目的 探讨胰性脑病的可能的发病机制、发病情况及防治措施.方法 计算机检索中文科技期刊全文数据库(1989～2004),收集有关胰性脑病的临床研究,并进行统计分析.结果 共纳入43篇文献,435例患者.胰性脑病在重症急性胰腺炎中的发病率远高于轻症急性胰腺炎;发病年龄趋向中、老年;病死率为43.67%;病因仍以胆系疾病为主;伴发低氧的几率不高于未并发胰性脑病患者.结论 胰性脑病的发生可能是多因素共同作用的结果,仍需进一步探讨其发病机制.血清髓鞘碱性蛋白有望成为有价值的诊断指标.防治以治疗原发病急性胰腺炎为主,重在预防.胰酶抑制剂和早期营养支持有一定预防作用.
Seventeen cases of pancreatic encephalopathy (PE) with acute pancreatitis were studied retrospectively. It was found that on the basis of brain damage caused by pancreatic enzyme, many factor might play a role in the development of PE. It suggests that PE should not be accepted as an operative indication separately in severe acute pancreatitis. Chinese medicine can benefit the patient in the treatment of this disease. Operation is the only choice while patient get worsened even after appropriate and enough nonoperative therapy, as well as while pancreatic necrosis become infected or pancreatic abcess formed. Mortality of PE in this series is 52.9%, slightly less than the level (66.7%-100%) reported by other authors.
Objective To study the effects of malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-α (TNF-α) on brain tissue in rats with pancreatic encephalopathy (PE). Methods Thirty-six Wistar rats were randomly divided into control group (n=6) and PE model group (n=30). In control group, rats were injected with normal saline by internal carotid artery (0.1 ml/100 g) and were killed on the first day after the injection. In PE model group, rats were injected with phospholipases A2 (0.1 ml/100 g, 1 000 U/0.1 ml) by internal carotid artery, to establish animal model of PE in rat and 10 rats were killed on day 1, 3, 7 respectively after the injection. The changes of water content in the brain were measured. Leucocytes aggregation and margination in the microvessels, and the changes of cerebral cells and nerve fibers were observed. The levels of MDA, TNF-α and the activity of SOD were tested in the brain homogenate in rats. Results In PE model group, water contents of brain increased; The phenomena of leucocytes accumulation and margination, cellular edema of neurons and demyelination of nerve fibers became more obvious; The levels of MDA and TNF-α increased significantly than those in the control group, while the activity of SOD reduced (P＜0．05， P＜0.01)． Conclusion Inthe rat model of PE, MDA, SOD, and TNF-α play important roles on the occurrence and development of brain injury.
ObjectiveTo discuss the changes of myelin basic protein (MBP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in serum and cerebrospinal fluid of experimental pancreatic encephalopathy rat model, analyze the relationship between each factor and the occurrence and development of pancreatic encephalopathy, and to provide the experimental basis for clinical diagnosis and treatment of pancreatic encephalopathy. MethodsSelecting 40 SD rats were randomly divided into sham operation group (SO group, n=10) and pancreatic encephalopathy group (PE group, n=30), respectively by the duodenal papilla retrograde pancreatic puncture injection of saline solution or 5% sodium taurocholic acid induced rat pancreatic encephalopathy model were set up. The rats in SO group were sacrificed on 1 d, and the PE group were sacrificed ten rats on 1 d, 3 d, and 7 d, respectively after surgery. The brain and pancreatic tissues of rats in each group were taken to observe the pathological changes of the rats and the brain white blood cells within microvessels gathered and coanda phenomenon. The water content of brain tissues, and the contents of MBP, TNF-α and TL-6 in serum and cerebrospinal fluid were detected. ResultsThe changes of brain nerve cell edema and nerve fiber demyelination were obvious in PE group rats after surgery with the extension of time. The contents of MBP, TNF-α and TL-6 in serum and cerebrospinal fluid on 1 d, 3 d, and 7 d after surgery in PE group were significantly higher than that SO group (P<0.05), and gradually increased with the extension of time. But by two two compared, the change trend of the above three indicators were different. ConclusionsMBP, TNF, and IL-6 on the occurrence and development of brain damage of pancreatic encephalopathy play a synergistic effect. To detecte the MBP, TNF-a, and IL-6 content in blood and cerebrospinal fluid could be diagnosed and evaluated the pancreatic encephalopathy.