[The evaluation of homoarginine and folic acid in patients with arterial hypertension.]
Оценка гомоаргинина и фолиевой кислоты у пациентов с артериальной гипертензией.
arterial hypertension
folic acid
homoarginine
homocysteine
Journal
Klinicheskaia laboratornaia diagnostika
ISSN: 0869-2084
Titre abrégé: Klin Lab Diagn
Pays: Russia (Federation)
ID NLM: 9432021
Informations de publication
Date de publication:
20 Jul 2020
20 Jul 2020
Historique:
entrez:
8
8
2020
pubmed:
8
8
2020
medline:
3
11
2020
Statut:
ppublish
Résumé
According to current data, a low level of folic acid (FA) contributes to the progression of arterial hypertension (AH), affecting the metabolism of cells that are involved in the vascular tone regulation, such as hypothalamic astrocytes of nervous tissue. It is also known that the level of FA in the nervous tissue and cerebrospinal fluid is 2-3 times higher than in plasma. There is another metabolic marker of cardiovascular diseases, the level of plasma homoarginine (hArg). The decrease in the level of plasma hArg is also known as a diagnostic sign. In our study, we established that in patients with AH (n = 60), the level of hArg was almost 2 times lower than in healthy individuals, and in 75% of cases the rate was below 1.80 μM. The insufficiency of FA taking into account its low level in plasma FA, as well as the level of total homocysteine (tHcy) higher than 10.9 μM, was observed in 78% of patients. HArg levels at values less than 1.80 μM corresponded to a statistically significant decrease in FA when its content was less than 13.5 nM. This relationship (r = 0.63, p = 0.020) appears in patients with AH, regardless of the number and severity of target organ damage (TOD). FA and hArg as metabolic markers exhibit various diagnostic capabilities when comparing subgroups of patients without TOD and with multiple TOD. Significant differences fared at an acceptable level (p = 0.007) only for the hArg levels, while for the FA concentrations there was only a trend to decrease. It is possible that metabolic disturbances in the central nervous system that are associated with the necessary to maintain high FA concentration contribute to the development of hypertensive status. The causal relationship of a parallel decrease in hArg and FA levels in patients with AH requires further research.
Identifiants
pubmed: 32762188
doi: 10.18821/0869-2084-2020-65-8-474-481
doi:
Substances chimiques
Homoarginine
156-86-5
Folic Acid
935E97BOY8
Types de publication
Journal Article
Langues
rus
Sous-ensembles de citation
IM
Pagination
474-481Subventions
Organisme : The Ministry of Health of the Russian Federation
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
Références
Ehret G.B., Munroe P.B., Rice K.M., Bochud M., Johnson A.D., Chasman D.I. et al. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Nature. 2011; 478(7367): 103–9. https://doi.org/10.1038/nature10405
McNulty H., Strain J. J., Hughes C. F., Pentieva, K., Ward M. Evidence of a role for one-carbon metabolism in blood pressure: can B vitamin intervention address the genetic risk of hypertension owing to a common folate polymorphism? Curr. Dev. Nutr. 2019; 4(1); nzz102. https://doi.org/10.1093/cdn/nzz102
Loehrer F.M., Angst C.P., Haefeli W.E., Jordan P.P., Ritz R., Fowler B. Low whole-blood S-adenosylmethionine and correlation between 5-methyltetrahydrofolate and homocysteine in coronary artery disease. Arterioscler. Thromb. Vasc. Biol. 1996; 16: 727–33.
Sobczynska-Malefora A., Harrington D.J., Voong K., Shearer M.J. Plasma and red cell reference intervals of 5-methyltetrahydrofolate of healthy adults in whom biochemical functional deficiencies of folate and vitamin B 12 had been excluded. Adv. Hematol. 2014; 2014: Article ID 465623: 7 pages. http://dx.doi.org/10.1155/2014/465623
Sobczyńska-Malefora A., Harrington D.J. Laboratory assessment of folate (vitamin B9) status. J. Clin. Pathol. 2018; 71 (11): 949-56. https://doi.org/10.1136/jclinpath-2018-205048
Kulyutsina E.R., Tatarchenko I.P., Levashova O.A., Denisova A.G., Druzhinina T.A. The relationship of homocysteine and genetic polymorphisms, causing disturbances of folate metabolism in a healthy population. Klinicheskaya laboratornaya diagnostika. 2017; 62(2): 82-7. (in Russian)
Zheng Y., Cantley L. C. Toward a better understanding of folate metabolism in health and disease. J. Exp. Med. 2019; 216(2): 253–66. https://doi.org/10.1084/jem.20181965
Scazzone C., Bono A., Tornese F., Arsena R., Schillaci R., Butera D. et al. Correlation between low folate levels and hyperhomocysteinemia, but not with vitamin B12 in hypertensive patients. Ann. Clin. Lab. Sci. 2014; 44(3): 286-90.
Zhloba A.A., Subbotina T.F. The evaluation of folate status using total homocysteine in hypertensive patients. Rossiiskii meditsinskii zhurnal. 2019; 25(3): 158-65. (in Russian) DOI: http://dx.doi.org/10.18821/0869-2106-2019-25-3-158-165 (in Russian)
Choe C.U., Atzler D., Wild P.S., Carter A.M., Boger R.H., Ojeda F. et al. Homoarginine levels are regulated by L-arginine: glycine amidinotransferase and affect stroke outcome: results from human and murine studies. Circulation. 2013; 128(13): 1451–61.
