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This study is being conducted to explore the clinical safety, local tolerability, convenience and effectiveness of self-treatment of hereditary angioedema (HAE) attacks with subcutaneous injections of icatibant.
Control: Uncontrolled, Endpoint Classification: Safety Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment
Universitätsklinik für Dermatologie und Venerologie
Shire Human Genetic Therapies, Inc.
Published on BioPortfolio: 2010-07-15T17:00:00-0400
Primary Outcome Measures: Symptom relief (patient) Secondary Outcome Measures: Safety and tolerability Additional efficacy assessments Pharmacoeconomics
This is a multicenter study recruiting patients with angioedema induced by ACEI. Open-label treatment with subcutaneous Icatibant compared to a historic group of 47 patients with ACE inhi...
Previous studies reported infraclinical modifications of the homeostasis in chronic urticaria, recurrent idiopathic angioedema and hereditary angioedema. This study aim to compare groups w...
The objectives of the study are to: 1. Evaluate the dose response and the pharmacokinetics (PK)/pharmacodynamics (PD) of intravenous (IV) administration of Cinryze for the treatmen...
Hereditary angioedema ("HAE") is a genetic disorder characterized by sudden recurrent attacks of local swelling (angioedema). These attacks are often painful and disabling, and, in some ca...
Hereditary angioedema is a rare autosomal dominantly inherited immunodeficiency disorder characterized by potentially life-threatening angioedema attacks.
Attacks of Hereditary Angioedema due to C1-inhibitor deficiency (C1-INH-HAE)are often triggered by stressful events/hormonal changes.
Hereditary angioedema is characterized by severe, episodic edema of the subcutaneous and mucosal tissue. The disease carries significant morbidity and mortality due to involvement of the gastrointesti...
The objective of this work was to assess resident education regarding contemporary management of hereditary angioedema using a web-based survey.
Objective Angioedema is a potentially life-threatening complication of angiotensin-converting enzyme inhibitor (ACEI) use, occurring in up to 0.5% of users. Although the pathophysiology of ACEI-induce...
Forms of hereditary angioedema that occur due to mutations in the gene for COMPLEMENT C1 INHIBITOR PROTEIN. Type I hereditary angioedema is associated with reduced serum levels of complement C1 inhibitor protein. Type II hereditary angioedema is associated with the production of a non-functional complement C1 inhibitor protein.
A form of hereditary angioedema that occurs in women and is precipitated or worsened by high ESTROGEN levels. It is associated with mutations in the gene for FACTOR XII that result in its increased activity.
Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.
An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.
Stable blood coagulation factor activated by contact with the subendothelial surface of an injured vessel. Along with prekallikrein, it serves as the contact factor that initiates the intrinsic pathway of blood coagulation. Kallikrein activates factor XII to XIIa. Deficiency of factor XII, also called the Hageman trait, leads to increased incidence of thromboembolic disease. Mutations in the gene for factor XII that appear to increase factor XII amidolytic activity are associated with HEREDITARY ANGIOEDEMA TYPE III.