Vromen A, Spira R M, Bercovier H, Berry E, Freund H R
Department of Surgery, Hebrew University Hadassak Medical School, Jerusalem, Israel.
JPEN J Parenter Enteral Nutr. 1997 Jul-Aug;21(4):233-4. doi: 10.1177/0148607197021004233.
We suggested that the continuous translocation of endotoxin from Gram-negative bacterial overgrowth during bowel rest and total parenteral nutrition (TPN) causes the release of tumor necrosis factor (TNF), resulting in liver damage and hepatic dysfunction. Because TPN-induced hepatic steatosis was significantly reduced by the monoclonal antibodies against TNF, we attempted a more clinically applicable approach using pentoxifylline and thalidomide.
A control group (group I) fed rat chow and four groups of rats receiving TPN were studied. Group II received TPN only; group III, TPN and 100 mg/kg/d pentoxifylline; group IV, TPN and 200 mg/kg/d pentoxifylline; and group V, TPN and 5 mg/kg/d thalidomide. On day 7, total liver fat was determined.
Bowel rest and TPN resulted in a significant (p < .0005) increase in liver fat content that was unaltered by either pentoxifylline or thalidomide.
Our results show no role for pentoxifylline or thalidomide in reducing TPN-associated hepatic steatosis.
我们曾提出，在肠道休息和全胃肠外营养（TPN）期间，革兰氏阴性菌过度生长导致内毒素持续移位，从而引起肿瘤坏死因子（TNF）释放，进而导致肝损伤和肝功能障碍。由于抗TNF单克隆抗体可显著减轻TPN诱导的肝脂肪变性，我们尝试采用更具临床适用性的方法，即使用己酮可可碱和沙利度胺。
研究一组喂食大鼠饲料的对照组（I组）和四组接受TPN的大鼠。II组仅接受TPN；III组接受TPN和100mg/kg/d己酮可可碱；IV组接受TPN和200mg/kg/d己酮可可碱；V组接受TPN和5mg/kg/d沙利度胺。在第7天，测定肝脏总脂肪含量。
肠道休息和TPN导致肝脏脂肪含量显著增加（p<.0005），己酮可可碱或沙利度胺对此均无影响。
我们的结果表明，己酮可可碱或沙利度胺在减轻TPN相关肝脂肪变性方面不起作用。
