Smith D W
Department of Pathology and Buehler Center on Aging, Northwestern University School of Medicine, Chicago, IL 60611-2611, USA.
Med Hypotheses. 1997 Dec;49(6):497-500. doi: 10.1016/s0306-9877(97)90067-0.
An hypothesis is offered here that the pathogenesis of avascular necrosis (AVN) of the femoral head is based on the inhibition of angiogenesis. Well-established facts supporting this hypothesis are: 1, the lesion of AVN is vascular obliteration often leading to infarction; 2, glucocorticoids, which are a risk factor for AVN, are inhibitors of angiogenesis; 3, interferons, which are now being used in the treatment of multiple sclerosis, hepatitis, leukemias, and hemangiomas are inhibitors of angiogenesis, and other endogenously produced cytokines are also inhibitors; 4, constituents of cartilage are inhibitors of angiogenesis, explaining the subchondral location of AVN; 5, angiography of the femoral head indicates the need for continual renewal of its blood supply, shows the inhibition of revascularization by steroids, and suggests that the stress of weight bearing makes the femoral head particularly vulnerable. This hypothesis has implications for the therapeutic use of inhibitors of angiogenesis.
本文提出一个假说，即股骨头缺血性坏死（AVN）的发病机制基于血管生成的抑制。支持这一假说的既定事实如下：1. AVN的病变是血管闭塞，常导致梗死；2. 糖皮质激素是AVN的一个危险因素，是血管生成的抑制剂；3. 目前用于治疗多发性硬化症、肝炎、白血病和血管瘤的干扰素是血管生成的抑制剂，其他内源性产生的细胞因子也是抑制剂；4. 软骨成分是血管生成的抑制剂，这解释了AVN的软骨下位置；5. 股骨头血管造影表明其血液供应需要持续更新，显示类固醇对血管再生的抑制作用，并表明负重压力使股骨头特别易受影响。这一假说对血管生成抑制剂的治疗应用具有启示意义。
