dc.creator | Magerl M., Germenis A.E., Maas C., Maurer M. | en |
dc.date.accessioned | 2023-01-31T08:55:38Z | |
dc.date.available | 2023-01-31T08:55:38Z | |
dc.date.issued | 2017 | |
dc.identifier | 10.1016/j.iac.2017.04.004 | |
dc.identifier.issn | 08898561 | |
dc.identifier.uri | http://hdl.handle.net/11615/76061 | |
dc.description.abstract | A new form of hereditary angioedema (HAE) was identified in the year 2000. Its clinical appearance resembles HAE types I and II, which are caused by mutations that result in a deficiency of C1 inhibitor (C1-INH). In patients with the new form of HAE, C1-INH plasma levels and function values are normal, so it's termed HAE with normal C1-INH (HAE-nC1). HAE-nC1, in a subgroup of patients, is thought to be caused by mutations that affect the F12 gene. The diagnosis of HAE-nC1 is based on history and clinical criteria. There are no licensed drugs with proven treatment effects for HAE-nC1. © 2017 Elsevier Inc. | en |
dc.language.iso | en | en |
dc.source | Immunology and Allergy Clinics of North America | en |
dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85021836423&doi=10.1016%2fj.iac.2017.04.004&partnerID=40&md5=55159388b12b4a28d8ad87fc53b39873 | |
dc.subject | bradykinin | en |
dc.subject | complement component C1s inhibitor | en |
dc.subject | ecallantide | en |
dc.subject | icatibant | en |
dc.subject | tranexamic acid | en |
dc.subject | blood clotting factor 12 | en |
dc.subject | bradykinin | en |
dc.subject | complement component C1s inhibitor | en |
dc.subject | plasmin | en |
dc.subject | protein binding | en |
dc.subject | SERPING1 protein, human | en |
dc.subject | angioneurotic edema | en |
dc.subject | clinical feature | en |
dc.subject | differential diagnosis | en |
dc.subject | evaluation study | en |
dc.subject | genetics | en |
dc.subject | human | en |
dc.subject | long term care | en |
dc.subject | pathophysiology | en |
dc.subject | priority journal | en |
dc.subject | prophylaxis | en |
dc.subject | Review | en |
dc.subject | short course therapy | en |
dc.subject | angioneurotic edema | en |
dc.subject | disease management | en |
dc.subject | genetic predisposition | en |
dc.subject | metabolism | en |
dc.subject | mutation | en |
dc.subject | phenotype | en |
dc.subject | premedication | en |
dc.subject | signal transduction | en |
dc.subject | treatment outcome | en |
dc.subject | Angioedemas, Hereditary | en |
dc.subject | Bradykinin | en |
dc.subject | Complement C1 Inhibitor Protein | en |
dc.subject | Diagnosis, Differential | en |
dc.subject | Disease Management | en |
dc.subject | Factor XII | en |
dc.subject | Fibrinolysin | en |
dc.subject | Genetic Predisposition to Disease | en |
dc.subject | Humans | en |
dc.subject | Mutation | en |
dc.subject | Phenotype | en |
dc.subject | Premedication | en |
dc.subject | Protein Binding | en |
dc.subject | Signal Transduction | en |
dc.subject | Treatment Outcome | en |
dc.subject | W.B. Saunders | en |
dc.title | Hereditary Angioedema with Normal C1 Inhibitor: Update on Evaluation and Treatment | en |
dc.type | other | en |