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目的评估阿托伐他汀对急性轻型胰腺炎患者的疗效及其机制。方法收集235例急性胰腺炎患者,将Ranson评分低于3分患者定义为急性轻型胰腺炎,共116例,将患者随机分为对照组及治疗组,分别给予安慰剂(20mg/qn,口服)及阿托伐他汀(20mg/qn,口服),共7d。分别于入院时,第3天及第7天评估患者外周血白细胞总数、谷草转氨酶、尿素氮、总胆固醇、C-反应蛋白和降钙素原水平,同时行腹部增强CT扫描,采用CT严重指数评估两组患者胰腺炎症及渗出情况。结果第3天时,治疗组患者血浆C-反应蛋白明显低于对照组(P<0.05),而白细胞总数、降钙素原及CT严重指数虽优于对照组,但差异无统计学意义;第7天时,治疗组患者外周血白细胞总数、C-反应蛋白、降钙素原水平明显低于对照组(P<0.05),且共有8例患者由CTSIⅡ级改善为Ⅰ级,而对照组仅有4例(P<0.05);两组患者谷草转氨酶、尿素氮和总胆固醇比较,差异无统计学意义。结论阿托伐他汀能够改善急性轻型胰腺炎患者全身及局部胰腺组织的炎症反应,其机制可能与阿托伐他汀能够下调C-反应蛋白及降钙素原表达有关。
Objective To evaluate the efficacy and mechanism of atorvastatin in patients with acute mild pancreatitis. Methods A total of 235 patients with acute pancreatitis were enrolled in this study. A total of 116 patients with acute pancreatitis with Ranson score less than 3 were randomly divided into control group and treatment group. The patients were given placebo (20 mg / qn orally) And atorvastatin (20 mg / qn, po) for a total of 7 days. Peripheral white blood cells, aspartate aminotransferase, urea nitrogen, total cholesterol, C-reactive protein and procalcitonin levels were assessed at admission, on day 3 and day 7, respectively, and abdominal enhanced CT scan was performed at the same time. CT severity index Pancreatic inflammation and exudation were assessed in both groups. Results On the third day, the plasma C-reactive protein in the treatment group was significantly lower than that in the control group (P <0.05), while the total number of leukocytes, procalcitonin and CT severity index were better than the control group, but the difference was not statistically significant; At 7 days, the total number of leukocytes, C-reactive protein and procalcitonin in the treatment group were significantly lower than those in the control group (P <0.05), and a total of 8 patients improved from grade CTSI to grade Ⅰ, while the control group only 4 cases (P <0.05). There was no significant difference in aspartate aminotransferase, urea nitrogen and total cholesterol between the two groups. Conclusions Atorvastatin can ameliorate systemic and local pancreatic inflammation in patients with acute mild pancreatitis. The mechanism of atorvastatin may be related to the downregulation of C-reactive protein and procalcitonin.