January 1998, Volume 7, Issue 1, Pages 42 – 48

Paper

Association of osteonecrosis in systemic lupus erythematosus with abnormalities of fibrinolysis JS Sheikh, GS Retzinger & EV Hess1 Departments of Medicine and Pathology, University of Cincinnati Medical Center, Cincinnati, Ohio, USA     1Correspondence: Dr EV Hess, M.L. 0563, 231 Bethesda Avenue, Cincinnati, Ohio 45267-0563, USA.

Keywords

osteonecrosis;   fibrinolysis;   systemic lupus erythematosus

Abstract

Patients with systemic lupus erythematosus (SLE) are at an increased risk of developing osteonecrosis (ON). Twenty-six patients with SLE were studied. Fifteen of these had ON and 11 did not. The latter were used as control subjects. Various coagulation analytes including antithrombin III (ATIII) activity, protein C activity, protein S activity, 2-antiplasmin activity, anticardiolipin antibodies (aCL), plasminogen activator inhibitor (PAI-1) activity and tissue type plasminogen activator (tPA) antigen were measured using citrated plasma samples from the patients. A significant proportion (80%) of patients had at least one laboratory abnormality that has been associated with a thrombotic predisposition. ON was significantly associated with elevated levels of PAI-1 activity; it was also associated with elevated PAI-1/tPA ratio. There was no association between ON of SLE and abnormalities of the other measured coagulation analytes. These results suggest that defective fibrinolysis seems to be operative in the pathogenesis of ON associated with SLE. The defect appears to involve an imbalance between tPA and its inhibitor, PAI-1. This imbalance could represent an important risk factor in the pathogenesis of ON.

Received 15 July 1997; Accepted 5 November 1997

^© Macmillan Publishers Ltd 1997