Resolution of Thrombocytopenia in a Patient with Lupus Anticoagulant Who Received Warfarin Therapy

Masahide Yamazaki, Department of Internal Medicine (III), Kanazawa University School of Medicine 13-1, Takaramachi Kanazawa, 920 (Japan) Although thrombocytopenia is a characteristic clinical finding in patients with anti-phospholipid antibody syndrome (APAS), neither the etiology nor the treatment of thrombocytopenia is clear [1]. We report the case of a 37-year-old Japanese man with APAS, whose thrombocytopenia was improved by oral warfarin. The patient had experienced multiple cerebral infarctions in 1984, at which time he was found to have thrombocytopenia (98 × 1071) and was given 200 mg/day of ticlo-pidine without effect on his thrombocytopenia. In 1987, he came to our hospital to consult for his early-onset cerebral infarction and thrombocytopenia. Several assays for lupus anticoagulant (LA), including kaolin clotting time (KCT), tissue thromboplastin inhibition test (TTI), and rabbit brain phos-pholipid neutralization procedure (RBNP) were performed as previously described [2-4]. Based on the results of these tests, he was diagnosed to have LA and was given mini-dose aspirin (40 mg/day), which was followed by a transient slight increase in his platelet count. In 1988, he developed venous thrombosis of the right lower limb and was thus readmitted to hospital. On admission, clinical and laboratory investigations revealed mild thrombocytopenia (85 × 109/1) and mild renal dysfunction (blood urea nitrogen 25 mg/dl and serum creatinine 1.2 mg/ dl), but electrolytes and hepatic function were normal. Antinuclear antibody (ANA) and anti-DNA antibody were positive. A falsepositive result was obtained on the VDRL test. Anticardiolipin antibody (ACA)-IgG was 48 U/ml (normal < IO), and ACA-IgM was below 5 U/ml (normal < 10). Anti-platelet antibody was negative but platelet-associated IgG (PA-IgG) was slightly elevated (23 ng/l07 cells). PT was normal but APTT was prolonged (12.7 and 52.2 s., respectively). Plasma fibrinogen was normal. Antithrombin III, plasminogen, α2-plasmi-nogen inhibitor and protein C activity was normal. Although plasma thrombin-anti-thrombin III complex (TAT) and prothrom-bin fragment 1+2 (Fl+2) were slightly elevated (3.8 ng/ml and 1.8 nmol/l, respectively), fibrin/fibrinogen degradation products (FDP), cross-linked fibrin degradation products (XDP), protein S, and plasmin-α2-plas-min inhibitor complex (PIC) were normal. The presence of LA was demonstrated by mixing tests based on KCT, the RBNP test, and the TTI test. From these findings, systemic lupus erythematosus (SLE) with APAS was diagnosed. 5 mg/day of warfarin was added to low-dose aspirin for recurrent thrombosis. His platelet count immediately