Richardson S G, Matthews K B, Stuart J, Geddes A M, Wilcox R M
Br J Haematol. 1979 Jan;41(1):95-103. doi: 10.1111/j.1365-2141.1979.tb03685.x.
Coagulation activity and whole-blood viscosity were measured in the steady state, and serially during painful crisis, in eight patients with sickle-cell anaemia. Platelet and coagulation activation occurred in the steady state and became more pronounced early in crisis. Whole-blood viscosity increased during crisis in parallel with plasma fibrinogen. Similar changes were found in a parallel study of 20 patients with localized bacterial or viral infection who did not have sickle-cell anaemia. Reports of platelet activation, hypercoagulability, and hyperviscosity during painful crisis therefore reflect secondary changes arising from vascular stasis, precipitating infection, and an acute-phase protein reaction. Although secondary, these changes may contribute to vascular occlusion by an additive effect in vessels already partially occluded by sickled cells.
对8例镰状细胞贫血患者在稳态时以及在疼痛危象期间进行了连续测量，测定了凝血活性和全血粘度。血小板和凝血激活在稳态时就已发生，在危象早期变得更加明显。在危象期间，全血粘度随血浆纤维蛋白原平行升高。在一项对20例无镰状细胞贫血的局部细菌或病毒感染患者的平行研究中也发现了类似变化。因此，关于疼痛危象期间血小板激活、高凝状态和高粘度的报告反映了由血管淤滞、感染诱发和急性期蛋白反应引起的继发性变化。尽管是继发性的，但这些变化可能通过在已经被镰状细胞部分阻塞的血管中产生累加效应而导致血管闭塞。
