Kimmings A N, van Deventer S J, Obertop H, Rauws E A, Huibregtse K, Gouma D J
Department of Surgery, Academic Medical Centre, Amsterdam, The Netherlands.
Gut. 2000 May;46(5):725-31. doi: 10.1136/gut.46.5.725.
Obstructive jaundice is associated with postoperative complications related to increased endotoxaemia and the inflammatory response. In animals obstructive jaundice is associated with endotoxaemia and cytokine induction, which are reversed by internal biliary drainage.
To study endotoxaemia and the subsequent inflammatory response in obstructive jaundiced patients and after endoscopic biliary drainage.
In 15 patients with malignant distal obstructive jaundice, inflammatory and bacteriological parameters were assessed before endoscopic stent placement and after three weeks endoscopic drainage.
Drainage reduced bilirubin from 252.5 to 45.1 micromol/l. At baseline low level endotoxaemia was detected (4.3 pg/ml) which was not affected after drainage (4.5 pg/ml). Serum interleukin 8 (IL-8) and endotoxin binding proteins were increased in jaundice and reduced after drainage (IL-8 113.6 to 20.7 pg/ml; lipopolysaccharide binding protein 24.2 to 16.5 microg/ml; sCD14 17.4 to 7.6 microg/ml; bactericidal/permeability increasing protein 2.9 to 1.8 ng/ml). Levels of other cytokines, augmented in animals, were only slightly increased and not changed after drainage (tumour necrosis factor (TNF): 21.7 and 18.4 pg/ml; sTNFr p55/75: 2.9/7.0 and 2.7/5.6 ng/ml; IL-6: 4.2 and 6.1 pg/ml; IL-10: 4.5 and 2.7 pg/ml). Elastase and lactoferrin tended towards reduction after drainage. All bile cultures were positive after stenting.
The effects of obstructive jaundice in humans on endotoxin and cytokines are different from those in animal models. Obstructive jaundice causes alterations in circulating endotoxin binding proteins and IL-8. Concentrations of other mediators (TNF, previously suggested as being responsible for systemic endotoxaemia effects) are low and not affected by drainage.
梗阻性黄疸与内毒素血症增加及炎症反应相关的术后并发症有关。在动物中,梗阻性黄疸与内毒素血症和细胞因子诱导有关,而经内镜胆管引流可逆转这些情况。
研究梗阻性黄疸患者及内镜胆管引流后的内毒素血症及随后的炎症反应。
对15例远端恶性梗阻性黄疸患者,在内镜下放置支架前及内镜引流3周后评估炎症和细菌学参数。
引流后胆红素从252.5微摩尔/升降至45.1微摩尔/升。基线时检测到低水平内毒素血症(4.3皮克/毫升),引流后未受影响(4.5皮克/毫升)。血清白细胞介素8(IL-8)和内毒素结合蛋白在黄疸时升高,引流后降低(IL-8从113.6皮克/毫升降至20.7皮克/毫升;脂多糖结合蛋白从24.2微克/毫升降至16.5微克/毫升;可溶性CD14从17.4微克/毫升降至7.6微克/毫升;杀菌/通透性增加蛋白从2.9纳克/毫升降至1.8纳克/毫升)。在动物中升高的其他细胞因子水平仅略有升高,引流后无变化(肿瘤坏死因子(TNF):21.7和18.4皮克/毫升;可溶性TNF受体p55/75:2.9/7.0和2.7/5.6纳克/毫升;IL-6:4.2和6.1皮克/毫升;IL-10:4.5和2.7皮克/毫升)。引流后弹性蛋白酶和乳铁蛋白有降低趋势。支架置入后所有胆汁培养均为阳性。
人类梗阻性黄疸对内毒素和细胞因子的影响与动物模型不同。梗阻性黄疸导致循环内毒素结合蛋白和IL-8发生改变。其他介质(TNF,先前认为是全身内毒素血症效应的原因)浓度较低,且不受引流影响。