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创伤性脑损伤患者血肿周围水肿形成延迟进展,该血肿表达高水平血管内皮生长因子(VEGF)和基质金属蛋白酶-9(MMP-9):病例报告

Delayed progression of edema formation around a hematoma expressing high levels of VEGF and mmp-9 in a patient with traumatic brain injury: case report.

作者信息

Hirose Tomoya, Matsumoto Naoya, Tasaki Osamu, Nakamura Hajime, Akagaki Fuyuko, Shimazu Takeshi

机构信息

Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine.

出版信息

Neurol Med Chir (Tokyo). 2013;53(9):609-12. doi: 10.2176/nmc.cr2012-0342.

DOI:10.2176/nmc.cr2012-0342
PMID:24067772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4508685/
Abstract

The mechanisms accounting for the development of tissue damage following traumatic brain injury (TBI) have been studied for several decades. A variety of mediators, such as vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9), which play a crucial role in edema formation after TBI, have been identified. We experienced a case of brain edema that progressed continuously at least until 13 days after head injury. The brain edema occurred around the hemorrhage from an intracerebral contusion. The evacuated hematoma was investigated based on the inference that the unexpected expansion of edema was induced by the mediators within the hematoma itself. A 64-year-old woman was admitted to our hospital following a traffic injury. Left brain contusion was revealed by head computed tomography (CT) on admission. Three hours later, formation of an intracerebral hematoma became evident. Serial CT examination revealed that brain edema had developed progressively till 13 days after the injury. A hematoma removal operation was performed on Day 13. The hematoma was centrifuged and the supernatant was analyzed for the expression of VEGF and MMP-9. The values of both (4400 pg/ml and 920 ng/ml, respectively) were extremely high compared with values reported previously in serum and cerebrospinal fluid collected from patients with intracranial infection or injury. This case suggested that the delayed exacerbation of edema following traumatic intracranial hemorrhage was possibly induced by secretory factors such as VEGF and MMP-9 released from within and around the hematoma.

摘要

几十年来,人们一直在研究创伤性脑损伤(TBI)后组织损伤发展的机制。已经确定了多种介质,如血管内皮生长因子(VEGF)和基质金属蛋白酶-9(MMP-9),它们在TBI后的水肿形成中起关键作用。我们遇到了一例脑水肿病例,该病例至少在头部受伤后13天持续进展。脑水肿发生在脑挫裂伤出血周围。基于血肿内介质诱发意外水肿扩展的推断,对清除的血肿进行了研究。一名64岁女性因交通伤入院。入院时头部计算机断层扫描(CT)显示左侧脑挫裂伤。三小时后,脑内血肿形成明显。系列CT检查显示,脑水肿在受伤后13天逐渐发展。在第13天进行了血肿清除手术。将血肿离心,分析上清液中VEGF和MMP-9的表达。与先前报道的从颅内感染或损伤患者收集的血清和脑脊液中的值相比,两者的值(分别为4400 pg/ml和920 ng/ml)极高。该病例表明,创伤性颅内出血后水肿的延迟加重可能是由血肿内部和周围释放的VEGF和MMP-9等分泌因子诱发的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e88d/4508685/4429f4524936/nmc-53-609-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e88d/4508685/33fe6c5adb7f/nmc-53-609-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e88d/4508685/4429f4524936/nmc-53-609-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e88d/4508685/33fe6c5adb7f/nmc-53-609-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e88d/4508685/4429f4524936/nmc-53-609-g2.jpg

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