Swerlick R A, Eckman J R, Kumar A, Jeitler M, Wick T M
Department of Dermatology, Emory University School of Medicine, Atlanta, GA 30322.
Blood. 1993 Sep 15;82(6):1891-9.
Important complications in sickle cell anemia occur secondary to vascular occlusion, which is postulated to be initiated by interactions of erythrocytes with vascular endothelial cells. In patients with sickle cell anemia, up to 25% of reticulocytes express the alpha 4 beta 1-integrin complex. Furthermore, erythrocytes from patients with sickle cell anemia bind to endothelial cells activated by tumor necrosis factor alpha via (TNF alpha) via interactions between erythrocyte alpha 4 beta 1 and endothelial cell vascular cell adhesion molecule-1 (VCAM-1). Thus, binding of alpha 4 beta 1-expressing reticulocytes to cytokine-activated endothelial cells may initiate vascular complications in sickle cell anemia and perhaps other hemolytic anemias during episodes of infection and inflammation.
镰状细胞贫血的重要并发症继发于血管闭塞，据推测这是由红细胞与血管内皮细胞的相互作用引发的。在镰状细胞贫血患者中，高达25%的网织红细胞表达α4β1整合素复合物。此外，镰状细胞贫血患者的红细胞通过红细胞α4β1与内皮细胞血管细胞黏附分子-1（VCAM-1）之间的相互作用，与由肿瘤坏死因子α（TNFα）激活的内皮细胞结合。因此，表达α4β1的网织红细胞与细胞因子激活的内皮细胞的结合可能引发镰状细胞贫血以及可能在感染和炎症发作期间的其他溶血性贫血的血管并发症。
