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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...
To explore the feasibility of a new Dried Blood Spot (DBS) filtercard-based screening algorithm and thereby analyzing the prevalence of the Hereditary Angioedema in patients with unclear r...
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...
The Icatibant Outcome Survey (IOS; NCT01034969) is a Shire-sponsored, international, observational study monitoring the safety and effectiveness of icatibant, a bradykinin B2 receptor antagonist appro...
Hereditary angioedema (HAE) is characterised by recurrent episodes of angioedema and can be fatal.
Incidence of angioedema associated with angiotensin-converting enzyme inhibitors (ACE-I) has been estimated at 0.1%-2.2% of patients receiving treatment. Despite the potential severity of this disease...
Hereditary angioedema is a life-threatening illness caused by mutations in the gene encoding C1 inhibitor (also called C1 esterase inhibitor) that lead to overactivation of the kallikrein-bradykinin c...
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.