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目的探讨重症急性胰腺炎(SAP)脓毒症的发生与肠道细菌易位、炎症及免疫抑制的关系。方法 2012年3月-2016年10月本院重症医学科收治的SAP患者160例,按脓毒症诊断标准分为脓毒症组(63例)和非脓毒症组(97例)。采集患者胰腺周围渗液进行细菌培养,同时留取尿液及血液标本用于肠粘膜通透性、炎症及免疫相关指标的检测。结果 160例SAP患者胰腺周围渗液中共分离出225株细菌,主要为革兰阴性菌(81.78%),包括大肠埃希菌、铜绿假单胞杆菌、产气杆菌、肺炎克雷伯菌,革兰阳性菌(18.22%)包括金黄色葡萄球菌、表皮葡萄球菌和肠球菌,脓毒症和非脓毒症组细菌构成基本一致;脓毒症组患者血清内毒素(ET)[(0.62±0.06)EU/ml]、肿瘤坏死因子α(TNF-α)[(4.44±0.07)g/L]、白细胞介素1β(IL-1β)[(1.86±0.22)μg/L、IL-6(239.40±38.93)]、IL-8[(0.55±0.12)μg/L]水平,乳果糖与甘露醇排泄率比值(L/M)(0.54±0.08)以及外周血调节性T细胞(Treg)水平[(10.64±1.50)%]均显著高于非脓毒症组(P<0.05),T辅助淋巴细胞1/2(Th1/Th2)值(0.84±0.34)低于非脓毒症组(P<0.05)。结论 SAP脓毒症的发生与肠源性细菌易位、炎症因子的过度释放及免疫抑制等因素所导致的肠屏障功能受损密切相关。
Objective To investigate the relationship between intestinal bacterial translocation, inflammation and immunosuppression in sepsis of severe acute pancreatitis (SAP). Methods From March 2012 to October 2016, 160 SAP patients admitted to the Department of Critical Care Medicine of our hospital were divided into sepsis group (63 cases) and non-sepsis group (97 cases) according to sepsis diagnostic criteria. Peripheral fluid from pancreas was collected for bacterial culture, and urine and blood samples were collected for detection of intestinal mucosal permeability, inflammation and immune related indicators. Results A total of 225 strains of bacteria were isolated from the peripancreatic fluid of the pancreas in 160 SAP patients, mainly including gram-negative bacteria (81.78%), including Escherichia coli, Pseudomonas aeruginosa, Aerobacter aerogenes, Klebsiella pneumoniae, Staphylococcus aureus, Staphylococcus epidermidis and Enterococcus were the same in the group of Langerhans bacteria (18.22%). The bacteria in sepsis group and non-sepsis group were basically the same in constitution. Serum endotoxin (ET) in patients with sepsis [(0.62 ± 0.06 ) EU / ml], IL-1β [(1.86 ± 0.22) μg / L, IL-6 [239.40 ± 38.93, IL-8 [(0.55 ± 0.12) μg / L], lactate to mannose excretion ratio (0.54 ± 0.08) and the level of Treg in peripheral blood [ (10.64 ± 1.50)%] were significantly higher than those in non - sepsis group (P <0.05), and the Th1 / Th2 (0.84 ± 0.34) T lymphocyte subsets were lower than those in non - sepsis group (P < 0.05). Conclusions The occurrence of SAP sepsis is closely related to impaired intestinal barrier function caused by factors such as intestinal bacterial translocation, excessive release of inflammatory cytokines and immunosuppression.