期刊文献+

急性胰腺炎的实验室检查改变及治疗 被引量:4

Laboratory Changes and the Treatment of Acute Pancreatitis
暂未订购
导出
摘要 目的:分析急性胰腺炎患者的肝肾功能损害、血脂改变以及其临床意义和治疗方法。方法:回顾分析358例急性胰腺炎患者的肝肾功能及血脂情况,对比病因和两型胰腺炎对肝肾功能损害的差异和预后,以及血脂与胰腺炎的因果关系,探讨其发生机制和药物治疗。结果:重型胰腺炎患者的肝肾功能损害比例及预后时间与轻型患者存在显著差异;伴有血脂异常的胰腺炎患者的TG、TC、LDL-C升高,而HDL-C降低,与无血脂改变组有显著差异。高甘油三酯性胰腺炎患者的甘油三酯浓度异常增高,血浆置换治疗有效。结论:高甘油三酯血症可能诱发或加重急性胰腺炎;急性胰腺炎可能导致一过性血脂增高;重型胰腺炎合并肝肾功能损害几率较高,随病情的发展可演变为多器官功能衰竭,增加死亡率;酶抑制剂和生长抑素用于急性胰腺炎疗效较好。 OBJECTIVE:To analyze functional lesion of the liver and the kidney, changes of blood fat, its clinical significance and the treatment. METHODS : To retrospect and analyze the functions of the liver and the kidney and blood fat of 358 patients with acute pancreatitis(AP), compare etiopathogenisis and the difference of functional lesion of the liver and the kidney and prognosis in two type of pancreatitis, and discuss causal relation between blood fat and pancreatitis and its possible mechanism of genesis. RESULTS:There was a notable difference between severe pancreatitic patients and mild pancreatitic patients in proportion of functional lesion of the liver and the kidney and prognosis time. TG, TC, LDL - C increased but HDL- C decreased in pancreatitic patients with abnormal blood fat, this was obviously different from that in the patients without abnormality of the blood fat. Concentration of TG greatly increased in pancreatitic patients with High TG, plasmapheresis obtained good result. CONCLUSION: Hypertriglyceridemia can induce or aggravate AP; AP can lead to transient increase of the blood fat ; Severe pancreatitis has high probability of complicating functional lesion of the liver and the kidney, it can develop into multiple organ failure with increased mortality. Enzyme inhibitor and somatostatin are used to treat AP and the effect is good.
作者 崔西玉 刘欣
出处 《中国医院用药评价与分析》 2005年第4期244-247,共4页 Evaluation and Analysis of Drug-use in Hospitals of China
关键词 急性胰腺炎 肝肾功能 甘油三酯 血脂 酶抑制剂 生长抑素 acute pancreatitis functions of the liver and the kidney TG blood fat enzymeinhibitor somatostatin
  • 相关文献

参考文献7

二级参考文献11

共引文献75

同被引文献25

引证文献4

二级引证文献14

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部