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ISSN: 1734-1922
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vol. 4

Invited commentary
Uric acid in chronic heart failure: marker or therapeutic target?
Commentary on: Pawan D. Patel, Rohit R. Arora. Uric acid and xanthine oxidase: perspectives in chronic heart failure (Arch Med Sci 2008; 4, 3: 219–225)

Wolfram Doehner
Stefan D. Anker
Gerasimos S. Filippatos

Arch Med Sci 2008; 4, 3: 226–228
Online publish date: 2008/10/15
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Heart failure is one of the leading medical problems in modern medicine regardless of whether we view it from the clinical, prognostic, epidemiological or socio-economic perspective. While current treatment strategies are targeting exclusively the neurohormonal activation, our pathophysiologic understanding has advanced significantly towards an increasingly complex picture including metabolic, inflammatory, and hormonal pathways. Recently, an increasing interest in uric acid (UA) has emerged, as a number of studies have shown that hyperuricaemia is a constant feature of metabolic imbalance within heart failure pathophysiology. In contrast to many other novel biomarkers, UA is an easily measured parameter with wide availability at low costs. The former perception of UA as the inert end product of the purin degradation has changed as recent evidence suggests a significant role of the purine degradation pathway within metabolic and immunologic regulation. In this issue, Patel and Arora provide a broad overview of current knowledge on UA and the xanthine oxidase metabolic pathway [1]. In combining the findings from pre-clinical and clinical studies the authors present a comprehensive picture of the diagnostic and therapeutic implications regarding UA metabolism in the context of CHF. In the ongoing discussion on hyperuricaemia in CHF several questions remain controversial. Fundamentally, the nature of UA as a good or bad guy in the field is still on debate. On one side, the enzyme xanthine oxidase (XO) has been established as a major source of oxygen radical accumulation and hence originator of a wealth of detrimental effect in acute and chronic disease conditions. In fact, XO was first documented biological generator of reactive oxygen species (ROS) [2]. On the other hand, UA accounts for much of the protective antioxidant capacity in plasma [3]. So a chicken and egg conundrum emerges if one looks at these two factors (i.e. XO and UA) separately. While several studies observed that exogenous administration of UA exerts protective effects against oxidative damage and endothelial dysfunction, it should be noted that in CHF hyperuricemia results mainly from up regulated XO activity [4] with the inevitable effect of increased ROS generation. Accordingly, inhibition of XO and hence preventing ROS accumulation yielded multiple protective effects on functional and metabolic capacity in CHF [5]. The specific organ distribution of XO with the highest activity...

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