Abstract
Intracerebral hemorrhage (ICH) is a subtype of stroke associated with high morbidity and mortality rates. No proven treatments are available for this condition. Iron-mediated free radical injury is associated with secondary damage following ICH. Deferoxamine (DFX), a ferric-iron chelator, is a candidate drug for the treatment of ICH. We performed a systematic review of studies involving the administration of DFX following ICH. In total, 20 studies were identified that described the efficacy of DFX in animal models of ICH and assessed changes in the brain water content, neurobehavioral score, or both. DFX reduced the brain water content by 85.7% in animal models of ICH (-0.86, 95% CI: -.48- -0.23; P < 0.01; 23 comparisons), and improved the neurobehavioral score by -1.08 (95% CI: -1.23- -0.92; P < 0.01; 62 comparisons). DFX was most efficacious when administered 2–4 h after ICH at a dose of 10–50 mg/kg depending on species, and this beneficial effect remained for up to 24 h postinjury. The efficacy was higher with phenobarbital anesthesia, intramuscular injection, and lysed erythrocyte infusion, and in Fischer 344 rats or aged animals. Overall, although DFX was found to be effective in experimental ICH, additional confirmation is needed due to possible publication bias, poor study quality, and the limited number of studies conducting clinical trials.
Highlights
Intracerebral hemorrhage (ICH) is associated with ~15% of all strokes and exhibits high morbidity and mortality[1]
Clinical studies have shown that an increased level of serum ferritin after ICH is closely related to exacerbation of brain edema and poor patient outcomes[7,8]
This review examines the impact of study quality and various study characteristics on effect size to determine whether the currently available evidence from animal experiments supports the therapeutic use of DFX for ICH
Summary
Intracerebral hemorrhage (ICH) is associated with ~15% of all strokes and exhibits high morbidity and mortality[1]. Nonheme iron catalyzes free radical formation, which is the critical hub in the toxic cascade causing brain edema, neuronal death, brain atrophy, and poor neurologic outcomes after ICH[4,5,6]. As a potent iron chelator, deferoxamine (DFX) has great potential to prevent poststroke injury caused by iron overload and iron-mediated toxicity[10]. Positive results of DFX treatment have been reported, including reductions in iron accumulation and brain edema, as well as improvements in neurologic outcomes[11,12,13]. Found that DFX treatment reduced neuronal loss and improved neurologic function, but did not reduce brain injury volume, edema, or swelling in ICH mice.
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