Abstract

The aim of the study was to evaluate the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in infants and children with congenital heart defects (CHD) in comparison with the levels in the control groups. Materials and methods. The volume study included 56 patients, including 35 cyanotic and 21 cyanotic with congenital heart disease, as well as 20 control subjects. We used a specific immunoassay to measure serum ghrelin, TNF-a and IL-6 levels. All patients' cardiac diagnoses were based on clinical examination, laboratory tests, electrocardiography and echocardiography; and none of the patients had pulmonary hypertension. The body mass index (BMI) was calculated as the ratio of body weight (kg) and height squared (m). The study also included 20 healthy infants and children corresponding to age and gender as a control group. Informed consent was obtained from the parents. Results. The results of the analysis indicate a significant increase in IL-6 and TNF-a levels in cyanotic and acyanotic patients with congenital heart defects compared with the control group (P < 0.0001). The findings highlight the importance of cytokines in the pathophysiology of congenital heart defects and their effect on patient growth. It is suggested that elevated levels of IL-6 and TNF-a may stimulate the process of apoptosis, which may play a key role in growth retardation. These data indicate the presence of growth disorders in a significant proportion of patients with congenital heart defects. These results provide additional details about the nature of growth disorders in patients with congenital heart defects and highlight the importance of further research to better understand the molecular and immunological mechanisms associated with this condition. Conclusion. The findings of this study support the hypothesis of the effect of cytokines on growth in congenital heart defects. Elevated levels of IL-6 and TNF-a are likely associated with chronic congestive heart failure and hypoxia. Further research is needed to confirm these results and develop therapeutic strategies for managing growth retardation in children with congenital heart defects.

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