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Procoagulants and Osteonecrosis
LYNNE C. JONES, MICHAEL A. MONT, TUNG B. LE, MICHELLE PETRI, DAVID S. HUNGERFORD, PING WANG, and CHARLES J. GLUECK
ABSTRACT.
Methods. Blood samples were drawn from 45 patients diagnosed with osteonecrosis. Etiologic associations included systemic lupus erythematosus (n = 9), inflammatory bowel disease (n = 1), corticosteroid therapy (n = 20), or history of heavy alcohol (n = 4) or tobacco (n = 3) use. No associated risk factors were identified in 5 patients; these individuals were labeled "idiopathic." The patient cohort was matched to a similarly studied cohort of 40 healthy individuals without documented osteonecrosis. The following factors were analyzed: plasminogen activator inhibitor (PAI-Fx), stimulated tissue plasminogen activator, lipoprotein (a), resistance to activated protein C, anticardiolipin antibodies (aCL IgG, IgM), protein C, protein S (free), and homocysteine. Results. Thirty-seven of the 45 patients (82.2%) with osteonecrosis were found to have at least one coagulopathy, versus 30% of controls (p < 0.0001). Twenty-one patients (46.7%) were identified with 2 or more abnormal test results versus 2.5% of controls (p < 0.0001). Patients were more likely than controls to have high levels of the hypofibrinolytic plasminogen activator inhibitor activity (42% vs 3%; p < 0.0001), and high anticardiolipin antibody IgG (34% vs 10%; p = 0.008). At least one coagulation factor abnormality was detected in all 5 idiopathic patients; elevated aCL IgG and PAI-Fx were evident in 4 patients. Conclusion. This study revealed a high incidence of thrombophilic and hypofibrinolytic coagulation abnormalities in patients with osteonecrosis. These findings have major implications for the diagnosis as well as the treatment of this disease. Since some of these abnormalities may be the result of autosomal dominant disorders, it may be possible to detect individuals at risk for development of this disease. (J Rheumatol 2003:30:783-91) Key Indexing Terms:
OSTEONECROSIS
From the Department of Orthopaedic Surgery and Department of Medicine (Rheumatology), Johns Hopkins University School of Medicine, Baltimore; the Institute for Advanced Orthopaedics, Sinai Hospital of Baltimore, Baltimore, Maryland; and the Cholesterol Center, The Jewish Hospital of Cincinnati, Cincinnati, Ohio, USA. L.C. Jones, PhD, Department of Orthopaedic Surgery; M.A. Mont, MD, Department of Orthopaedic Surgery, The Johns Hopkins University School of Medicine and Institute for Advanced Orthopedics, Sinai Hospital of Baltimore; T.B. Le, MD, Department of Orthopaedic Surgery; M. Petri, MD, Department of Medicine; D.S. Hungerford, MD, Department of Orthopaedic Surgery, The Johns Hopkins University School of Medicine; P. Wang, PhD; C.J. Glueck, MD, Cholesterol Center, The Jewish Hospital of Cincinnati. Address reprint requests to Dr. L.C. Jones, The Johns Hopkins University School of Medicine, Department of Orthopaedic Surgery, Suite 201, Good Samaritan Professional Building, 5601 Loch Raven Boulevard, Baltimore, MD 21239. E-mail: lcjones@jhmi.edu Submitted July 3, 2001; revision accepted September 19, 2002. |