Association of Increased Homocysteine Level with Impaired Folate Metabolism and Vitamins B Deficiency in Early Onset of Multiple Sclerosis

The study analyzed the homocysteine, cyanocobalamin (vitamin B12), folic acid (vitamin B9) and pyridoxine (vitamin B6) levels in the blood of children with confirmed demyelinating lesions of the central nervous system. The genotypes of the main polymorphisms of the folate cycle genes such as C677T and A1298C of the MTHFR gene, A2756G of the MTR gene and A66G of the MTRR gene were determined. A comparison of the studied parameters was carried out for five groups: a control group – healthy children under 18 years old, children at the onset of MS (with disease duration of no more than six months), healthy adults without neurological pathology, adult patients with MS at the onset stage of the disease and patients with long-term MS. A significant increase in homocysteine amount was revealed in children at the onset of MS compared to healthy children of the corresponding age. A high predictive value of determining homocysteine levels in children has been established. It has been demonstrated that an increased above safe values level of homocysteine is not accompanied by the presence of a vitamin deficiency state, assessed by the amount of folic acid, vitamins B6 and B12 in the blood. The lack of correlation between laboratory signs of vitamin deficiency and homocysteine levels may be due to the carriage of polymorphic variants of folate cycle genes, and an increased homocysteine level should be considered as a marker of functional disorders of folate metabolism that accompany the onset of the pathological process in MS in children. The identified patterns can be used in the development of treating strategies and preventing of the demyelination process in children with multiple sclerosis.