急性胰腺炎早期肠道通透性改变与并发SIRS关系的临床研究

Clinical study on relationship between intestinal permeability alteration and acute pancreatitis associated with SIRS in early period of acute pancreatitis

目的探讨急性胰腺炎(AP)早期肠道通透性改变与AP并发全身炎症反应综合症(SIRS)的关系。方法对62例AP患者的临床资料进行前瞻性分析,将AP患者分为轻型急性胰腺炎(MAP)和重型急性胰腺炎(SAP),并按有无并发SIRS分为SIRS组与非SIRS组。另取30例健康志愿者为正常对照组。选定血清D-乳酸作为肠道通透性改变的监测指标,动态观测血清D-乳酸、血清内毒素及血清肿瘤坏死因子(TNF-α)的变化。结果SIRS在AP患者中总发生率为67.74%,其中MAP组发生SIRS为52.38%,SAP组则100.00%发生;AP并发SIRS组第1、4及7天血清D-乳酸水平均较非SIRS组明显升高,且AP发病第1天血清D-乳酸水平越高,则SIRS在AP病程中持续时间越长,程度越严重;AP发病第1、4及7天血清D-乳酸水平、内毒素含量及TNF-α活性较正常对照组明显升高,且发现病程中血清D-乳酸水平与内毒素含量及TNF-α活性之间均呈显著正相关。结论AP早期肠道通透性改变可引发SIRS的发生,推测肠道通透性改变是AP并发SIRS的重要病理因素之一。

[Objective]To investigate the relationship between intestinal permeability alteration and acute panereatitis （AP） associated With systemic inflammatory response syndrome （SIRS） in the early period of AP. [Methods] A prospective analysis was made in 62 patients with AP, by dividing the patients into mild acute pancreatitis （MAP） and severe acute pancreatitis （SAP）. All the cases were divided into SIRS group and non-SIRS group. 30 healthy people were selected as control group. Serum D-lactic acid was selected as monitoring index of intestinal permeability alteration and the change of serum D-lactic acid, endotoxin and TNF-ct were dynamiely observed. [Results] The total incidence of SIRS in AP group was 67.74%, of the total, the incidence of SIRS in MAP group was 52.38%, and it was 100% in SAP group. The serum D-lactic acid of SIRS group was signifandy higher than that of non-SIRS group and higher the level of D-lactic acid, longer the duration of SIRS, and more severe the degree of SIRS. The level of serum D-lactic acid, endotoxin and TNF-α of SIRS group was obviously higher than that of control group, and the serum D-lactic acid showed significant direct correlation with the level of endotoxin and TNF-α [ Conclusion] Intestinal permeability alteration could induce the ensuing SIRS in early period of AP. Intestinal permeability alteration could be one of the important pathological factor of the ensuing SIRS during the course of AP.