Noncirrhotic portal vein thrombosis exhibits neuropsychological and MR changes consistent with minimal hepatic encephalopathy
Noncirrhotic portal vein thrombosis exhibits neuropsychological and MR changes consistent with minimal hepatic encephalopathy
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DOI：
10.1002/hep.21126
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发表时间：
2006-04-01
期刊：
影响因子：
13.5
通讯作者：
Córdoba, J
中科院分区：
文献类型：
--
作者：
Mínguez, B;García-Pagán, JC;Córdoba, J
肝性脑病可以在没有内在肝病的情况下由门体分流引起。然而，对这种形式的脑病的描述很少。门静脉血栓形成是一种罕见的疾病，导致门体分流。在门静脉血栓形成的患者中曾描述过发作性肝性脑病，但尚不清楚这些患者是否会发生轻微的肝性脑病。我们设计了一项研究，以探讨门静脉血栓形成的神经系统的后果，在病人没有肝硬化和临床症状的脑病。为此，10例患者进行了神经心理学测试，口服谷氨酰胺激发试验，和脑磁共振（MR）成像。并与10例健康对照者进行比较。门静脉血栓形成患者的神经心理学测试、口服谷氨酰胺激发试验和MR结果异常，与肝硬化相关肝性脑病相似。磁共振波谱显示肌醇减少和谷氨酰胺增加。谷氨酰胺的增加与口服谷氨酰胺激发试验后氨的增加、脑水增加的体征（磁化转移率降低）和注意力试验受损相关。总之，非肝性门静脉血栓形成患者发生亚临床神经系统异常，并伴有轻微肝性脑病。这些障碍，其中包括增加的迹象，脑水和补偿性渗透反应（减少脑肌醇），似乎是继发于脑暴露于氨门体分流诱导。
Hepatic encephalopathy can a-rise from portal-systemic shunting in the absence of intrinsic liver disease. However, there are few descriptions of this form of encephalopathy. Portal vein thrombosis is an infrequent disease that causes portal-systemic shunting. Episodic hepatic encephalopathy has been described in patients with portal vein thrombosis, but it is not known if these patients develop minimal hepatic encephalopathy. We designed a study to investigate the neurological consequences of portal vein thrombosis in patients without cirrhosis and no clinical signs of encephalopathy. For this purpose, 10 patients underwent neuropsychological tests, an oral glutamine challenge test, and brain magnetic resonance (MR) imaging. The results were compared with those obtained in 10 healthy controls. Patients with portal vein thrombosis exhibited abnormalities in the results of neuropsychological tests, oral glutamine challenge test, and MR similar to those described in hepatic encephalopathy associated with cirrhosis. MR spectroscopy revealed a decrease in myoinositol and an increase in glutamine. The increase in glutamine correlated with an increase in ammonia following the oral glutamine challenge test, signs of increased brain water (decrease in magnetization transfer ratio), and impairment of attention tests. In conclusion, patients with noncirrhotic portal vein thrombosis develop subclinical neurological abnormalities compatible with minimal hepatic encephalopathy. These disturbances, which include signs of increase in brain water and a compensatory osmotic response (decrease in brain myo-inositol), appear to be secondary to brain exposure to ammonia induced by portal-systemic shunting.