Pentoxifylline in the treatment of acute ischaemic stroke--a reappraisal in Chinese stroke patients. Pentoxifylline in acute nonhemorrhagic stroke. A randomized, placebo-controlled double-blind trial. Effect of propentofylline on regional cerebral glucose metabolism in acute ischemic stroke.
A double-blind, randomized and placebo-controlled trial was conducted on 110 Chinese patients with ischaemic stroke who were stratified into 2 subtypes (cortical and lacunar infarcts) according to their clinical and CT findings. Treatment was started within 36-48 hours after the stroke onset. Pentoxifylline was administered intravenously in a dose of 600 mg daily for 5 days, together with oral aspirin 150 mg daily. Neurological deficits were scored on admission and at one week. Demographic data were comparable between the treatment and placebo groups. For cortical infarcts, there were significantly more patients in the placebo group who deteriorated and died than in the treatment group (p < 0.02). As for the lacunar infarcts, there was no difference between groups in the numbers of patients who improved or deteriorated. Our study shows that the positive effect of pentoxifylline can be demonstrated only in patients with cortical infarction. Early deterioration and mortality were significantly decreased in these patients. The clinical course of lacunar infarction was not affected by pentoxifylline. It is not clear whether aspirin may potentiate the antiplatelet function of pentoxifylline and contribute to its temporary clinical efficacy in this way. The efficacy and safety of pentoxifylline were assessed in 297 adult patients with ischemic stroke in a multicenter, double-blind, randomized and placebo-controlled trial. Treatment was started within 12 hours after the stroke onset. Study medication was administered intravenously continuously (16 mg/kg/day, maximum 1,200 mg/day) for 3 days and per os (400 mg t.i.d.) for the remainder of 28 days. Demographic data were comparable, and functional impairment and mortality (pentoxifylline 12%, placebo 10%) were not different between the two groups. Neurologic deficit scores improved from baseline admission scores during the 4-week study in both groups but did not differ between groups at admission or throughout the study except during the first few days when the consciousness level (Days 1 and 2), motor function (Days 1 and 2), cranial nerve function (Days 1-4), and total neurologic deficit scores (Days 1 and 2) were better in the pentoxifylline group than in the placebo group, especially in a subset of patients with severe deficits at admission. Laboratory values and side effects were also comparable between groups. Our study indicates that pentoxifylline can be given safely in patients with acute ischemic stroke. Although pharmacologic effects were present during the first few days, the clinical benefits were small and not sustained. In a randomized double-blind placebo-controlled study in 30 patients with acute ischemic stroke, the effect of the adenosine uptake blocker propentofylline on regional brain glucose metabolism (rCMRglu) was investigated using repeated positron emission tomography (PET) with 2-[18F]fluoro-2-deoxy-D-glucose (FDG). Treatment was initiated within 48 h after onset of symptoms. The clinical course was followed for 3 months. In the propentofylline group, after 14 days rCMRglu was increased in the infarct by 37.3% and was practically unchanged in other brain regions, whereas in the control group glucose metabolism had decreased in all regions (1.4-13.4%). These differences were significant between the two groups [Analysis of variance (ANOVA) p = 0.005]. Although there was a trend toward greater clinical improvement in the propentofylline-treated patients, this did not reach statistical significance. The results correspond to experimental data showing that propentofylline improves energy metabolism in cerebral ischemia. A clinical trial is needed to determine whether this new therapeutic principle can be successfully used in acute human stroke.
There is not enough evidence to assess adequately the effectiveness and safety of methylxanthines after acute ischaemic stroke.