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Interventional Study in Adult Subjects With Immune Thrombocytopenia Purpura Receiving Romiplostim

2014-08-27 03:12:56 | BioPortfolio

Summary

The purpose of this study is to describe the number of months with a subject platelet response over a 12 month treatment period and to describe ITP Remission Rates in Adult Subjects with Immune Thrombocytopenia Purpura Receiving Romiplostim

Study Design

Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Idiopathic Thrombocytopenic Purpura

Intervention

AMG 531

Status

Not yet recruiting

Source

Amgen

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:12:56-0400

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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.

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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