Hurley J C
Division of Infectious Diseases, Children's Hospital and Medical Center, Seattle, Washington 98105.
Lancet. 1993 May 1;341(8853):1133-5. doi: 10.1016/0140-6736(93)93139-r.
There is strong evidence to implicate endotoxin released from gram negative bacteria in the pathogenesis of the sepsis syndrome and related conditions, but equally compelling data bring the role of endotoxin into doubt. Reappraisal of endotoxin and its release from gram negative bacteria suggests that it is not directly responsible for the complications of sepsis syndrome. Rather, release of endotoxin is a marker for the transition of gram negative organisms to cell-wall-deficient forms (L-forms) that may persist undetected despite antibiotic therapy directed against the parental form. This transition has two consequences in compromised patients: L-forms cause organ failure, and they serve as a sanctuary from which cell-wall-intact revertants may arise.
有强有力的证据表明革兰氏阴性菌释放的内毒素与脓毒症综合征及相关病症的发病机制有关,但同样有说服力的数据让人对内毒素的作用产生怀疑。对内毒素及其从革兰氏阴性菌中的释放进行重新评估表明,它并非脓毒症综合征并发症的直接原因。相反,内毒素的释放是革兰氏阴性菌向细胞壁缺陷型(L型)转变的一个标志,尽管针对亲代形式使用了抗生素治疗,但L型可能仍未被检测到而持续存在。这种转变在身体虚弱的患者中会产生两个后果:L型会导致器官衰竭,并且它们成为可能产生细胞壁完整回复菌的庇护所。