The pathogenesis of sepsis involves not only microbial toxins but also activated host inflammatory mediators. Therefore, besides conventional antibiotic or surgical treatment of infection and supportive intensive therapy, modulating host inflammatory mediators as a conjunctive therapeutic option has been explored in the past decade. Although successful in animal models of sepsis, inhibiting host inflammatory response in human sepsis has failed to improve survival or otherwise show efficacy. Studies are needed which better describe the circumstances under which these therapies may ultimately prove successful.
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Karzai et al. (1997) studied this question.
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