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Effect of paracetamol (acetaminophen) and ibuprofen on body temperature in acute ischemic stroke PISA, a phase II double-blind, randomized, placebo-controlled trial [ISRCTN98608690]

DOI: 10.1186/1471-2261-3-2

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Seventy-five patients with acute ischemic stroke confined to the anterior circulation were randomized to treatment with either 1000 mg acetaminophen, 400 mg ibuprofen, or placebo, given 6 times daily during 5 days. Treatment was started within 24 hours from the onset of symptoms. Body temperatures were measured at 2-hour intervals during the first 24 hours, and at 6-hour intervals thereafter.No difference in body temperature at 24 hours was observed between the three treatment groups. However, treatment with high-dose acetaminophen resulted in a 0.3°C larger reduction in body temperature from baseline than placebo treatment (95% CI: 0.0 to 0.6 °C). Acetaminophen had no significant effect on body temperature during the subsequent four days compared to placebo, and ibuprofen had no statistically significant effect on body temperature during the entire study period.Treatment with a daily dose of 6000 mg acetaminophen results in a small, but potentially worthwhile decrease in body temperature after acute ischemic stroke, even in normothermic and subfebrile patients. Further large randomized clinical trials are needed to study whether early reduction of body temperature leads to improved outcome.During the first days after stroke, between one and two fifths of the patients develop fever or subfebrile temperatures. [1-4] Increased temperatures have been associated with relatively large infarct volumes, high case fatality, and poor functional outcome, even after adjustment for initial stroke severity [2-6]. The period in which hyperthermia is associated with poor outcome is probably limited to the first 12 or 24 hours from stroke onset.[6,7]The harmful effects of an early rise in body temperature have been attributed to increased cerebral metabolic demands,[8] changes in the blood-brain barrier permeability, acidosis, and an increased release of excitatory amino acids.[9] In animal models of temporary focal cerebral ischemia, mild intra-ischemic hyperthermia increased infa


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