Glueck C J, Freiberg Richard A, Wang Ping
Cholesterol Center, ABC Building, 3200 Burnet Avenue, Cincinnati, OH 45229, USA.
Curr Hematol Rep. 2003 Sep;2(5):417-22.
We think that osteonecrosis, to a large degree, develops because of familial and acquired thrombophilia and hypofibrinolysis causing venous thrombosis in the femoral head. We postulate that venous thrombosis leads to increased intraosseus venous pressure, reduced arterial flow, and hypoxic bone death. Many studies suggest that familial and acquired thrombophilia and hypofibrinolysis may play an important etiologic role in adults with osteonecrosis of the hip and jaw and in children with Legg-Perthes disease (pediatric osteonecrosis). We have limited pilot data in adults with osteonecrosis associated with familial thrombophilia and hypofibrinolysis that suggest that 12 weeks of therapy with enoxaparin, if started early (Ficat stages I/II) before femoral head collapse (Ficat stages III/IV), may interrupt the progression of osteonecrosis of the hip. Placebo-controlled trials with a 2-year follow-up or longer in adults will be required to assess the promise of the pilot anticoagulant studies in osteonecrosis.
我们认为,在很大程度上,骨坏死是由于家族性和后天性血栓形成倾向以及纤维蛋白溶解功能减退导致股骨头静脉血栓形成而发展的。我们推测静脉血栓形成会导致骨内静脉压升高、动脉血流减少以及骨缺氧性坏死。许多研究表明,家族性和后天性血栓形成倾向以及纤维蛋白溶解功能减退可能在成人髋部和颌骨骨坏死以及患有Legg-Perthes病(小儿骨坏死)的儿童中起重要的病因学作用。我们在患有与家族性血栓形成倾向和纤维蛋白溶解功能减退相关的骨坏死的成人中获得的初步数据有限,这些数据表明,如果在股骨头塌陷(Ficat分期III/IV)之前早期(Ficat分期I/II)开始使用依诺肝素治疗12周,可能会中断髋部骨坏死的进展。需要对成人进行为期2年或更长时间的安慰剂对照试验,以评估抗凝治疗在骨坏死初步研究中的前景。