Database : MEDLINE
Search on : Hereditary and Angioedema and Type and III [Words]
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Baracat, Edmund Chada
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[PMID]: 28715060
[Au] Autor:Iahn-Aun M; Aun MV; Motta AA; Kalil J; Giavina-Bianchi P; Hayashida SA; Baracat EC; Maciel GA
[Ad] Address:Gynecologist/Obstetrician, Disciplina de Ginecologia.
[Ti] Title:The Complex Interaction Between Polycystic Ovary Syndrome and Hereditary Angioedema: Case Reports and Review of the Literature.
[So] Source:Obstet Gynecol Surv;72(7):417-424, 2017 Jul.
[Is] ISSN:1533-9866
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: Hereditary angioedema (HAE) is a rare but severe disease, with high risk of death, and attacks have been associated to high estrogen levels. Polycystic ovary syndrome (PCOS) is a common hyperandrogenic condition, which is frequently treated with combined oral contraceptives. Objective: The aim of this study was to describe 2 clinical cases of young women diagnosed as having PCOS who developed HAE attacks after the introduction of combined estrogen-progestin pills to treat PCOS symptoms. Evidence Acquisition: Literature review of sex hormones' role in genesis of HAE attacks and possible mechanisms involved. Results: In the cases reported, after initiation of combined contraceptives, patients presented with facial swelling with airway involvement (laryngeal edema) and abdominal pain. They had a familial history of angioedema and normal C1 inhibitor (C1-INH) levels, leading to the diagnosis of HAE with normal C1-INH (HAEnC1-INH) or HAE type III. After suspension of exogenous estrogen, patients remained asymptomatic from HAE. Conclusions and Relevance: HAEnC1-INH is an estrogen-dependent form of HAE. It is well established that exogenous estrogen triggers attacks of all types of HAE. However, this is the first description of the association between PCOS and HAE, in which PCOS could be masking HAE symptoms. We propose that PCOS might have a protective role regarding HAE attacks, because of its particular hormonal features, that is, hyperandrogenism and relative stable levels of estradiol. The use of combined estrogen-progestin compounds in women with PCOS and HAE must be avoided, and treatment must be individualized.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1707
[Cu] Class update date: 170717
[Lr] Last revision date:170717
[St] Status:In-Process
[do] DOI:10.1097/OGX.0000000000000457

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[PMID]: 28346966
[Au] Autor:Naudin C; Burillo E; Blankenberg S; Butler L; Renné T
[Ad] Address:Clinical Chemistry, Department of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital, Stockholm, Sweden.
[Ti] Title:Factor XII Contact Activation.
[So] Source:Semin Thromb Hemost;43(8):814-826, 2017 Nov.
[Is] ISSN:1098-9064
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Contact activation is the surface-induced conversion of factor XII (FXII) zymogen to the serine protease FXIIa. Blood-circulating FXII binds to negatively charged surfaces and this contact to surfaces triggers a conformational change in the zymogen inducing autoactivation. Several surfaces that have the capacity for initiating FXII contact activation have been identified, including misfolded protein aggregates, collagen, nucleic acids, and platelet and microbial polyphosphate. Activated FXII initiates the proinflammatory kallikrein-kinin system and the intrinsic coagulation pathway, leading to formation of bradykinin and thrombin, respectively. FXII contact activation is well characterized in vitro and provides the mechanistic basis for the diagnostic clotting assay, activated partial thromboplastin time. However, only in the past decade has the critical role of FXII contact activation in pathological thrombosis been appreciated. While defective FXII contact activation provides thromboprotection, excess activation underlies the swelling disorder hereditary angioedema type III. This review provides an overview of the molecular basis of FXII contact activation and FXII contact activation-associated disease states.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1703
[Cu] Class update date: 171101
[Lr] Last revision date:171101
[St] Status:In-Process
[do] DOI:10.1055/s-0036-1598003

