Abstract 481: Characteristics of Two Thrombotic Thrombocytopenic Purpura (TTP) Syndromes Associated with Ticlopidine and Clopidogrel: Results From the Surveillance, Epidemiology, and Risk Factors for Thrombotic Thrombocytopenic Purpura (SERF-TTP) Research Group
Background: Most idiopathic TTP cases have ADAMTS13 deficiency. We evaluated clinical and laboratory findings for patients with TTP caused by the thienopyridines, ticlopidine and clopidogrel, the most common TTP-associated drugs.
Methods: Information on thienopyridine schedule, thrombocytopenia, renal insufficiency, therapeutic plasma exchange (TPE), and survival were obtained for thienopyridine-associated TTP cases. For 39 individuals, plasma was examined for ADAMTS13 deficiency (<15% activity) and inhibitors.
Results: In comparison to clopidogrel-associated TTP patients (n=35), ticlopidine-associated TTP patients (n=93) were more likely to have received >2 weeks of thienopyridines (90% vs 26%), be thrombocytopenic (84% vs 60%), have normal renal function (82% vs 55%), and have ADAMTS13 deficiency (80% vs 22%) (p<0.015 for each) (Table 1⇓). Among patients who developed TTP after >2 weeks of ticlopidine, survival rates were greater with TPE (84% vs 38%, p<0.05) (Table 2⇓). Among patients who developed TTP after ≤2 weeks of clopidogrel, survival was 70% with TPE and 67% without. Among deficient ADAMTS13 patients, 85% received >2 weeks of ticlopidine, and survival was 91% with TPE vs 50% without (p<0.10). Among nondeficient ADAMTS13 patients, 54% had received clopidogrel and 58% survived with TPE.
Conclusions: Thienopyridine-associated TTP occurs most commonly by an immune-mediated ADAMTS13 deficiency syndrome that develops mainly after 2 weeks of ticlopidine use and has high survival rates following TPE. A less common but more immediate syndrome occurs following ticlopidine or clopidogrel use, has preserved ADAMTS13 activity, and is less responsive to TPE.