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文献详情 >肝性脑病患者大脑“外周型苯二氮结合位点”的体内成像 收藏

肝性脑病患者大脑“外周型苯二氮结合位点”的体内成像

In vivo imaging of cerebral “peripheral benzodiazepine binding sites” in patients with hepatic encephalopathy

作     者:Cagnin A. Taylor-Robinson S.D. Forton D.M. Banati R.B. 陈瑜 

作者机构:School of Medical Radiation SciencesRamaciotti Centre for Brain ImagingUniversity of SydneyEast St PO Box 170LidcombeNSW 1825Australia.Prof 

出 版 物:《世界核心医学期刊文摘(胃肠病学分册)》 (Core Journals in Gastroenterology)

年 卷 期:2006年第2卷第10期

页      面:39-40页

学科分类:1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

主  题:肝性脑病 苯二氮 外周型 胶质细胞 神经甾体 苍白球 认知障碍 脑功能 壳核 特异性配体 

摘      要:Background and aim: One proposed mechanism whereby hepatic encephalopathy (HE) leads to loss of brain function is dysregulated synthesis of neurosteroids. Mitochondrial synthesis of neurosteroids is regulated by “peripheral benzodiazepine binding sites (PBBS). Expressed in the brain by activated glial cells, PBBS can be measured in vivo by the specific ligand [11C](R)-PK11195 and positron emission tomography (PET). Recently, it has been suggested that PBBS expressing glial cells may play a role in the general inflammatory responses seen in HE. Therefore, we measured PBBS in vivo in the brains of patients with minimal HE using [11C](R)-PK11195 PET. Methods: Five patients with minimal HE and biopsy proven cirrhosis of differing aetiology were assessed with a neuropsychometric battery. Regional expression of PBBS in the brain was detected by [11C](R)-PK11195 PET. Results: All patients showed brain regions with increased [11C](R)-PK11195 binding. Significant increases in glial [11C](R)-PK11195 binding were found bilaterally in the pallidum, right putamen, and right dorsolateral prefrontal region. The patient with the most severe cognitive impairment had the highest increases in regional [11C](R)-PK11195 binding. Conclusion: HE is associated with increased cerebral binding of [11C](R)-PK11195 in vivo, reflecting increased expression of PBBS by glial cells. This supports earlier experimental evidence in rodent models of liver failure, suggesting that an altered glial cell state, as evidenced by the increase in cerebral PBBS, might be causally related to impaired brain functioning in HE.

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