Marshall J C, Nathens A B
Department of Surgery, University of Toronto, Ontario, Canada.
Shock. 1996;6 Suppl 1:S10-6.
Data from a large number of published human studies support the hypothesis that the gastrointestinal tract of the critically ill patient is an important factor in ICU morbidity and mortality. Changes in proximal gut flora in the critically ill patient predict nosocomial infection with the same organism, while gut-directed therapeutic measures clearly reduce rates of nosocomial infection and may have an impact on mortality Modulation of the systemic inflammatory response through gut derived measures has been no more successful than modulation of that response through more conventional systemic forms of mediator-directed therapy. But if the gastrointestinal tract is an important factor in nosocomial ICU-acquired infection, the bigger unanswered question is, to what extent does infection per se alter outcome in critical illness? Current articulations of the gut hypothesis challenge long-held and probably outmoded views of host-microbial interactions. The challenge to replace them is no less compelling and no less treacherous than it was in the era of Metchnikoff, Lane, or their ancient forebears.
大量已发表的人体研究数据支持这样一种假设，即重症患者的胃肠道是影响重症监护病房（ICU）发病率和死亡率的一个重要因素。重症患者近端肠道菌群的变化预示着由相同病原体引起的医院感染，而针对肠道的治疗措施显然能降低医院感染率，并且可能对死亡率产生影响。通过肠道衍生措施调节全身炎症反应并不比通过更传统的全身性介质导向治疗形式调节该反应更成功。但是，如果胃肠道是ICU获得性医院感染的一个重要因素，那么更大的未解决问题是，感染本身在多大程度上会改变危重病的预后？目前对肠道假说的阐述挑战了长期以来可能已过时的宿主-微生物相互作用观点。取代这些观点的挑战与梅契尼科夫、莱恩或他们古代前辈那个时代相比，同样紧迫且同样充满风险。
