Perihematoma edema: a potential translational target in intracerebral hemorrhage?
Perihematoma edema: a potential translational target in intracerebral hemorrhage?
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DOI:
10.1007/s12975-015-0389-7
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发表时间:
2015-04
影响因子:
6.9
通讯作者:
Sheth, Kevin N.
中科院分区:
文献类型:
--
作者:
Selim, Magdy;Sheth, Kevin N.
Secondary injury in intracerebral hemorrhage (ICH) is becoming increasingly well characterized and is the subject of intense investigations. After the initial injury caused by tissue disruption and mass effect of the hematoma, products of coagulation, clot retraction, and hemoglobin breakdown initiate a secondary cascade of deleterious events including apoptosis, necrosis, iron-mediated oxidative stress, inflammation, autophagy, and edema formation [1–3]. Tissue swelling, in particular, may contribute to neurological deterioration and disability.Vasogenic (extracellular) edema is most commonly described after ICH. However, there is evidence that cytotoxic (intracellular) edema also contributes, at least in part, to perihematomal edema (PHE)[4]. A number of clinical studies examined several drugs targeting these secondary processes and PHE formation over the past years [5]. These included the glycine antagonist, gavestinel [6]; the free radical trapping agent, NXY-059 [7]; citicoline [8]; mannitol and glycerol [9, 10]; the sphingosine-1-phosphate receptor agonist, fingolimod [11]; and the PPAR-γ receptor agonist, pioglitazone [12]. Currently, the iron chelator deferoxamine mesylate is being investigated in a phase II trial [13], and several other agents are in the pipeline for future clinical investigations. Unlike interventions targeting hematoma expansion where the targeted effects of therapy on ICH growth can be easily assessed in proof-of-concept pre-phase III studies, there are
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