Hyperhomocysteinemia and endothelial dysfunction in multiple sclerosis

For a comprehensive study of such a socially significant disease as multiple sclerosis (MS), which occurs predominantly in people of working age and in which neuroinflammation and neurodegeneration go hand in hand, resulting in irreversible damage to the brain and spinal cord, the key point is to decipher the pathophysiological mechanisms of its development and progression. Despite the established relationship between hyperhomocysteinemia and secondary endothelial damage, data on the possible role of homocysteine (Hcy) in disease progression are quite contradictory. Objective: to investigate the informative value of determining the content of markers of oxidative stress, mitochondrial and endothelial dysfunction in patients with MS. Material and methods . The study included 63 patients with MS (40 women, 23 men) aged 35 [30; 43] years. The control group consisted of 43 healthy volunteers (22 men, 21 women) aged 37 [32; 44] years. Depending on the therapy received, patients were divided into two groups: those receiving first-line and second-line therapy; patients receiving natalizumab therapy were considered separately. A neurological examination of patients was performed with an assessment of disease severity using the EDSS scale, and the disease progression index was calculated. The following biomarkers were also determined in the blood of patients and volunteers using enzyme-linked immunosorbent assay: intercellular adhesion molecules (ICAM-1), S-adenosylmethionine, S-adenosylhomocysteine, cysteine, cysteinylglycine, glutathione, and Hcy. Results. A statistically significant correlation was found between disease severity (EDSS disability level) and increased Hcy levels. A statistically significant increase in ICAM-1 levels was also found in patients during periods of disease activity (clinical exacerbation, activity according to MRI data), which allows this molecule to be considered as a biomarker of endothelial dysfunction and inflammation. Conclusion. The results of the study indicate the need to continue studying the pathophysiological causes of the onset and progression of MS, further identifying new biomarkers for predicting the course of MS, and evaluating the effectiveness of drugs that alter the course of MS.