Serum endotoxin and inflammatory mediators in patients with cirrhosis and hepatic encephalopathy

被引:52
|
作者
Jain, Lokesh [1 ]
Sharma, Barjesh Chander [1 ]
Sharma, Praveen [2 ]
Srivastava, Siddharth [1 ]
Agrawal, Amit [1 ]
Sarin, Shiv Kumar [2 ]
机构
[1] GB Pant Hosp, Dept Gastroenterol, New Delhi 110002, India
[2] ILBS, Dept Hepatol, New Delhi, India
关键词
IL-6; IL-18; TNF-alpha; TUMOR-NECROSIS-FACTOR; CHRONIC LIVER-FAILURE; FACTOR-ALPHA; INDUCED HYPERAMMONEMIA; IBUPROFEN RESTORES; PORTACAVAL SHUNTS; RATS; AMMONIA; PATHOGENESIS; NEUROINFLAMMATION;
D O I
10.1016/j.dld.2012.07.002
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Recent observations suggest that inflammatory response may be important in the pathogenesis of hepatic encephalopathy. The aim of the study was to measure arterial ammonia, tumour necrosis factor-alpha, Interleukin-6, Interleukin-18, and serum endotoxin levels and their correlation with different grades of hepatic encephalopathy. Methods: 120 patients with cirrhosis were enrolled: 20 patients each of cirrhosis with grades I. II, III and IV hepatic encephalopathy, cirrhosis with and without minimal hepatic encephalopathy and healthy controls were tested for arterial ammonia, tumour necrosis factor-alpha, Interleukin-6, Interleukin-18 and serum endotoxin levels. Results: Median arterial ammonia, tumour necrosis factor-alpha, Interleukin-6, Interleukin-18 and serum endotoxin levels were significantly higher in patient with hepatic encephalopathy and minimal hepatic encephalopathy as compared to patients without minimal hepatic encephalopathy and healthy controls. Arterial ammonia (r=0.72. p=0.03), tumour necrosis factor alpha (r=0.87, p=0.02), Interleukin-6 (r=0.50, p=0.05), Interleukin-18 (r=0.76, p=0.02) and serum endotoxin (r=0.91, p=0.01) correlated with higher grades of hepatic encephalopathy. Conclusion: In hepatic encephalopathy arterial ammonia, inflammatory mediators, and serum endotoxin are elevated and correlate with encephalopathy grade. (C) 2012 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:1027 / 1031
页数:5
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