凯时与生长抑素联合应用治疗重症急性胰腺炎的临床研究

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目的评价凯时(LipoPGE1)和生长抑素(SS)联合应用对重症急性胰腺炎(SAP)的治疗效果, 并试图揭示两者联合应用的作用机制。方法依据Ranson标准、APACHEⅡ评分或Balthazar CT积分,将确诊为SAP的患者分为SS治疗组和SS联合LipoPGE1治疗组,对比观察临床症状的缓解和血清学指标的变化情况。结果两组患者入院时年龄、性别、病因构成及SAP严重度评分诸方面差异均无显著性。与单用 SS治疗组相比,SS联合LipoPGE1治疗组患者的血清白蛋白于入院2周后显著升高,但血清淀粉酶和乳酸脱氢酶(LDH)活性于治疗后无明显差别;自入院后第3天开始,血浆MDA显著降低、SOD显著升高、肿瘤坏死因子TNF-α及白细胞介素IL-6水平明显降低;血清胰岛素样生长因子(IGF-1)水平于入院后2周显著升高;APACHEⅡ评分及Binder合并症积分明显改善;并发症和平均住院时间明显缩短,死亡率降低。住院费用两组差异无显著性。结论 SS和LipoPGE1联合应用可显著改善SAP患者的预后,缩短住院时间,其可能的作用机制是通过减轻急性期炎症介质和细胞因子的过度释放、减轻过氧化反应、促进IGF-1释放, 促进胰腺细胞的再生等多途径阻断SAP时的高应激反应,避免并发多器官功能障碍。 Objective To evaluate the therapeutic effect of combined use of LipoPGE1 and somatostatin (SS) on severe acute pancreatitis (SAP), and try to reveal the mechanism of the combination of the two. Methods According to Ranson criteria, APACHE Ⅱ score or Balthazar CT score, patients diagnosed with SAP were divided into SS treatment group and SS combined with LipoPGE1 treatment group. The clinical symptoms and serological changes were observed. Results There were no significant differences in age, gender, etiology and severity of SAP on admission between the two groups. Serum albumin in SS combined LipoPGE1 group was significantly higher than that in SS group only after two weeks of admission, but serum amylase and lactate dehydrogenase (LDH) activity had no significant difference after treatment After 3 days, plasma MDA decreased significantly, SOD increased significantly, tumor necrosis factor TNF-α and interleukin IL-6 levels decreased significantly; serum insulin-like growth factor (IGF-1) Increased; APACHE Ⅱ score and Binder complications significantly improved; complications and the average hospitalization time was significantly reduced, the mortality rate decreased. There was no significant difference in hospitalization costs between the two groups. Conclusions The combination of SS and LipoPGE1 can significantly improve the prognosis and shorten the hospital stay in SAP patients. The possible mechanism is to reduce the over-release of inflammatory mediators and cytokines, reduce the peroxidation, promote the release of IGF-1, and promote the pancreas Cell regeneration and other ways to block the SAP when the high-stress response, to avoid concurrent multiple organ dysfunction.
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