| Excerpt | Reference |
|---|
| "Hereditary angioedema is an episodic swelling disorder with autosomal dominant inheritance." | ( Frank, MM, 2008) |
| "Hereditary angioedema is a rare genetic disorder, manifested by recurrent edema leading to disfigurement, organ dysfunction and life-threatening respiratory impairment that may become fatal." | ( Goren, A; Leibovich, I; Reshef, A, 2008) |
| "Hereditary angioedema is a rare genetic disorder characterized by acute, intermittent, and potentially life-threatening attacks of edema of the skin and mucosa." | ( Campion, M; Cicardi, M; Horn, PT; Levy, RJ; Li, HH; McNeil, DL; Pullman, WE; Sheffer, AL, 2010) |
| "Hereditary angioedema is characterized by recurrent attacks of angioedema of the skin, larynx, and gastrointestinal tract." | ( Aberer, W; Anné, S; Arcoleo, F; Banerji, A; Bas, M; Bernstein, JA; Bier, H; Björkander, J; Bork, K; Bouillet, L; Bracho, F; Bull, C; Cicardi, M; Cillari, E; Dong, L; Fan, WT; Farkas, H; Feighery, C; Fernández Romero, DS; Floccard, B; Gleich, G; Grabbe, J; Greve, J; Hébert, J; Hoffmann, TK; Hurewitz, D; Jacobson, KW; Kaatz, M; Katelaris, CH; Keith, P; Kirkpatrick, CH; Kivity, S; Knolle, J; Kravec, I; Kreuz, W; Langton, D; Levy, RJ; Luger, T; Lumry, W; Malbrán, A; Martin, L; Maurer, M; Merk, H; Obtulowicz, K; Pichler, C; Reshef, A; Resnick, D; Riedl, M; Ritchie, B; Rosen, K; Rosenkranz, B; Schmid-Grendelmeier, P; Sitkauskiene, B; Smith, WB; Toubi, E; Werner, S; Wombolt, D; Yang, W; Zanichelli, A; Zimmermann, J, 2010) |
| "Hereditary angioedema is a severe genetic disorder due to C1 esterase inhibitor deficiency, which leads to an excess of bradykinin." | ( , 2010) |
| "Hereditary angioedema is caused by a C1-inhibitor deficiency." | ( Majluf-Cruz, A; Nieto-Martínez, S, 2011) |
| "Hereditary angioedema is a disease which develops as a result of a deficiency or dysfonction of C1-inhibitor, a key regulator of the complement, coagulation and contact cascades, resulting among others in excessive release of bradykinin." | ( Leimgruber, A, 2011) |
| "Hereditary angioedema is a rare and potentially fatal autosomal dominant disorder characterised by unpredictable skin, gastrointestinal tract or respiratory tract oedema." | ( Wiednig, M, 2013) |
| "Hereditary angioedema is a heterogeneous disorder with a complex pathophysiology." | ( Walford, HH; Zuraw, BL, 2014) |
| "The acquired C1 inhibitor deficiency is associated with clonal disorders of B cell hyperreactivity, including lymphoma and monoclonal gammopathy." | ( Kaplan, AP, 2014) |
| "C1 Inhibitor deficiency is a rare disorder, characterised by recurrent angio-oedema of skin, upper respiratory and gastrointestinal tracts." | ( Chandini, R; Neeraj, M; Philip, A; Shajith, S; Soopy, K; Thulseedharan, NK, 2013) |
| "Hereditary angioedema is a rare disease, potentially life-threatening." | ( Bouillet, L, 2015) |
| "Acute attacks of hereditary angioedema are characterized by recurrent localized edema." | ( Adnet, F; Boccon-Gibod, I; Boubaya, M; Bouillet, L; Cantin, D; Carpentier, F; Fain, O; Gompel, A; Javaud, N; Launay, D; Smaiti, N, 2015) |
| "Hereditary angioedema is a rare but known cause of compartment syndrome of the upper extremity, and must be considered when patients present with compartment syndrome of unknown etiology." | ( Jager, Z; LoGiudice, J; Matloub, H; Venditto, C, 2017) |
| "However, hereditary angioedema is a burdensome disease that can lead to debilitating and dangerous angioedema episodes associated with significant costs for individuals and society." | ( Chen, M; Riedl, MA, 2017) |
