Patient Registry Study of Berinert® in Normal Clinical Practice

2014-07-23 21:09:28 | BioPortfolio


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.

Study Design

Observational Model: Cohort, Time Perspective: Prospective


Hereditary Angioedema


Berinert® (C1 Esterase Inhibitor)


United States, California
Granada Hills
United States




CSL Behring

Results (where available)

View Results


Published on BioPortfolio: 2014-07-23T21:09:28-0400

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Medical and Biotech [MESH] Definitions

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.

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