Lepper P M, Held T K, Schneider E M, Bölke E, Gerlach H, Trautmann M
Dept. of Medical Microbiology and Hygiene, University Hospital, Steinhövelstr. 9, 89075 Ulm, Germany.
Intensive Care Med. 2002 Jul;28(7):824-33. doi: 10.1007/s00134-002-1330-6. Epub 2002 May 30.
Antibiotic-induced release of bacterial cell wall components can have immediate adverse effects for the patient. This article reviews the data on endotoxin release after initiation of antibiotic therapy and its role in the pathogenesis of sepsis and septic shock. Antibiotics differ in their potential to liberate endotoxins from bacterial cell walls. When used for treatment of systemic Gram-negative infection, some classes of beta-lactam antibiotics lead to markedly increased levels of free endotoxins while treatment with carbapenems and aminoglycosides produces relatively low amounts of endotoxins. Antibiotics that induce the formation of long, aberrant bacterial cells before effectively killing the microorganisms show the highest degree of endotoxin liberation. There is increasing evidence from animal models and clinical studies of sepsis that the antibiotic-mediated release of biologically active cell wall components derived from Gram-positive, Gram-negative or fungal organisms is associated with a rapid clinical deterioration.
抗生素诱导的细菌细胞壁成分释放可能会对患者产生直接不良影响。本文综述了抗生素治疗开始后内毒素释放的数据及其在脓毒症和脓毒性休克发病机制中的作用。不同抗生素从细菌细胞壁释放内毒素的潜力有所不同。在用于治疗全身性革兰氏阴性菌感染时,某些类别的β-内酰胺抗生素会导致游离内毒素水平显著升高,而碳青霉烯类和氨基糖苷类药物治疗产生的内毒素量相对较少。在有效杀灭微生物之前诱导形成长而异常的细菌细胞的抗生素,其释放内毒素的程度最高。来自脓毒症动物模型和临床研究的证据越来越多,表明抗生素介导的源自革兰氏阳性菌、革兰氏阴性菌或真菌的生物活性细胞壁成分的释放与临床快速恶化有关。