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Study of Doxil in the Treatment of Patients With Refractory Idiopathic Thrombocytopenic Purpura

2014-08-27 03:53:26 | BioPortfolio

Summary

This study is designed to evaluate the efficacy and safety of single agent Doxil in the treatment of patients with refractory ITP (Idiopathic Thrombocytopenic Purpura).

Description

Eligible patients will receive Doxil 20 mg/m2 IV over 1 hour every 2 weeks. Treatment will be continued for 1 course beyond return of the platelet count to normal with a maximum of 18 courses.

Study Design

Allocation: Non-Randomized, Control: Uncontrolled, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Autoimmune Thrombocytopenic Purpura

Intervention

Doxil

Location

Hematology and Oncology Specialists
Metairie
Louisiana
United States
70006

Status

Recruiting

Source

Hematology and Oncology Specialists

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:53:26-0400

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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.

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.

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.

An acquired, congenital, or familial disorder caused by PLATELET AGGREGATION with THROMBOSIS in terminal arterioles and capillaries. Clinical features include THROMBOCYTOPENIA; HEMOLYTIC ANEMIA; AZOTEMIA; FEVER; and thrombotic microangiopathy. The classical form also includes neurological symptoms and end-organ damage, such as RENAL FAILURE.

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