Hypofibrinolysis, lipoprotein(a), and plasminogen activator inhibitor

Parameters of hypofibrinolysis and thrombophilia were assessed in 20 consecutive patients with bone marrow edema syndrome of the hip who lacked typical risk factors for osteonecrosis. Twenty healthy subjects, matched for age and gender, served as the control subjects. In patients with bone marrow edema syndrome, elevated levels of lipoprotein(a) and plasminogen activator inhibitor were found in nine (45%) and two patients (10%), respectively. Elevation of lipoprotein(a) was present in two patients in the control group; however, plasminogen activator inhibitor levels were normal in this group. Mean levels of lipoprotein(a) were 34.8 mg/dL in the patients with bone marrow edema versus 13.8 mg/dL in the control subjects. Mean concentrations of plasminogen activator inhibitor, apolipoproteins, lipid metabolism parameters, and indicators of thrombophilia did not differ in both groups. Pulsed field gel electrophoresis and Southern blots confirmed the presence of pathologic allelotypes in three patients with elevated levels of lipoprotein(a) who had a familial occurrence of bone marrow edema syndrome. These findings also underline a fundamental role of hypofibrinolysis, mediated by elevated levels of lipoprotein(a) or plasminogen activator inhibitor, or both, in the former idiopathically considered etiology of the bone marrow edema syndrome of the hip.