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The objectives of this survey are to collect data to report the safety and efficacy of Firazyr (Icatibant acetate) in the post-marketing phase in participants diagnosed with Hereditary Angioedema (HAE).
Hereditary Angioedema (HAE)
Published on BioPortfolio: 2019-08-20T20:17:15-0400
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 objective is to compare the gene expression of B1 and / or B2 monocyte receptors between patients with hereditary bradykinetic angioedema and control subjects.
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 serious disease with unpredictable attacks. It has an impact on patients' health-related quality of life. This study aimed to assess the quality of life of the hereditary an...
For the prevention of attacks of hereditary angioedema (HAE), the efficacy and safety of subcutaneous human C1-esterase inhibitor (C1-INH[SC]; HAEGARDA, CSL Behring) was established in the 16-week COM...
Many notable advances in drug allergy, urticaria, angioedema and anaphylaxis were reported in 2018. Broad spectrum antibiotic use and consequently antibiotic resistance is widespread, and algorithms t...
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.