| "Hereditary angioedema is characterized by severe, episodic edema of the subcutaneous and mucosal tissue." | ( Johnson, NM; Phillips, MA, 2018) |
| "Hereditary angioedema is a rare disease associated with unpredictable, recurrent attacks of potentially life-threatening edema." | ( Adnet, F; Baker, E; Bertrand, P; Boccon-Gibod, I; Bouillet, L; Coppere, B; Durand-Zaleski, I; Fain, O; Floccard, B; Gompel, A; Javaud, N; Kanny, G; Lapostolle, F; Launay, D; Martin, L; Mezaour, M; Petrovic, T; Rabetrano, H; Reuter, PG; Sobel, A; Vicaut, E; Woimant, M, 2018) |
| "Hereditary angioedema is a life-threatening illness caused by mutations in the gene encoding C1 inhibitor (also called C1 esterase inhibitor) that lead to overactivation of the kallikrein-bradykinin cascade." | ( Aberer, W; Aygören-Pürsün, E; Baeza, ML; Bygum, A; Cancian, M; Cicardi, M; Clemons, D; Collis, P; Cornpropst, M; Dobo, S; Du-Thanh, A; Fain, O; Fang, L; Farkas, H; Gompels, M; Gonzalez-Quevedo, T; Graff, J; Greve, J; Grivcheva-Panovska, V; Guilarte, M; Huissoon, A; Katelaris, C; Kinaciyan, T; Lleonart, R; Longhurst, HJ; Magerl, M; Maurer, M; Rae, W; Sheridan, W; Smith, WB; Steiner, UC; Triggiani, M; Zanichelli, A, 2018) |
| "hereditary angioedema) is important for correct and rational treatment." | ( Magerl, M; Zampeli, V, 2019) |
| "Hereditary angioedema is characterized by recurrent and unpredictable episodes of subcutaneous and mucosal swelling that can be life threatening." | ( Alexander, VJ; Baker, BF; Cohn, DM; Fijen, LM; Geary, RS; Kaeser, GE; Levi, M; Meijers, JCM; Nanavati, C; Schneider, E; Stroes, ESG; Viney, NJ; Xia, S, 2020) |
| "Hereditary angioedema is a rare, autosomal dominant genetic disorder that leads to sporadic episodes of swelling, which can affect any part of the body." | ( Manning, ME, 2020) |
| "Hereditary angioedema is a rare inherited condition leading to recurrent, sometimes life-threatening angioedema attacks in subcutaneous tissues and gastrointestinal and oropharyngeal mucosa dating back to childhood or adolescence." | ( Gülbahar, O, 2021) |
| "Hereditary angioedema is classified into HAE owing to a deficiency of functional C1INH (HAE-C1INH) or HAE with normal C1INH (HAE-nl-C1INH)." | ( Busse, P; Kaplan, A, 2022) |
| "Hereditary angioedema is a hereditary life-threatening disease characterized by recurrent angioedema of various strength and localization." | ( Latysheva, EA; Latysheva, TV; Manto, IA; Sorokina, LE, 2021) |
| "Hereditary angioedema is an autosomal dominant genetic disease, associated with increased levels of bradykinin." | ( Marcílio Santos, G; Oliveira Dos Santos, F; Pimenta E Silva, LM; Rodrigues de Oliveira, F; Wolff Dick, JMJ, 2023) |
| "The various forms of hereditary angioedema are included in this category, requiring specific tests of C4 and C1 inhibitor level and function to confirm the diagnosis." | ( Bork, K; Grumach, AS; Katelaris, CH, 2023) |
| Excerpt | Reference |
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| "First, the results for the treatment of hereditary angioedema are promising." | ( Lehmann, A, 2008) |
| "The aim of treatment of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency (HAE-C1-INH) is either treating acute attacks or preventing attacks by using prophylactic treatment." | ( Bork, K, 2012) |
| "Recently, the Hereditary Angioedema International Working Group (HAWK) consensus recommended early, on-demand treatment for HAE." | ( Aberer, W, 2012) |
