Hyperhomocysteinemia: a modern view of the problem (literature review)

Abstract

Annotation. The purpose of the work was to systematize modern scientific information on the etiology and mechanisms of development of hypohomocysteinemia, to argue its possible role in pathology and the expediency of correcting a low level of homocysteine. The analysis and generalization of the results of scientific research for the years 2012-2023, selected on the basis of information search in the scientometric databases Scopus, Web of Science, PubMed, MEDLINE, Google Scholar, was carried out. Hypohomocysteinaemia is a metabolic disorder that occurs in 0.5-1% of the population and is genetically determined or acquired. Recognised causes of hypohomocysteinaemia include a mutation of the NFE2L2 gene, and acquired causes include high doses of vitamins and trace elements with hypohomocysteinemic effects, primarily vitamins B6, B9, B12. Hypohomocysteinaemia can be caused by factors such as nutritional deficiency of methionine, N-acetylcysteine, insulin, pregnancy, and coronavirus disease, but this disorder is often idiopathic. The biochemical mechanisms of hypohomocysteinemia include excessive activation of methyltransferase reactions, increased need for homocysteine and cysteine in the face of increased glutathione intake, increased activity of transsulfuration processes involving cystathionine beta-synthase, separation of homocysteine from blood proteins and increased urinary excretion. The clinical significance of hypohomocysteinemia is due to a decrease in numerous physiological functions of homocysteine, which leads to a reduced ability to respond to oxidative stress and certain types of toxins, and increases the risk of developing idiopathic peripheral neuropathy, Parkinson's and Alzheimer’s diseases. There are no special approaches to the prevention and correction of hypohomocysteinaemia, which indicates the prospects for further research into this metabolic phenomenon and the development of new pharmacotherapeutic approaches.