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Genetic association studies related to septic shock have traditionally evaluated 2 end points: susceptibility to development of septic shock and mortality due to septic shock. Recently, Lorenz et al¹ reported an association between toll-like receptor 4 (TLR4) mutations and susceptibility to gram-negative septic shock in the ARCHIVES. The C3H/HeJ mice, which are lipopolysaccharide hyporesponsive due to mutations within the Toll gene, were more susceptible to dissemination of gram-negative bacteria.² In in vitro studies, when cells with the Asp299Gly mutation were exposed to lipopolysaccharide, they released less tumor necrosis factor and interleukin 1, which are important mediators of septic shock.³ Although it is difficult to extrapolate these results to humans, one may hypothesize that patients who develop gram-negative infections and have the Asp299Gly mutation are more susceptible to bacteremia. However, whether these patients would be more or less susceptible to develop septic shock, which is mediated by proinflammatory cytokines, remains unknown. . . . [Full Text of this Article]

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