Ácido Urico

EXPERTOPINION
By Scott Pello, MD, Torrey Boland, MD, Valerie Dechant, MD, Shatabdi Patel, MD, Tsao-Wei Liang, MD, and Steven Mandel, MD

Uric Acid’s Relationship with Stroke and Parkinson’s Disease: A Review
Could uric acid levels be modulated to help prevent or manage neurologic diseases? Here’s what recent data show.
n recent years, much attention has been paid to the role of uric acid indisease modification. It has been hypothesized that uric acid reduces oxidative stress on neurons. This may have a significant bearing on therapeutic management of disease, as many neurological disorders are believed to result from oxidative stress. As a potentially modifiable risk factor, the prospect for uric acid and its derivatives to play a role in disease modification or prevention has greatpotential. Uric acid is primarily produced as an end product of purine metabolism. Dietary purine intake accounts for a smaller percentage of the body’s total uric acid production; however, it is more commonly formed from de novo synthesis or degradation of nucleic acids. Its chemical composition consists of carbon, nitrogen, oxygen, and hydrogen with the formula C5H4N4O3. Uric acid is excretedin the urine.1 Stroke and Parkinson’s Disease (PD) are two disorders that carry a correlation with uric acid. This review is designed to help clarify the relationship, if any, that exists between uric acid and these two extremely widespread disorders.

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Uric Acid and Stroke
Hyperuricemia has long been associated with cardiovascular disease, hypertension, metabolic syndrome, and renaldisease.2 The link between uric acid and stroke is less clear. Some authors have suggested that elevated uric acid levels are closely associated with stroke risk factors and therefore hyperuricemia is a marker in patients at high risk for stroke. Others contend that uric acid is an independent risk factor for stroke and is directly involved with the pathophysiology of cerebrovascular disease. Stillothers believe that the antioxidant properties of uric acid may provide some protection against ischemic damage in the brain. Currently, the role uric acid plays in cerebrovascular disease is a matter of ongoing debate. UA can act as an antioxidant and therefore is part of the body’s protective mechanism against oxygen radical induced toxicity.3 Oxidants cause lipid peroxidation, which results inthe generation of reactive species, which in turn can damage cellular components including DNA, cellular membranes, and other organelles.3 UA may suppress lipid peroxidation, thereby reducing oxidative damage.2,3 Theoretically, owing to its antioxidant properties, UA could be protective against oxidative and ischemic damage in the brain. Following this logic, investigators have examined thepossibility of a protective relationship between hyperuricemia and stroke. Low plasma antioxidant levels have been associated with poor outcome from ischemic stroke.4 Yet only one small study has confirmed the hypothetical protective effect of hyperuricemia in stroke patients. Chamorro et al. report a 12 percent increase in the odds of a good recovery from ischemic stroke for each milligram per deciliterincrease of uric acid.5 Based on these results the same group has suggested giving uric acid as a therapeutic agent in patients with acute stroke.6,7 In contrast to these studies, several researchers have implicated uric acid as a marker for vascular disease or even a direct agent of vascular damage. Several studies have reported increased risk of stroke in patients with elevated UAlevels.8,9,10,11 Hyperuricemia has also been found to predict poor outcome in patients with previous stroke.10,11,12,13 These patients may be at increased risk of recurrent stroke and cardiac causes of mortality. Elevations in UA have been linked to stroke risk factors such as insulin resistance,9 hypertension,2,9 obesity, lipid abnormalities as well as coronary artery disease.8 Even when other cardiovascular...