness of rapid testing of pneumococcal antigens in urine has been shown, and their use in routine pediatric practice has made it possible to timely identify a group of severe community-acquired pneumonia and reasonably prescribe antibacterial medications. It has been demonstrated that pneumococcal-induced pneumonia is characterized by higher levels of proinflammatory cytokines. These levels, along with the clinical course of the disease, confirm the high level of systemic inflammation. Relatively lower levels of proinflammatory cytokines corresponded to a more mild clinical picture of community-acquired pneumonia of non-pneumococcal etiology, which on the one hand may reflect a relatively «balanced» inflammatory response, and on the other hand determine the protracted and polyclinic course of the infectious process. Conclusion. The etiology of community-acquired pneumonia in school-age children is dominated by atypical pathogens. Community-acquired pneumonia of pneumococcal etiology has more severe clinical courses, and their early identification will allow for the appropriate prescription of initial antibacterial treatment.