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Cost savings to hospital of rituximab use in severe autoimmune acquired thrombotic thrombocytopenic purpura.

ABSTRACT: Patients with severe autoimmune thrombotic thrombocytopenic purpura (TTP) experience acute hematologic emergencies during disease flares and a lifelong threat for relapse. Rituximab, in addition to steroids and therapeutic plasma exchange (TPE), has been shown to mitigate relapse risk. A barrier to care in initiating rituximab in the inpatient setting has been the presumed excessive cost of medication to the hospital. Retrospectively reviewing TTP admissions from 2004 to 2018 at our academic center, we calculated the actual inpatient cost of care. We then calculated the theoretical cost to the hospital of initiating rituximab in the inpatient setting for both initial TTP and relapse TTP cohorts, with the hypothesis that preventing sufficient future TTP admissions offsets the cost of initiating rituximab in all patients with TTP. At a median follow-up of 55 months in the initial TTP cohort, rituximab use produced a projected cost savings of $905?906 and would have prevented 185 inpatient admission days and saved 137 TPE procedures. In the relapse TTP setting, rituximab use produced a projected cost savings of $425?736 and would have prevented 86 inpatient admission days and saved 64 TPE procedures. From a hospital cost standpoint, cost of rituximab should no longer be a barrier to initiating inpatient rituximab in both initial and relapse TTP settings.

SUBMITTER: Goshua G

PROVIDER: S-EPMC7013262 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Cost savings to hospital of rituximab use in severe autoimmune acquired thrombotic thrombocytopenic purpura.

Goshua George G Gokhale Amit A Hendrickson Jeanne E JE Tormey Christopher C Lee Alfred Ian AI

Blood advances 20200201 3

Patients with severe autoimmune thrombotic thrombocytopenic purpura (TTP) experience acute hematologic emergencies during disease flares and a lifelong threat for relapse. Rituximab, in addition to steroids and therapeutic plasma exchange (TPE), has been shown to mitigate relapse risk. A barrier to care in initiating rituximab in the inpatient setting has been the presumed excessive cost of medication to the hospital. Retrospectively reviewing TTP admissions from 2004 to 2018 at our academic cen ...[more]

PMID: 32045473

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Project description:BackgroundAcquired thrombotic thrombocytopenic purpura (TTP) is an autoimmune disease in which anti-ADAMTS13 autoantibodies cause severe enzyme deficiency. ADAMTS13 deficiency causes the loss of regulation of von Willebrand factor multimeric size and platelet-tethering function, which results in the formation of disseminated microvascular platelet microthrombi. Precisely how anti-ADAMTS13 autoantibodies, or antibody subsets, cause ADAMTS13 deficiency (ADAMTS13 activity generally < 10%) has not been formally investigated.MethodsWe analysed 92 acquired TTP episodes at presentation, through treatment and remission/relapse using epitope mapping and functional analyses to understand the pathogenic mechanisms of anti-ADAMTS13 IgG.Results89/92 of TTP episodes had IgG recognising the ADAMTS13 N-terminal domains. The central spacer domain was the only N-terminal antigenic target detected. 38/92 TTP episodes had autoantibodies recognising the N-terminal domains alone; 54/92 TTP episodes also had antibodies against the ADAMTS13 C-terminal domains (TSP2-8 and/or CUB domains). Changes in autoantibody specificity were detected in 9/16 patients at relapse, suggesting a continued development of the disease. Functional analyses on IgG from 43 patients revealed inhibitory IgG were limited to anti-spacer domain antibodies. However, 15/43 patients had autoantibodies with no detectable inhibitory action and as many as 32/43 patients had autoantibodies with inhibitory function that was insufficient to account for the severe deficiency state, suggesting that in many patients there is an alternative pathogenic mechanism. We therefore analysed plasma ADAMTS13 antigen levels in 91 acquired TTP presentation samples. We demonstrated markedly reduced ADAMTS13 antigen levels in all presentation samples, median 6% normal (range 0-47%), with 84/91 patients having < 25% ADAMTS13 antigen. ADAMTS13 antigen in the lowest quartile at first presentation was associated with increased mortality (odds ratio 5.7).ConclusionsAnti-spacer domain autoantibodies are the major inhibitory antibodies in acquired TTP. However, depletion of ADAMTS13 antigen (rather than enzyme inhibition) is a dominant pathogenic mechanism. ADAMTS13 antigen levels at presentation have prognostic significance. Taken together, our results provide new insights into the pathophysiology of acquired TTP.

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Cost savings to hospital of rituximab use in severe autoimmune acquired thrombotic thrombocytopenic purpura.

Publications

Cost savings to hospital of rituximab use in severe autoimmune acquired thrombotic thrombocytopenic purpura.

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