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Complement C3Complement C4Complement C4aComplement C3aComplement C1qComplement C5aComplement ActivationComplement C4bComplement C5Complement C3bComplement System ProteinsComplement C6Phosphatidylethanolamine Binding ProteinComplement C3cComplement C3dComplement C2Complement C9Receptors, ComplementComplement C1sComplement Membrane Attack ComplexComplement C1rComplement Inactivator ProteinsComplement C7Complement C3-C5 ConvertasesComplement Factor BComplement Pathway, AlternativeComplement Pathway, ClassicalComplement C1 Inactivator ProteinsComplement C8Complement C1Receptors, Complement 3bComplement Factor HComplement C5bComplement C2aReceptor, Anaphylatoxin C5aComplement Activating EnzymesComplement Inactivating AgentsComplement Hemolytic Activity AssayMolecular Sequence DataReceptors, Complement 3dAnaphylatoxinsAmino Acid SequenceProton-Translocating ATPasesMitochondria, HeartAngioedemaSubmitochondrial ParticlesComplement Fixation TestsProteinsAurovertinsComplement Factor DComplement C1 Inhibitor ProteinProtein BindingComplement Factor IComplement C4b-Binding ProteinComplement C3b Inactivator ProteinsAntigens, CD55Complement C3-C5 Convertases, Classical PathwayCattleComplement C2bAndrogen-Binding ProteinCarrier ProteinsAntigens, CD59Base SequenceKineticsEnzyme InhibitorsCobra VenomsElectrophoresis, Polyacrylamide GelAntigen-Antibody ComplexSteroid 21-HydroxylaseComplement C3-C5 Convertases, Alternative PathwayAlpha-GlobulinsBinding SitesPeptide FragmentsImmunoglobulin GHemolysisComplement C3 Convertase, Alternative PathwayComplement C5 Convertase, Classical PathwaySequence Homology, Amino AcidComplement C3 Convertase, Classical PathwayAntigens, CD46Molecular WeightCloning, MolecularOpsonin ProteinsPlacental HormonesCells, CulturedI-kappa B ProteinsBlood ProteinsRibonuclease, PancreaticMutationCell LineMice, Inbred C57BLLupus Erythematosus, SystemicModels, MolecularComplement C5 Convertase, Alternative PathwayPhagocytosisProtein ConformationRecombinant ProteinsAdenosine TriphosphateRNA, MessengerUracil-DNA Glycosidase

Micrurus snake venoms activate human complement system and generate anaphylatoxins. (57/83)

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Alterations of coagulation and fibrinolysis in patients with angioedema due to C1-inhibitor deficiency. (58/83)

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Type I hereditary angioedema in Taiwan -- clinical, biological features and genetic study. (59/83)

BACKGROUND: Hereditary angioedema (HAE) is a rare, autosomal dominant inherited disease which is caused by a genetic deficiency of C1 esterase inhibitor (C1 INH). There have only been a few case reports in Taiwan to date. OBJECTIVE: To describe the clinical features of type I HAE in Taiwanese patients. METHODS: Three unrelated Taiwanese families with type I HAE are reported, and one case of a family from a review of PubMed was reviewed. Clinical manifestations, diagnostic examinations, management and genetic studies were analyzed. RESULTS: Including this report, 19 patients had low C1 INH and low C4 levels and were diagnosed with type I HAE. Only 11 (57.9%) patients were symptomatic. Recurrent skin swelling and edema over the four extremities or trunk were reported in all symptomatic patients (100%). 45.5% of the patients recalled laryngeal attacks and one patient died from asphyxia. 18.2% of the patients experienced abdominal symptoms. The age at the beginning of clinical symptoms ranged from 5 to 30 years (mean +/- SD: 20.82 +/- 7.88 years). The diagnosis tended to be delayed (range from 1 to 39 years; mean +/- SD: 8.45 +/- 11.04 years). Nine patients had a mutant C1 INH gene, and two patients received long-term prophylaxis with danazol. CONCLUSION: The prevalence of hereditary angioedema in Taiwan is low. Persons with low levels of C1 INH who were clinically symptomatic accounted for only 57.9% of the cases in our study, which is far lower than previous reports from other countries. Ethnic differences may be the reason for this finding. Further genomic studies are needed to elucidate the genetic penetrance of C1 INH deficiency in Taiwan.  (+info)

Hereditary and acquired complement component 1 esterase inhibitor deficiency: a review for the hematologist. (60/83)

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Hereditary angioedema (HAE) in children and adolescents--a consensus on therapeutic strategies. (61/83)

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The effect of C1 inhibitor on myocardial ischemia and reperfusion injury. (62/83)

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C1-inhibitor protects from brain ischemia-reperfusion injury by combined antiinflammatory and antithrombotic mechanisms. (63/83)

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Update on treatment of hereditary angioedema. (64/83)

BACKGROUND: Hereditary Angioedema (HAE) is a rare disease characterized by recurrent, self-limiting episodes of swelling. New therapies have recently emerged and are now available; however, many physicians are not aware of the new medications, and their indications and contraindications. OBJECTIVE: To update allergists and primary care physicians on new advances in HAE therapies. DATA SOURCES: A PubMed literature search was used to develop this manuscript. STUDY SELECTIONS: English language peer-reviewed angioedema articles were selected. High quality Phase II and III placebo-controlled clinical trials were reviewed and summarized. RESULTS: Until 2008, therapy for HAE consisted of symptom relief with narcotics, hydration and fresh frozen plasma (FFP). Androgens and FFP are frequently used despite multiple, significant side effects. Newer therapies include C1-inhibitor--both human plasma derived and recombinant--as well as contact system modulators such as ecallantide and icatibant. All of these products can be used for treatment of acute attacks of HAE, and C1-inhibitors can also be used for prophylaxis. CONCLUSION: New, disease-specific therapies have recently emerged which are more efficacious, are proven to work by placebo-controlled studies, have minimal adverse effects, and can be utilized for the treatment of HAE.  (+info)