Prognostic significance of uric acid serum concentration in patients with acute ischemic stroke.
OBJECTIVE
We sought to assess in 881 consecutive patients with acute ischemic stroke the clinical relevance in regard to functional outcome of the natural antioxidant uric acid measured at hospital admission.


METHODS
Patients had serum uric acid (mg/dL) measured by standard procedures 18.2+/-15.5 hours from clinical onset. At hospital discharge (11.0+/-6.0 days), neurological impairment was classified as moderate/severe (Mathew score < or =75; n=304) or mild/absent (Mathew score >75; n=577). Demographics, atherosclerotic risk factors, history of organ disease, baseline neurological score, stroke subtype, infarction size, renal function, aspirin use before stroke, stroke therapy, diuretic use, and laboratory markers, including erythrocyte sedimentation rate, were analyzed in both outcome groups with the use of backward logistic regression.


RESULTS
Increased uric acid values were found in men, hypertensives, alcohol drinkers, and patients with coronary, pulmonary, or renal diseases. Diabetic patients had lower uric acid levels on admission. Uric acid was directly associated with hematocrit (P=0.001), sodium (P=0.001), creatinine (P=0.001), and triglycerides (P=0.001) and inversely related with nonfasting glucose (P=0.001) levels. Neurological impairment on admission (P=0.001) and final infarction size on CT/MRI (P=0.01) were also inversely associated with uric acid. A logistic regression adjusted for confounders confirmed the following independent (odds ratio, 95% CI) good outcome predictors: age (0.97, 0.96 to 0.99), Mathew score on admission (1.14, 1.12 to 1.17), erythrocyte sedimentation rate (0.98, 0.97 to 0.99), infarction volume (0.98, 0.98 to 0.99), and uric acid (1.12, 1.00 to 1.25).


CONCLUSIONS
In patients with acute ischemic stroke, there is a 12% increase in the odds of good clinical outcome for each milligram per deciliter increase of serum uric acid. This finding reinforces the relevance of oxidative damage in ischemic stroke.
Chamorro
Angel
A
Neurology Service and Institut d'Investigació Biomédica August Pi i Sunyer, Hospital Clínic, Barcelona, Spain. chamorro@medicina.ub.es
Obach
Victor
V
Cervera
Alvaro
A
Revilla
Marian
M
Deulofeu
Ramón
R
Aponte
John H
JH
D000208:Acute Disease; D000367:Age Factors; D000368:Aged; D000975:Antioxidants / Q000032:analysis; D001786:Blood Glucose; D001799:Blood Sedimentation; D002545:Brain Ischemia / Q000097:blood* / Q000175:diagnosis* / Q000453:epidemiology; D002784:Cholesterol / Q000097:blood; D015897:Comorbidity; D003710:Demography; D005260:Female; D006400:Hematocrit; D006801:Humans; D016015:Logistic Models; D008297:Male; D011237:Predictive Value of Tests; D011379:Prognosis; D012042:Registries; D012307:Risk Factors; D012720:Severity of Illness Index; D012737:Sex Factors; D013030:Spain / Q000453:epidemiology; D020521:Stroke / Q000097:blood* / Q000175:diagnosis* / Q000453:epidemiology; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D014527:Uric Acid / Q000097:blood*
D000975:Antioxidants; D001786:Blood Glucose; D014280:Triglycerides; D014527:Uric Acid; D002784:Cholesterol