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Serum uri acid: neuroprotection in thrombolysis. The Bergen NORSTROKE study

Nicola Logallo12*, Halvor Naess, Titto T Idicula1, Jan Brogger1, Ulrike Waje-Andreassen1 and Lars Thomassen12

Author Affiliations

1 Department of Neurology, Haukeland University Hospital, Bergen, Norway

2 Department of Clinical Medicine, University of Bergen, Bergen, Norway

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BMC Neurology 2011, 11:114  doi:10.1186/1471-2377-11-114

Published: 25 September 2011



A possible synergic role of serum uric acid (SUA) with thrombolytic therapies is controversial and needs further investigations. We therefore evaluated association of admission SUA with clinical improvement and clinical outcome in patients receiving rt-PA, early admitted patients not receiving rt-PA, and patients admitted after time window for rt-PA.


SUA levels were obtained at admission and categorized as low, middle and high, based on 33° and 66° percentile values. Patients were categorized as patients admitted within 3 hours of symptom onset receiving rt-PA (rt-PA group), patients admitted within 3 hours of symptom onset not receiving rt-PA (non-rt-PA group), and patients admitted after time window for rt-PA (late group). Short-term clinical improvement was defined as the difference between NIHSS on admission minus NIHSS day 7. Favorable outcome was defined as mRS 0 - 3 and unfavorable outcome as mRS 4 - 6.


SUA measurements were available in 1136 patients. Clinical improvement was significantly higher in patients with high SUA levels at admission. After adjustment for possible confounders, SUA level showed a positive correlation with clinical improvement (r = 0.012, 95% CI 0.002-0.022, p = 0.02) and was an independent predictor for favorable stroke outcome (OR 1.004; 95% CI 1.0002-1.009; p = 0.04) only in the rt-PA group.


SUA may not be neuroprotective alone, but may provide a beneficial effect in patients receiving thrombolysis.