tailieunhanh - Báo cáo y học: "Impact of the factor V Leiden mutation on the outcome of pneumococcal pneumonia: a controlled laboratory study"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Impact of the factor V Leiden mutation on the outcome of pneumococcal pneumonia: a controlled laboratory study. | Schouten et al. Critical Care 2010 14 R145 http content 14 4 R145 c CRITICAL CARE RESEARCH Open Access Impact of the factor V Leiden mutation on the outcome of pneumococcal pneumonia a controlled laboratory study ifard 2 malic x arVt x ddr1 2 ITI I Pcidcitc3 I c. i4 Hdr Pr .ll1 2 4 Mcucel sci louten I Cornelis van t Veer Joris Jin Roelois Marcel Levi on van del roll Abstract Introduction Streptococcus S. pneumoniae is the must common cause of community-acquired pneumonia. The factor V Leiden FVL mutation results in resistance of activated FV to inactivation by activated protein c and thereby in a prothrombotic phenotype. Human heterozygous FVL carriers have been reported to be relatively protected against sepsis-related mortality. We here determined the effect of the FVL mutation on coagulation inflammation bacterial outgrowth and outcome in murine pneumococcal pneumonia. Methods Wild-type mice and mice heterozygous or homozygous for the FVL mutation were infected intranasally with 2 106 colony forming units of viable S. pneumoniae. Mice were euthanized after 24 or 48 hours or observed in a survival study. In separate experiments mice were treated with ceftriaxone intraperitoneally 24 hours after infection and euthanized after 48 hours or observed in a survival study. Results The FVL mutation had no consistent effect on activation of coagulation in either the presence or absence of ceftriaxone therapy as reflected by comparable lung and plasma levels of thrombin-antithrombin complexes and fibrin degradation products. Moreover the FVL mutation had no effect on lung histopathology neutrophil influx cytokine and chemokine levels or bacterial outgrowth. Remarkably homozygous FVL mice were strongly protected against death due to pneumococcal pneumonia when treated with ceftriaxone which was associated with more pronounced FXIII depletion this protective effect was not observed in the absence of antibiotic therapy. Conclusions Homozygosity for the FVL .

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