| "Both prophylactic and acute treatment of hereditary angioedema have been revolutionized in the past decade." | ( Frank, MM, 2013) |
| "Historically, treatment for hereditary angioedema (HAE) attacks has been administered by healthcare professionals (HCPs)." | ( Aberer, W; Bloom, B; Bygum, A; Caballero, T; Kivity, S; Longhurst, H; Malbrán, A; Maurer, M; Nair, N; Reshef, A, 2014) |
| "Several types of angioedema exist beyond hereditary angioedema (HAE) types I/II; however, the diagnostic and treatment needs of these conditions are not well understood." | ( Bernstein, JA; Boccon-Gibod, I; Bouillet, L; Craig, TJ; Farkas, H, 2014) |
| "Icatibant is used to treat acute hereditary angioedema with C1 inhibitor deficiency types I/II (C1-INH-HAE types I/II) and has shown promise in angioedema due to acquired C1 inhibitor deficiency (C1-INH-AAE)." | ( Aberer, W; Andresen, I; Bouillet, L; Caballero, T; Fabien, V; Fain, O; Longhurst, HJ; Maurer, M; Zanichelli, A, 2017) |
| "Bradykinin-mediated angioedema (such as hereditary angioedema due to C1-inhibitor deficiency) does not respond to the standard therapy used for histamine-mediated angioedema." | ( Cicardi, M; Mansi, M; Wu, MA; Zanichelli, A, 2016) |
| "Patients with hereditary angioedema with C1 inhibitor deficiency were randomly assigned in a 2:1 ratio to receive either lanadelumab (24 patients) or placebo (13 patients), in two administrations 14 days apart." | ( Adelman, B; Al-Ghazawi, A; Baker, J; Banerji, A; Bernstein, JA; Biedenkapp, JC; Busse, P; Chyung, Y; Cicardi, M; Craig, T; Davis-Lorton, M; Faucette, R; Iarrobino, R; Jacobs, J; Kenniston, JA; Kushner, H; Li, HH; Lockey, R; Lumry, W; Mensah, R; Riedl, M; Sexton, DJ; Shennak, M; Soo, C; Stevens, C; Still, JG; TenHoor, C; Wedner, HJ, 2017) |
| "Recent advances in the treatment of hereditary angioedema include new techniques used to isolate and purify human-derived C1 inhibitor, the production of a recombinant form of C1 inhibitor, and the development of drugs that target the kallikrein-kinin pathway." | ( Johnson, NM; Phillips, MA, 2018) |
| "The future therapies for hereditary angioedema will likely involve the development of oral agents as alternatives to parenteral administration of drugs, specific targeting of proteins and/or enzymes that are not yet possible (e." | ( Kaplan, AP, 2020) |
| "Emerging treatments of hereditary angioedema including targets of prekallikrein, DNA vector technology replacing C1-INH protein, and CRIPSR technology targeting prekallikrein among many others are explored." | ( Bernstein, JA; Kesh, S, 2022) |
| "In bradykinin mediated hereditary angioedema, C1-esterase inhibitor (C1INH) is an effective and approved treatment since many years." | ( Bas, M; Greve, J; Gröger, M; Hahn, J; Hoffmann, TK; Kehl, V; Kojda, G; Stelter, K; Strassen, U; Trainotti, S; Volkenstein, S; Wirth, M, 2023) |
| "In bradykinin mediated hereditary angioedema, C1-esterase inhibitor (C1INH) is an effective and approved treatment since many years." | ( Bas, M; Greve, J; Gröger, M; Hahn, J; Hoffmann, TK; Kehl, V; Kojda, G; Stelter, K; Strassen, U; Trainotti, S; Volkenstein, S; Wirth, M, 2023) |
| "Therapeutic management of hereditary angioedema first consists in treating severe attacks with a selective B2 bradykinin receptor antagonist or a C1 inhibitor concentrate." | ( Boccon-Gibod, I; Bouillet, L; Fain, O; Gobert, D; Launay, D; Trumbic, B, 2023) |