Davì G, Giammarresi C, Vigneri S, Ganci A, Ferri C, Di Francesco L, Vitale G, Mansueto S
Department of Internal Medicine, University of Chieti, Italy.
Thromb Haemost. 1995 Aug;74(2):631-4.
Endothelial injury in vivo induced by Rickettsia Conorii, the etiologic agent of Mediterranean Spotted Fever (MSF) has been recently demonstrated. We sought to determine whether platelet and/or coagulative activation in vivo can be demonstrated in the acute phase of MSF, through measurements of a major metabolite of thromboxane (TX) in the urine (11-dehydro-TXB2) and of plasma prothrombin fragment 1 + 2, whose levels reflect activation of prothrombin to thrombin. Moreover, we measured plasma endothelin-1 as marker of endothelial dysfunction. Our results provide biochemical evidence for the occurrence of TXA2-dependent platelet activation and thrombin generation in vivo, together with endothelial dysfunction. These phenomena could account for clinical manifestations of MSF, such as vasculitis and focal microthrombus formation. These results could also provide a rationale for testing the efficacy of aspirin or heparin in reducing the prothrombotic status of Rickettsiae diseases.
最近已证实,地中海斑疹热(MSF)的病原体康氏立克次体可在体内诱导内皮损伤。我们试图通过测量尿液中血栓素(TX)的主要代谢产物(11-脱氢-TXB2)和血浆凝血酶原片段1 + 2来确定在MSF急性期体内是否可表现出血小板和/或凝血激活,其水平反映凝血酶原向凝血酶的激活。此外,我们测量了血浆内皮素-1作为内皮功能障碍的标志物。我们的结果为体内TXA2依赖性血小板激活和凝血酶生成以及内皮功能障碍的发生提供了生化证据。这些现象可能解释了MSF的临床表现,如血管炎和局灶性微血栓形成。这些结果还可为测试阿司匹林或肝素在降低立克次体病血栓形成状态方面的疗效提供理论依据。