Adjuvant rituximab to prevent TTP relapse

Cuker, Adam

doi:10.1182/blood-2016-04-710475

Cited by 20 publications

(9 citation statements)

References 10 publications

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“…The authors did not conclude that rituximab is warranted for all acquired TTP patients because they did observe some long‐term remissions with prednisone . However, an accompanying editorial argued that by treating all acquired TTP patients with rituximab the “overtreatment” of some patients for the benefit of those who do need additional therapy (a tenant of adjuvant therapy in oncology) could be justified in this potentially deadly disease . Ultimately, we currently have no reliable biomarkers for relapse and providers are faced with the dilemma to use a reactionary strategy to treat those whose disease demonstrates its severity versus choosing a preventive strategy in which some patients will be overtreated but many will have relapses prevented.…”

Section: Discussionmentioning

confidence: 99%

Treatment of acquired Thrombotic Thrombocytopenic Purpura in the U.S. remains heterogeneous: Current and future points of clinical equipoise

Mazepa

Raval

Brecher

et al. 2017

J of Clinical Apheresis

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Section: Discussionmentioning

confidence: 99%

Treatment of acquired Thrombotic Thrombocytopenic Purpura in the U.S. remains heterogeneous: Current and future points of clinical equipoise

Mazepa

Raval

Brecher

et al. 2017

J of Clinical Apheresis

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“…Fewer and later relapses were also observed in rituximab-treated patients by the French TMA Reference Center Network 82 and the Oklahoma TTP registry. 93,95 As a consequence, frontline treatment with rituximab is a reasonable indication, although it may expose patients to overtreatment, as in up to 50% of cases, acquired TTP recovers with standard treatment. 96 Further studies should determine whether rituximab allows for improving the poorer outcome of the more severe forms of the disease (ie, old patients with cerebral and/ or cardiac involvement).…”

Section: Treatmentmentioning

confidence: 99%

Thrombotic thrombocytopenic purpura

Joly

Coppo

Veyradier

2017

Blood

512

592

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Thrombotic thrombocytopenic purpura (TTP) is a rare and life-threatening thrombotic microangiopathy characterized by microangiopathic hemolytic anemia, severe thrombocytopenia, and organ ischemia linked to disseminated microvascular platelet rich-thrombi. TTP is specifically related to a severe deficiency in ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13), the specific von Willebrand factor-cleaving protease. ADAMTS13 deficiency is most frequently acquired via ADAMTS13 autoantibodies, but rarely, it is inherited via mutations of the ADAMTS13 gene. The first acute episode of TTP usually occurs during adulthood, with a predominant anti-ADAMTS13 autoimmune etiology. In rare cases, however, TTP begins as soon as childhood, with frequent inherited forms. TTP is ∼2-fold more frequent in women, and its outcome is characterized by a relapsing tendency. Rapid recognition of TTP is crucial to initiate appropriate treatment. The first-line therapy for acute TTP is based on daily therapeutic plasma exchange supplying deficient ADAMTS13, with or without steroids. Additional immune modulators targeting ADAMTS13 autoantibodies are mainly based on steroids and the humanized anti-CD20 monoclonal antibody rituximab. In refractory or unresponsive TTP, more intensive therapies including twice-daily plasma exchange; pulses of cyclophosphamide, vincristine, or cyclosporine A; or salvage splenectomy are considered. New drugs including N-acetylcysteine, bortezomib, recombinant ADAMTS13, and caplacizumab show promise in the management of TTP. Also, long-term follow-up of patients with TTP is crucial to identify the occurrence of other autoimmune diseases, to control relapses, and to evaluate psychophysical sequelae. Further development of both patients’ registries worldwide and innovative drugs is still needed to improve TTP management.

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“…Relapsing and refractory cases of TTP like our first case have been effectively treated with rituximab, a monoclonal antibody against CD20 receptors on memory B cells. 20 - 24 Further studies are needed to delineate the role, dosing, and frequency of rituximab in TTP, including TTP-related MI.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Infarction as an Early Presentation in Thrombotic Thrombocytopenic Purpura: A Rare Case Series

Dahal

Ghimire

Sapkota

et al. 2018

Journal of Investigative Medicine High Impact Case Reports

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Renal and neurological involvements are frequently seen in thrombotic thrombocytopenic purpura (TTP). Cardiac involvement, however, has been rarely reported. In this article, we present 2 cases of myocardial infarction in patients with TTP. In the first case, a young man presented with non–ST-segment elevation myocardial infarction that resolved promptly with plasmapheresis. The second patient developed ST-segment elevation myocardial infarction early in the course of the disease and died before plasmapheresis could be initiated. Hence, a high degree of suspicion with prompt diagnosis and treatment is needed to prevent mortality associated with cardiac involvement in TTP.

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Adjuvant rituximab to prevent TTP relapse

Cited by 20 publications

References 10 publications

Treatment of acquired Thrombotic Thrombocytopenic Purpura in the U.S. remains heterogeneous: Current and future points of clinical equipoise

Treatment of acquired Thrombotic Thrombocytopenic Purpura in the U.S. remains heterogeneous: Current and future points of clinical equipoise

Thrombotic thrombocytopenic purpura

Myocardial Infarction as an Early Presentation in Thrombotic Thrombocytopenic Purpura: A Rare Case Series

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