A prospective study of platelets and plasma proteolytic systems during the early stages of Rocky Mountain spotted fever.
A prospective study of platelets and plasma proteolytic systems during the early stages of Rocky Mountain spotted fever.
复制标题
落基山斑疹热早期阶段血小板和血浆蛋白水解系统的前瞻性研究。
DOI：
10.1056/nejm198804213181603
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Sobel,E
中科院分区：
文献类型：
--
作者：
Rao,AK;Schapira,M;Clements,ML;Niewiarowski,S;Budzynski,AZ;Schmaier,AH;Harpel,PC;Blackwelder,WC;Scherrer,JR;Sobel,E
We prospectively examined early changes in platelets and plasma proteolytic systems in 12 vaccinated and 6 unvaccinated volunteers in whom Rocky Mountain spotted fever developed after challenge withRickettsia rickettsii.The platelet counts declined while the plasma concentration of β-thromboglobulin and the ratio of β-thromboglobulin to platelet factor 4 increased, indicating in vivo activation of platelets. Plasma levels of antithrombin III decreased and levels of fibrinopeptide A increased, indicating in vivo activation of the coagulation system. Plasma fibrinogen levels peaked at 24 hours and gradually declined; this is consistent with the behavior of fibrinogen as an acute-phase reactant.Prolongation of the prothrombin time and a decrease in plasma levels of factor VII in the absence of evidence of liver injury suggested possible activation of the extrinsic pathway of coagulation. A decline in plasma prekallikrein levels with an increase in plasma C1-inhibitor–kallikrein complexes suggested activation of kallikrein, probably through the intrinsic coagulation system. Elevations in levels of plasma fibrin-degradation products and α2-antiplasmin–plasmin complexes with declines in plasminogen and α2-antiplasmin levels provided evidence of activation of the fibrinolytic system. Elevated plasma levels of tissue plasminogen activator and von Willebrand factor reflected endothelial stimulation.Thus, even early in the course of Rocky Mountain spotted fever that is treated promptly, there is activation of platelets, coagulation pathways, and the fibrinolytic system. These changes may be related to endothelial perturbation, a major pathogenetic mechanism in the disorder. (N Engl J Med 1988; 318:1021–8.)
