急性胰腺炎患者致炎与抗炎因子的变化及生长抑素的调节作用

The Effect of Somatostatin on Inflammatory and Anti-inflarnmatory Cytokines Response in Patients with Acute Pancreatitis

目的:探讨急性胰腺炎患者血浆中致炎因子肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)和抗炎因子转化细胞生长因子-β(TGF-β)、白介素-10(IL-10)的变化、意义及生长抑素的调节作用。方法:急性胰腺炎48例,随机分成生长抑素治疗组和常规治疗组,分别在治疗前(入院时)、治疗后8 h和第2、3、4 d清晨空腹抽肘静脉血3 ml,测定TNF-α、IL-6、TGF-β和IL-10,并设对照组。结果:TNF-α和IL-6各监测点均比对照组显著升高(P<0.05,P<0.01),高峰在入院时。TGF-β和IL-10入院后8 h以后各监测点均比对照组显著升高(P<0.05,P<0.01);第2天达高峰。生长素抑素治疗组TNT-α、IL-6、和TGF-β、IL-10含量治疗后8 h明显低于常规治疗组。治疗后各观察点持续降低(P<0.05,P<0.01)。结论:急性胰腺炎患者血中致炎因子与抗炎因子均升高,机体免疫功能紊乱。生长抑素对致炎因子与抗炎因子的升高有抑制作用。

Purpose: To investigate the significance of changes in inflammatory cytokines [tumor necrosis factor-α(TNF-α) , interleukin-6(IL-6)] and anti-infiammatory cytokines [ transforming growth factor-β(TGF-β), interleukin-10( IL-10) ] in plasma and to assess the effect of somatostatin on modulation of them. Methods: 48 patients diagnosed as acute pancreatitis were observed and were randomly divided into somatostatin treatment group and routine treatment group while health people were in the control one.3 ml blood was drown from every patients elbow vein and TNF-α, IL-6,TCF-β and IL-10 were de-tected respectively at the time of admission before the treatment,at the 8th hour,in the 2nd,3rd,and 4th days after the treatment. Results: TNF-α and 1L-6 were significantly higher in the acute pancreatitis group at every observation points than in the control group ( P < 0. 05, P < 0. 01), and their peak values appeared at the time of admission. TGF-β and IL-10 were manifestly higher from the 8th hour to 4th day in the acute pancreatitis group than in the control group (P < 0.05, P < 0.01) , and their peak values showed in the 2nd day. The contents of TNT-α, IL-6 and TGF-β , IL-10 in patients of somatostain treatment group at the 8th hour after treatment were obviously less than those in patients of routine treatment group, then persistently declined after that ( P < 0.05, P < 0.01). Conclusion: Both inflammatory cytokines and anti-inflammatory cytokines were markedly increased and immune function was disturded in acute pancreatitis. Somatostatin can modulate the disorder of these cytokines in acute pancreatitis.