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Is Hyperhomocysteinemia due to the Oxidative Depletion of Folate rather than to Insufficient Dietary Intake?

  • Dietmar Fuchs , Matthias Jaeger , Bernhard Widner , Barbara Wirleitner , Erika Artner-Dworzak and Friedrich Leblhuber
Published/Copyright: June 1, 2005
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Clinical Chemistry and Laboratory Medicine (CCLM)
From the journal Volume 39 Issue 8

Abstract

Hyperhomocysteinemia is considered as a risk factor for cardiovascular diseases. Usually, an inverse relationship exists between homocysteine and folate levels, and supplementation with folate lowers homocysteine concentrations in patients. Therefore, hyperhomocysteinemia is mainly ascribed to the insufficient dietary intake of folate. Hyperhomocysteinemia has also been observed in infections and inflammatory diseases. Oxidative stress appears to be involved in the pathogenesis of these disorders, and associations have been found between homocysteine and e.g., neopterin concentration. Increased neopterin concentration indicates immune system activation and also allows an estimate of thus elicited oxidative stress. It may be relevant that the active cofactor, tetrahydrofolate, is very susceptible to oxidation. Immunologically induced oxidative stress could lead to folate depletion resulting in hyperhomocysteinemia. Thus, hyperhomocysteinemia in patients can be considered as an indirect consequence of hyperconsumption of antioxidant vitamins during prolonged states of immune activation.

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Published Online: 2005-06-01
Published in Print: 2001-08-31

Copyright © 2001 by Walter de Gruyter GmbH & Co. KG

Articles in the same Issue

  1. Historical Aspects and Perspectives in Homocysteine Research
  2. The Importance of Hyperhomocysteinemia as a Risk Factor for Diseases: An Overview
  3. Pre-analytical Conditions Affecting the Determination of the Plasma Homocysteine Concentration
  4. Total Plasma Homocysteine and Related Amino Acids in End-Stage Renal Disease (ESRD) Patients Measured by Gas Chromatography-Mass Spectrometry – Comparison with the Abbott IMx Homocysteine Assay and the HPLC Method
  5. Is Hyperhomocysteinemia due to the Oxidative Depletion of Folate rather than to Insufficient Dietary Intake?
  6. Hyperhomocysteinemia in Advanced Age
  7. Genetic Defects as Important Factors for Moderate Hyperhomocysteinemia
  8. Heterogeneity of the Association between Plasma Homocysteine and Atherothrombotic Disease: Insights from Studies of Vascular Structure and Function
  9. Hyperhomocysteinemia as a Risk Factor for Venous Thrombosis
  10. Hyperhomocysteinaemia in Patients with Peripheral Arterial Occlusive Disease
  11. Homocysteine, Vascular Dementia and Alzheimer's Disease
  12. Homocysteine in Cerebrovascular Disease: an Independent Risk Factor for Subcortical Vascular Encephalopathy
  13. Vascular Dysfunction in Hyperhomocyst(e)inemia. Implications for Atherothrombotic Disease
  14. Hyperhomocysteinemia in Chronic Renal Failure Patients: Relation to Nutritional Status and Cardiovascular Disease
  15. Homocysteine, Cystathionine, Methylmalonic Acid and B-Vitamins in Patients with Renal Disease
  16. Hyperhomocysteinemia Is Related to Residual Glomerular Filtration and Folate, but not to Methylenetetrahydrofolate-Reductase and Methionine Synthase Polymorphisms, in Supplemented End-Stage Renal Disease Patients Undergoing Hemodialysis
  17. Effect of Treatment of Hypothyroidism on the Plasma Concentrations of Neuroactive Steroids and Homocysteine
  18. Hyperhomocysteinaemia and Human Reproduction
  19. Homocysteine in Postmenopausal Women and the Importance of Hormone Replacement Therapy
  20. Does a Single Vitamin B-Supplementation Induce Functional Vitamin B-Deficiency?
  21. IFCC News – July 2001
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