As shown in Table II, six patients (cases 1, 2, 3, 10, 11 and 13) received IFN-α, three patients (cases 4, 6 and 8) received conventional AITP therapy and four patients (cases 5, 7, 9 and 12) did not receive any treatment at all (because they refused IFN-α treatment and had moderate thrombocytopenia). The six IFN-α-treated HCV-positive thrombocytopenic patients were women, median age 58·6 years (range 48–66). At admission, thrombocytopenia duration ranged from 1 to 240 months (median 54·6). Patients had not received prior specific treatments. Median platelet count was 61 × 109/l (range 18–87) at the onset of IFN-α therapy. The median duration of IFN-α treatment was 14 months (range 6–24 months). After 6 months, two patients (cases 1 and 3) discontinued IFN-α treatment because of side-effects. The remaining four patients have received 11–24 months of IFN-α therapy and are still on treatment. Patients were evaluated periodically during and after therapy. Changes in the platelet counts of IFN-α-treated patients are detailed in Table IV. After initiation of IFN-α treatment, all patients had a significant increase in platelet counts. Five patients (cases 2, 3, 10, 11 and 13) had > 100 × 109/l platelets by the 6th month of therapy with IFN-α. In patient 1, however, the increase in platelet count was minor, with a maximum increase to 38 × 109/l platelets after 6 months of IFN-α therapy. All of our IFN-α-treated patients had a durable (> 1 year) platelet responses. Even two patients (cases 1 and 3), who were treated with a short course of IFN-α, had a durable platelet response. Follow-up of these six IFN-α-treated patients ranged from 11 to 36 months (median 23 months). Interestingly, one patient (case 2) presented with an acute relapse (platelet count 17 × 109/l) 12 months after starting IFN-α therapy. In this patient, the platelet count rapidly returned to 130 × 109/l after a short course of low-dose prednisone (0·25 mg/kg/d for 2 weeks), although IFN-α treatment was continued. PAIgG was not determined at this time. Currently (at 24 months of IFN-α treatment), her platelet count is maintained above 100 × 109/l on a standard dose of IFN-α. Serum ALT levels were normalized in one patient (case 2), reduced to less than twice the upper normal limit in two patients (cases 3 and 10) and did not change in three patients (cases 1, 11 and 13).
In two patients (cases 1 and 3), treatment with IFN-α had to be stopped after 6 months because of depression. In the other four patients, side-effects were moderate, generally limited to asthenia. No clinical symptoms of anaemia or leucopenia were observed during follow-up and no autoimmune diseases occurred.
On the other hand, three patients with HCV-positive thrombocytopenia were managed with conventional therapy for AITP (Table II). Patient 4 had no platelet response after treatment with prednisone and IVIg. Then, she was splenectomized and achieved a good long-term response (platelet count 180 × 109/l), which persisted for longer than 1 year. Patient 6 was treated with prednisone without platelet response. She was subsequently treated with splenectomy and danazol without effect (platelet count 20 × 109/l). Because of bleeding episodes during follow-up, she was treated with IVIg, which produced a very transient response (platelet count 58 × 109/l). In patient 8, treatment with prednisone had no impact on the platelet count, then he responded to splenectomy and maintains a stable platelet count (platelet count 168 × 109/l) after 3 years.