Zhang Qiankun, L V Jin, Jin Lie
1 Department of Nephrology, Lishui Central Hospital, Lishui, Zhejiang, China.
2 Department of Neurology, Lishui People's Hospital, Lishui, Zhejiang, 323000, China.
J Int Med Res. 2018 Jun;46(6):2141-2148. doi: 10.1177/0300060517700299. Epub 2017 May 1.
The two major theories of glucocorticoid (GC)-induced osteonecrosis of the femoral head (ONFH) are apoptosis and ischaemia. The traditional theory implicates ischaemia as the main aetiological factor because the final common pathway of ONFH is interruption of blood supply to the bone. The most common causes of interruption of blood supply include fat embolism and coagulation disorders. GCs can directly or indirectly lead to coagulation disorders, producing a hypercoagulable state, followed by poor blood flow, ischaemia, and eventually ONFH. This review summarizes the existing knowledge on coagulation disorders in the context of GC-induced ONFH, including hypofibrinolysis and thrombophilia, endothelial cell dysfunction and damage, endothelial cell apoptosis, lipid metabolism, platelet activation, and the effect of anticoagulant treatment.
糖皮质激素（GC）诱导的股骨头缺血性坏死（ONFH）的两大主要理论是细胞凋亡和缺血。传统理论认为缺血是主要病因，因为ONFH的最终共同途径是骨供血中断。供血中断最常见的原因包括脂肪栓塞和凝血障碍。GC可直接或间接导致凝血障碍，产生高凝状态，继而血流不畅、缺血，最终导致ONFH。本综述总结了GC诱导的ONFH背景下有关凝血障碍的现有知识，包括纤溶功能减退和血栓形成倾向、内皮细胞功能障碍和损伤、内皮细胞凋亡、脂质代谢、血小板活化以及抗凝治疗的效果。
