Key result
Hyperhomocysteinemia in chronic heart failure is linked to elevated purines, lower glutathione, and heightened oxidative stress.
Cross-Sectional (n=75)
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Background Oxidative stress (OS) represents the primary mediator of chronic heart failure (CHF) development and progression. It is well established that homocysteine is able to generate reactive oxygen species. Small amounts of allantoin in human serum result from free radical action on urate and may provide a stable marker for in vivo free radical activity. To investigate whether some easily measurable indexes such as antioxidants (uric acid, glutathione) and related molecules (allantoin, homocysteine and cysteine) can serve as OS biomarkers. Methods We investigated 75 stable CHF patients. Aminothiols and purine compound levels were determined by capillary electrophoresis. Results The homocysteine level was markedly elevated in CHF patients, whatever the aetiology. Parameters of the transsulfuration pathway and the investigated purine compounds were significantly increased. Conversely, total glutathione was decreased. The allantoin/uric acid ratio was significantly higher in CHF patients with an hyperhomocysteinaemia >17 μmol/L. All parameters of the transsulfuration and purine degadation pathways were significantly correlated, suggesting an OS in CHF patients. Conclusion Our data show an imbalance of serum aminothiols and purine compounds in these CHF patients on adapted therapy. We suggest that the evaluation and control of these new markers may help improve the OS that participates in the progression of the disease.
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Caussé et al. (2017) conducted a cross-sectional in chronic heart failure (n=75). Serum aminothiols and purine compounds was evaluated on Levels of aminothiols and purine compounds. In stable chronic heart failure, serum homocysteine and purine compounds were elevated, glutathione decreased, and allantoin/uric acid ratio was higher with hyperhomocysteinemia >17 μmol/L.
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