García-Urkia N, Asensio A B, Cano A, Samprón N, García-Arenzana J M, Bachiller P, Aldazabal P, Eizaguirre I
Unidad Experimental, Hospital Donostia, San Sebastián.
Cir Pediatr. 2006 Jul;19(3):147-50.
Selective intestinal decontamination (SID) has been useful restraining Bacterial translocation (BT) in both animal models and human clinics. The not well known parenteral nutrition-related liver disease is a serious problem associated to short bowel and long-term parenteral nutrition (PN) use, and BT is also frequent in those patients. Germs reach liver through portal vein and activate Kupffer cells, which release cytokines as IL-1 or TNF-alpha. The aim of this study was to test the use of SID restraining BT in a PN undergoing experimental short bowel model, and its possible favourable consequences on hepatic injury determined by IL-1 and TNF-alpha levels. Twenty-five 240-280 g Wistar rats were divided into two groups and maintained in individual metabolic cages for ten days: Resection-PN group (n=15): animals with a bowel resection of the 80% and a continuous PN infusion. Resection-PN-SID (n=10) group: similar to previous group and a daily oral administration of Tobramycine (20mg/kg/day) and Polymyxine-E (25mg/kg/day). Animals were sacrificed and mesenteric lymph nodes (MLN), and both peripheral and portal blood samples were recovered for TB determination in bacterial culture. Determination of both IL-l and TNF-alpha seric levels were carried out by ELISA. Bacterial translocation incidence was higher in RES-NPT group (66.6%) than RES-NPT-SID group (30%) (P>0,05). The relative risk was 2.22 (IC 95% 0,81-6,11) and the number needed to treat was 3 (IC 95% 2-235). Seric levels of IL-1 and TNF-alpha were also higher in RES-NPT group (7,537 and 5,399 pg/ml, respectively) than in RES-NPT-SID group (6,397 and 5,032 pg/ml respectively) (p<0,001). 1. SID reduces TB in a PN undergoing experimental short bowel resection murine model. 2. Parenteral nutrition-related liver disease decreases in DIS receiving animals.
选择性肠道去污（SID）在动物模型和人类临床中对抑制细菌移位（BT）均有作用。肠外营养相关肝病这一鲜为人知的问题与短肠及长期使用肠外营养（PN）相关，且这些患者中细菌移位也很常见。细菌通过门静脉到达肝脏并激活库普弗细胞，库普弗细胞会释放如白细胞介素-1或肿瘤坏死因子-α等细胞因子。本研究的目的是在接受肠外营养的实验性短肠模型中测试SID抑制细菌移位的作用，以及其对由白细胞介素-1和肿瘤坏死因子-α水平所确定的肝损伤可能产生的有利影响。将25只体重240 - 280克的Wistar大鼠分为两组，并在个体代谢笼中饲养10天：切除 - PN组（n = 15）：进行80%肠切除并持续输注肠外营养的动物；切除 - PN - SID组（n = 10）：与前一组相似，但每日口服妥布霉素（20毫克/千克/天）和多粘菌素 - E（25毫克/千克/天）。处死动物后，回收肠系膜淋巴结（MLN）以及外周血和门静脉血样本，用于细菌培养中的细菌定量测定。通过酶联免疫吸附测定法（ELISA）测定血清白细胞介素 - 1和肿瘤坏死因子-α水平。切除 - PN组的细菌移位发生率（66.6%）高于切除 - PN - SID组（30%）（P>0.05）。相对风险为2.22（95%置信区间0.81 - 6.11），治疗所需人数为3（95%置信区间2 - 235）。切除 - PN组的血清白细胞介素 - 1和肿瘤坏死因子-α水平（分别为7537和5399皮克/毫升）也高于切除 - PN - SID组（分别为6397和5032皮克/毫升）（p<0.001）。1. SID可降低接受肠外营养的实验性短肠切除小鼠模型中的细菌定量。2. 接受SID的动物中肠外营养相关肝病有所减轻。
