Hemostatic defects are common in patients with systemic lupus erythematosus (SLE), estimated as occurring in 20% of cases.1 The usual defects detected are thrombocytopenia, abnormal platelet function, circulating anticoagulants, and hypoprothrombinemia. These hemostatic defects are thought to be due to autoantibodies. The circulating anticoagulants found in SLE are of two types as follows: one is called the "lupus anticoagulant" and the others are inhibitors directed against specific coagulation factors.2 The lupus anticoagulant is not a cause for hemorrhage unless it is associated with reduced factor II (hypoprothrombinemia), thrombocytopenia, and/or platelet dysfunction. Thrombotic disease, however, has been described in patients with this type of anticoagulant. Inhibitors against specific coagulation factors (eg, factors VIII, IX, and XI), on the other hand, cause a moderate to severe hemorrhagic condition that is clinically similar to the congenital factor deficiency diseases.
In this issue, Bernstein et al call our attention to those patients