Introduction. Inflammatory bowel diseases (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory diseases with an autoimmune attack on the gastrointestinal tract. Insufficient knowledge of the pathogenesis and the lack of reliable biomarkers of the severity of the condition in IBD dictates the need to search for new prognostic markers to assess the condition and effectiveness of therapy in IBD patients during remission and exacerbation of diseases.
The aim of the work was to evaluate the protein profile, the amount of ischemia-modified albumin (IMA) and the content of 3-nitrotyrosine (3-NT) in the blood serum in IBD children.
Materials and methods. In the blood serum of twenty two children in accordance with the pediatric indices of PCDAI/PUC disease activity in remission and exacerbation of IBD, electrophoretic separation of serum proteins was performed on the Hydrases 2 scan focusing device (Sebia). The content of IMA was determined by colorimetric method, 3-NT — by enzyme immunoassay (Hycult-Biotech, USA).
Results. The article presents data on the content of fractions of albumin (A) and globulins, IMA, and 3-NT in the blood serum in children with different severity of IBD (CD and UC), corresponding to remission and exacerbation of diseases. It was shown that the more severe the condition, the more pronounced the decrease in A with an increase in the fraction of acute phase proteins and a decrease in the albumin/globulin index (A/G). Simultaneously with a decrease in the level of A, the content of IMA and 3-NT indicators of oxidative and nitrosative stress increases.
Conclusion. The results obtained indicate modifications of serum proteins and the presence of oxidative and nitrosative stress in children with severe IBD. Due to the fact that such changes are typical for hypoxic brain damage and hyperstimulation of glutamate receptors (GluRc) of neurons, it is suggested that the indicators of oxidative and nitrosative stress in IBD children are associated with the possible development of disorders in the brain through GluRc activation.