An association between raised serum uric acid (UA) concentration and increased cardiovascular risk has been recognized for over 50 years.1 A number of major epidemiological studies have identified high UA concentrations as an important risk marker for stroke in unselected populations. Furthermore, raised serum UA concentrations are associated with increased risk of stroke in high risk patient groups, for example those with hypertension or type 2 diabetes mellitus.2,,3 However, the significance of these relationships remains subject to considerable debate. Both in vitro and in vivo studies have shown UA to be a powerful free radical scavenger in humans and, paradoxically, these antioxidant properties could be expected to offer a number of benefits within the cardiovascular system.4 No potential biological mechanisms are known by which raised UA concentrations could influence the development of stroke. Therefore, it is unclear whether high UA concentrations promote or protect against the development of cardiovascular disease, or simply act as a passive marker of increased risk. Not only has there been speculation surrounding the possible effects of UA on development of atherosclerosis but, over recent years, increasing attention has been paid to its potential role in the disease manifestations that ensue. In particular, emerging evidence suggests that UA plays an important role in acute ischaemic stroke, as a consequence of its antioxidant properties. Cerebral infarction initiates a complex cascade of metabolic events in the surrounding tissue, and free‐radical‐mediated oxidative damage plays a key role in the pathogenesis of cerebral ischaemia.5 Free radicals are …
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W. Stephen Waring (2002) studied this question.
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