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Phase II Study of Rituximab in Patients With Immune Thrombocytopenic Purpura

2014-08-27 03:57:44 | BioPortfolio

Summary

OBJECTIVES: I. Determine the response rate and response duration to rituximab in patients with immune thrombocytopenic purpura.

II. Evaluate the toxicity associated with this treatment regimen in these patients.

III. Evaluate the alteration in antiplatelet antibody with this treatment regimen in these patients.

Description

PROTOCOL OUTLINE: Patients receive rituximab IV on days 1, 8, 15, and 22. Patients who achieve a clinical response lasting over 4 months may receive a second course of rituximab.

Patients are followed at 5, 6, 8, and 12 weeks, and then at 6 and 9 months.

Study Design

Primary Purpose: Treatment

Conditions

Purpura, Thrombocytopenic, Idiopathic

Intervention

rituximab

Location

University of Alabama Comprehensive Cancer Center
Birmingham
Alabama
United States
35294

Status

Completed

Source

Office of Rare Diseases (ORD)

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:57:44-0400

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PubMed Articles [960 Associated PubMed Articles listed on BioPortfolio]

Relapse Rate in Survivors of Acute Autoimmune Thrombotic Thrombocytopenic Purpura Treated with or without Rituximab.

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Child-onset thrombotic thrombocytopenic purpura caused by p.R498C and p.G259PfsX133 mutations in ADAMTS13.

Patients suffering from congenital thrombotic thrombocytopenic purpura (cTTP) have a deficiency in ADAMTS13 due to mutations in their ADAMTS13 gene.

Ticagrelor-induced thrombotic thrombocytopenic purpura: A case report and review of the literature.

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Multiple total hip arthroplasties in refractory immune thrombocytopenic purpura: A case report and literature review.

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Medical and Biotech [MESH] Definitions

Any form of purpura in which the PLATELET COUNT is decreased. Many forms are thought to be caused by immunological mechanisms.

Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.

Immunoglobulin preparations used in intravenous infusion, containing primarily IMMUNOGLOBULIN G. They are used to treat a variety of diseases associated with decreased or abnormal immunoglobulin levels including pediatric AIDS; primary HYPERGAMMAGLOBULINEMIA; SCID; CYTOMEGALOVIRUS infections in transplant recipients, LYMPHOCYTIC LEUKEMIA, CHRONIC; Kawasaki syndrome, infection in neonates, and IDIOPATHIC THROMBOCYTOPENIC PURPURA.

A systemic non-thrombocytopenic purpura caused by HYPERSENSITIVITY VASCULITIS and deposition of IGA-containing IMMUNE COMPLEXES within the blood vessels throughout the body, including those in the kidney (KIDNEY GLOMERULUS). Clinical symptoms include URTICARIA; ERYTHEMA; ARTHRITIS; GASTROINTESTINAL HEMORRHAGE; and renal involvement. Most cases are seen in children after acute upper respiratory infections.

An ADAMTS protease that contains eight thrombospondin (TS) motifs. It cleaves VON WILLEBRAND FACTOR to control vWF-mediated THROMBOSIS. Mutations in the ADAMTS13 gene have been identified in familial cases of PURPURA, THROMBOTIC THROMBOCYTOPENIC and defects in ADAMTS13 activity are associated with MYOCARDIAL INFARCTION; BRAIN ISCHEMIA; PRE-ECLAMPSIA; and MALARIA.

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