Huisse Marie-Geneviève, Pease Sebastian, Hurtado-Nedelec Margarita, Arnaud Bertrand, Malaquin Cécile, Wolff Michel, Gougerot-Pocidalo Marie-Anne, Kermarrec Nathalie, Bezeaud Annie, Guillin Marie-Claude, Paoletti Xavier, Chollet-Martin Sylvie
Department of Hematology, AP-HP, Hospital Bichat, Paris, France.
Crit Care Med. 2008 Aug;36(8):2288-95. doi: 10.1097/CCM.0b013e318180dd43.
The mechanisms linking severe inflammation and coagulation during heatstroke are poorly understood. Here, we examined the roles of the tissue factor pathway, leukocyte activation, and mediators of innate immunity in patients admitted to an intensive care unit for heatstroke during an intense heat wave in Paris.
Retrospective observational study.
Intensive care unit of a university medical center.
Eighteen critically ill severe patients with heatstroke were enrolled in the study and 14 age-matched patients with severe sepsis as controls.
None.
High circulating levels of some inflammation and stress mediators (interleukin-6, -8, C5a, interleukin-1 receptor antagonist, heat shock protein 60 and 70) were observed. Blood leukocyte activation was shown by beta2 integrin up-regulation, L-selectin down-regulation, and strong production of reactive oxygen species and interleukin-8 ex vivo. High levels of circulating promatrix metalloproteinase-9 were detected in all the patients studied, and its active form was present in two patients. Overt disseminated intravascular coagulation according to the International Society of Thrombosis and Hemostasis score was present in five patients. Whole-blood tissue factor was present in all the patients and part of this activity was associated with microparticles in five patients. The degrees of inflammation and disseminated intravascular coagulation are correlated with clinical severity.
These results suggest that neutrophil activation plays a key role in the acute activation of coagulation observed during severe heatstroke, despite a rapid and sustained antiinflammatory response. The comparison with a group of patients with severe sepsis suggests some common mechanisms, but more intense responses during heatstroke.
中暑期间严重炎症与凝血之间的联系机制尚不清楚。在此，我们研究了组织因子途径、白细胞活化和先天免疫介质在巴黎酷热期间入住重症监护病房的中暑患者中的作用。
回顾性观察研究。
大学医学中心的重症监护病房。
18例中暑重症患者纳入研究，14例年龄匹配的严重脓毒症患者作为对照。
无。
观察到一些炎症和应激介质（白细胞介素-6、-8、C5a、白细胞介素-1受体拮抗剂、热休克蛋白60和70）的循环水平升高。β2整合素上调、L-选择素下调以及体外活性氧和白细胞介素-8的大量产生表明血液白细胞被激活。在所有研究患者中均检测到循环中高水平的前基质金属蛋白酶-9，其中两名患者存在其活性形式。根据国际血栓与止血学会评分，五名患者出现明显的弥散性血管内凝血。所有患者均存在全血组织因子，其中五名患者的部分活性与微粒有关。炎症程度和弥散性血管内凝血与临床严重程度相关。
这些结果表明，尽管有快速且持续的抗炎反应，但中性粒细胞活化在严重中暑期间观察到的凝血急性激活中起关键作用。与一组严重脓毒症患者的比较表明存在一些共同机制，但中暑期间的反应更为强烈。