Tommasi S., Elliot D.J., Da Boit M., Gray S.R., Lewis B.C., Mangoni A.A. Homoarginine and inhibition of human arginase activity: kinetic characterization and biological relevance. Sci. Rep. 2018; 8(1): 3697. http://dx.doi.org/ 10.1038/s41598-018-22099-x
März W, Meinitzer A, Drechsler C. Pilz S., Krane V., Kleber M.E. et al. Homoarginine, cardiovascular risk, and mortality. Circulation. 2010; 122(10): 967–75.
Atzler D., Gore M.O., Ayers C.R., Choe C.U., Böger R.H., de Lemos J.A., et al. Homoarginine and cardiovascular outcome in the population-based Dallas Heart Study. Arterioscler. Thromb. Vasc. Biol. 2014; 34(11): 2501–7.
Drechsler C., Kollerits B., Meinitzer A., März W., Ritz E., König P. et al. Homoarginine and progression of chronic kidney disease: results from the mild to moderate kidney disease study. PLoS One. 2013; 8(5): e63560.
Ravani P., Maas R., Malberti F., Pecchini P., Mieth M., Quinn R. et al. Homoarginine and mortality in pre-dialysis chronic kidney disease (CKD) patients. PLoS One 2013; 8(9): e72694.
Raedle-Hurst T., Mueller M., Meinitzer A., März W., Dschietzig T. Homoarginine - A prognostic indicator in adolescents and adults with complex congenital heart disease? Fukumoto Y., ed. PLoS One 2017; 12(9): e0184333.
März W., Meinitzer A., Drechsler C., Pilz S., Krane V., Wanner C. Homoarginine as a biomarker for the risk of mortality. United States Patent US 9,506,909 B2; 2016.
Atzler D., Appelbaum S., Cordts K., Ojeda F.M., Wild P.S., Münzel T., et al. Reference intervals of plasma homoarginine from the German Gutenberg Health Study. Clin. Chem. Lab. Med. 2016; 54(7): 1231-7.
Zhloba A.A., Subbotina T.F., Molchan N.S., Polushin Yu.S. Homoarginine level and methionine-homocysteine balance in patients with ischemic heart disease. Klinicheskaya Laboratornaya Diagnostika. 2019; 64 (9): 516-24. DOI: http://dx.doi.org/10.18821/0869-2084-2019-64-9-516-524 (in Russian)
Zhloba A.A. Laboratory diagnosis of hyperhomocysteinemia. Kliniko-laboratornyy konsilium. 2009; 26(1): 49-60. (in Russian)
Zhloba A.A., Subbotina T.F. Homocysteinylation score of high molecular weight plasma proteins. Amino Acids. 2014; 46(4): 893-9.
Zhloba A.A., Subbotina T.F., Shipaeva K.A. The way for determining the content of homoarginine in blood plasma and other biological fluids of human. Patent RF N 2609873; 2017. (in Russian)
Bokeriya L.A., Samuilova D.Sh., Appolonova M.V., Surganov V.A., Klyuchnikov I.V., Merzlyakov V.Yu. et al. Homocysteine in patients before and after coronary artery bypass grafting on a working heart and in cardiopulmonary bypass. Byulleten’ Nauchnogo Tsentra serdechno-sosudistoy khirurgii im. A.N. Bakuleva RAMN. Serdechno-sosudistye zabolevaniya. 2008; 9(S3): 147. (in Russian)
Knowles L., Morris A.A., Walter J.H. Walter treatment with mefolinate (5-methyltetrahydrofolate), but not folic acid or folinic acid, leads to measurable 5-methyltetrahydrofolate in cerebrospinal fluid in methylenetetrahydrofolate reductase deficiency // JIMD Rep. 2016; 29: 103-7.
Zorilova I.V., Suslina Z.A., Illarioshkin S.N., Kistenev B.A. Inherited hyperhomocysteinemia in the pathogenesis of ischemic strokes of young persons. Nevrologicheskiy zhurnal. 2005; 10(2): 14–7. (in Russian)
Litvinenko I.V., Odinak M.M., Sologub O.S., Mogil´naya V.I., Shmeleva V.M., Sakharovskaya A.A. Hyperhomocysteinemia with Parkinson’s disease: a new variant of complications of the therapy performed or a specific biochemical marker of the diseases? Annaly klinicheskoy i eksperimental’noy nevrologii. 2008; 2(2): 13–7. (in Russian)
Wu Y., Yang X., Li X., Wang H., Wang T. Elevated cerebrospinal fluid homocysteine is associated with blood-brain barrier disruption in amyotrophic lateral sclerosis patients. Neurol. Sci. 2020 Feb 21. DOI: http://dx.doi.org/10.1007/s10072-020-04292-x [Epub ahead of print].
Marina N., Christie I.N., Korsak A., Doronin M., Brazhe A., Hosford P.S. et al. Astrocytes monitor cerebral perfusion and control systemic circulation to maintain brain blood flow. Nat. Commun. 2020; 11(1): 131. DOI: http://dx.doi.org/10.1038/s41467-019-13956-y
Li W., Ma Y., Li Z., Lv X., Wang X., Zhou D. et al. Folic acid decreases astrocyte apoptosis by preventing oxidative stressinduced telomere attrition. Int. J. Mol. Sci. 2020; 21(1): E62; https://doi.org/10.3390/ijms21010062
Shao Y., Tan B., Shi J., Zhou Q. Methotrexate induces astrocyte apoptosis by disrupting folate metabolism in the mouse juvenile central nervous system. Toxicol. Lett. 2019; 301: 146–56.
Mattson M.P., Shea T.B. Folate and homocysteine metabolism in neural plasticity and neurodegenerative disorders. Trends Neurosci. 2003; 26(3): 137-46.