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The objective of this patient registry is to collect data on the safety of Berinert® in normal clinical practice in the United States. The patient registry will be maintained for a period of 3 years. The duration of individual patient participation will vary and is determined by the frequency of hereditary angioedema (HAE) attacks and the patient's need for Berinert® treatment.
Observational Model: Cohort, Time Perspective: Prospective
Berinert® (C1 Esterase Inhibitor)
United States, California
Published on BioPortfolio: 2014-07-23T21:09:28-0400
The study is performed to investigate the subcutaneous (s.c.) versus intravenous (i.v.) administration of Berinert P in patients with hereditary angioedema (HAE) to establish a second admi...
The purpose of this study is to assess the efficacy and safety of subcutaneous administration of a liquid formulation of C1 esterase inhibitor for the prevention of angioedema attacks in a...
The study objective was to describe the pharmacokinetics (PK) of one or two doses of C1 esterase inhibitor (C1INH-nf) in hereditary angioedema (HAE) subjects who were not experiencing an H...
Hereditary angioedema (HAE) is a rare disorder characterized by congenital lack of functional C1 esterase inhibitor. If not treated adequately, the acute attacks of HAE can be life-threate...
The study objective was to evaluate the safety and efficacy of repeat use of C1INH-nf for the treatment of acute HAE attacks.
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...
Attacks of Hereditary Angioedema due to C1-inhibitor deficiency (C1-INH-HAE)are often triggered by stressful events/hormonal changes.
Subcutaneous C1-inhibitor (HAEGARDA, CSL Behring), is a US Food and Drug Administration (FDA)-approved, highly concentrated formulation of a plasma-derived C1-esterase inhibitor (C1-INH), which, in th...
Hereditary angioedema (HAE) with normal C1 inhibitor (C1-INH) is a rare condition with clinical features similar to those of HAE with C1-INH deficiency. Mutations in the F12 gene have been identified ...
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.
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.
Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.
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.