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Xanthine oxidase and uric acid in cardiovascular disease: clinical impact and therapeutic options


Doehner, W; Landmesser, U (2011). Xanthine oxidase and uric acid in cardiovascular disease: clinical impact and therapeutic options. Seminars in Nephrology, 31(5):433-440.

Abstract

The association between increased uric acid (UA) levels and cardiovascular disease (CVD) has been observed and studied for many decades. The value of UA as an independent factor within the metabolic risk profile for prediction of CVD in the normal population remains an issue of ongoing discussion. In turn, increasing evidence suggests that among patients with established CVD such as heart failure UA is an independent marker of disease state and prognosis. Increased UA levels may be an indicator of up-regulated activity of xanthine oxidase, a powerful oxygen radical-generating system in human physiology. Increased reactive oxygen species (ROS) accumulation contributes to endothelial dysfunction, metabolic and functional impairment, inflammatory activation, and other features of cardiovascular pathophysiology. Accordingly, inhibition of xanthine oxidase activity has been shown to improve a range of surrogate markers in patients with CVD, but this effect seems to be confined to hyperuricemic patients because disappointing results were reported in studies with normouricemic patients. In this review we summarize current evidence on hyperuricemia in CVD. The value of UA as a biomarker and as a potential therapeutic target for tailored metabolic treatment in CVD is discussed.

Abstract

The association between increased uric acid (UA) levels and cardiovascular disease (CVD) has been observed and studied for many decades. The value of UA as an independent factor within the metabolic risk profile for prediction of CVD in the normal population remains an issue of ongoing discussion. In turn, increasing evidence suggests that among patients with established CVD such as heart failure UA is an independent marker of disease state and prognosis. Increased UA levels may be an indicator of up-regulated activity of xanthine oxidase, a powerful oxygen radical-generating system in human physiology. Increased reactive oxygen species (ROS) accumulation contributes to endothelial dysfunction, metabolic and functional impairment, inflammatory activation, and other features of cardiovascular pathophysiology. Accordingly, inhibition of xanthine oxidase activity has been shown to improve a range of surrogate markers in patients with CVD, but this effect seems to be confined to hyperuricemic patients because disappointing results were reported in studies with normouricemic patients. In this review we summarize current evidence on hyperuricemia in CVD. The value of UA as a biomarker and as a potential therapeutic target for tailored metabolic treatment in CVD is discussed.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology

04 Faculty of Medicine > University Hospital Zurich > Clinic for Cardiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2011
Deposited On:22 Jan 2012 11:27
Last Modified:21 Nov 2017 15:47
Publisher:Elsevier
ISSN:0270-9295
Publisher DOI:https://doi.org/10.1016/j.semnephrol.2011.08.007
PubMed ID:22000650

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