plasma and blood transfusions, infections, autoimmune disorders, pregnancies, malignancies, and antibiotics [ 2 4 ] . We report the first case of an acquired factor V inhibitor in the setting of HIV infection.A 32-year-old man with HIV infection presented 10 days prior to admission with fever and weight loss for 2 months and diffuse lymphadenopathy. His hemoglobin (Hb) and platelet count were normal with a CD4 count of 220/pl (nl 410-1,840) and a CD8 count of 173O/pl (nl 270-870). On admission, he had a temperature of 100.5"F, and a Hb of 82 g/L (nl 120-150), platelet count of 7 X 10YL (nl ISWSO), reticulocyte % of3.9 (nlO.5-1.5), and LDH of 1,725 U/L (nl 2 9 7 4 1 1). Prothrombin time (PT), international normalized ratio (INR), and partial thromboplastin time (P'IT) were normal. A direct Coomb's antibody test was negative. The peripheral smear contained schistocytes and large platelets. His mental status, creatinine, and urinalysis were normal. A diagnosis of thrombotic thrombocytopenic purpura (TTP) was made and plasma exchange was begun. After initial improvement (Fig. I), the platelet count decreased. A bone marrow biopsy showed plasmacytosis and increased megakaryocytes. Elevated antiplatelet antibodies 2) and IgG 37.4% (nl2.1-12.1)] suggested a diagnosis of AIT. Plasma exchange was discontinued, and intravenous immunoglobulin (IVIG) was started. A cervical lymph node showed Kaposi sarcoma (KS), and an abdominal CT scan showed lymphadenopathy and splenomegaly. His thrombocytopenia was thought due to HIV-associated AIT and splenomegalic-KS, so he was treated with azidothymidine and vincristine plus interferon-a (IFF-a). A preoperative evaluation for a splenectomy revealed a PT of 21.9 sec (nl 11.1-12.9), INR of 4.3 (nl ratio I .O), and PTT of 61.2 sec (nl20.&33.5). These did not correct with vitamin K or fresh frozen plasma. His measured factor 11 activity was 64% (nl 83-126), factor V was 12% (nl 66152). factor VII was 59% (nl 66-156) and factor X was 75% (nl 65-142). A factor V mixing study was 9% (nl 85%) and factor V 50:5O mixed study was 28% (nl 47%), demonstrating the presence of a factor V inhibitor. Splenectomy was postponed, and on hospital day 17 his platelet count increased. He was discharged home with aplatelet count of 13 1 X 109/L. His coagulation indices normalized 1 month later while receiving weekly vincristine.During plasma exchange, he was exposed to 156 units of foreign factors that likely served as the antigenic stimulus to develop the inhibitor. Patients with coagulation factor inhibitors have been treated with FFP, cyclophosphamide, and prednisolone; platelets are used specifically for factor V inhibitors [ S ] . Specific therapy was not instituted because the patient was asymptomatic, the risk of further immunosuppression, and the possibility his inhibitor might disappear spontaneously. His asymptomatic course suggests that expectant management may be appropriate
REFERENCES1 . Sande MA, Volberding PA (eds): The Medical Management of AIDS, 2nd ed., pp 33, Philadelphia, PA: W.B. Saunder...