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[PMID]: 28291095
[Au] Autor:LoVerde D; Files DC; Krishnaswamy G
[Ad] Address:1Division of Pulmonary, Critical Care, Allergy and Immunology, Department of Medicine, Wake Forest Baptist Medical Center, Winston-Salem, NC.2Division of Allergy and Clinical Immunology, Department of Medicine, W.G. (Bill) Hefner VA Medical Center, Salisbury, NC.
[Ti] Title:Angioedema.
[So] Source:Crit Care Med;45(4):725-735, 2017 Apr.
[Is] ISSN:1530-0293
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Angioedema is a potentially life-threatening occurrence that is encountered by critical care providers. The mechanistic understanding of angioedema syndromes has improved in recent years, and novel medications are available that improve outcomes from these syndromes. This clinically focused review will describe the underlying genetics, pathophysiology, classification and treatment of angioedema syndromes, with an emphasis on the novel pharmacologic agents that have recently become available for acute treatment. DATA SOURCES: A MEDLINE search was conducted with the MeSH terms angioedema, acquired angioedema, hereditary angioedema type III, and angiotensin converting enzyme inhibitor-induced angioedema. STUDY SELECTION: Selected publications describing angioedema, clinical trials, diagnosis, management, and genetics were retrieved (reviews, guidelines, clinical trials, case series), and their bibliographies were also reviewed to identify relevant publications. DATA EXTRACTION: Data from the relevant publications were reviewed, summarized and the information synthesized. DATA SYNTHESIS: The data obtained were used to describe the current state of diagnosis and management of various angioedema syndromes. CONCLUSIONS: Angioedema is a life-threatening syndrome with multiple subtypes, each with a distinct pathophysiology. We present an evidence-based approach to the diagnosis and suggested management of various subtypes of angioedema. Securing the airway remains the most important intervention, followed by administration of both established and more novel pharmacologic interventions based on disease pathology.
[Mh] MeSH terms primary: Airway Management
Angioedema/classification
Angioedema/therapy
[Mh] MeSH terms secundary: Angioedema/diagnosis
Angioedema/genetics
Bradykinin/analogs & derivatives
Bradykinin/therapeutic use
Bradykinin B2 Receptor Antagonists/therapeutic use
Complement C1 Inactivator Proteins/therapeutic use
Complement C1 Inhibitor Protein/therapeutic use
Critical Care
Humans
Kallikreins/antagonists & inhibitors
Peptides/therapeutic use
Recombinant Proteins/therapeutic use
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Bradykinin B2 Receptor Antagonists); 0 (Complement C1 Inactivator Proteins); 0 (Complement C1 Inhibitor Protein); 0 (Peptides); 0 (Recombinant Proteins); 0 (SERPING1 protein, human); 0 (conestat alpha); 5Q6TZN2HNM (ecallantide); 7PG89G35Q7 (icatibant); EC 3.4.21.- (Kallikreins); S8TIM42R2W (Bradykinin)
[Em] Entry month:1705
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170315
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0000000000002281

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[PMID]: 27905115
[Au] Autor:Bork K; Wulff K; Witzke G; Hardt J
[Ad] Address:Department of Dermatology, Johannes Gutenberg University, Mainz, Germany.
[Ti] Title:Treatment for hereditary angioedema with normal C1-INH and specific mutations in the F12 gene (HAE-FXII).
[So] Source:Allergy;72(2):320-324, 2017 Feb.
[Is] ISSN:1398-9995
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:Hereditary angioedema with normal C1 esterase inhibitor and mutations in the F12 gene (HAE-FXII) is associated with skin swellings, abdominal pain attacks, and the risk of asphyxiation due to upper airway obstruction. It occurs nearly exclusively in women. We report our experience treating HAE-FXII with discontinuation of potential trigger factors and drug therapies. The study included 72 patients with HAE-FXII. Potential triggers included estrogen-containing oral contraceptives (eOC), hormonal replacement therapy, or angiotensin-converting enzyme inhibitors. Drug treatment comprised plasma-derived C1 inhibitor (pdC1-INH) for acute swelling attacks and progestins, tranexamic acid, and danazol for the prevention of attacks. Discontinuation of eOC was effective in 25 (89.3%) of 28 women and led to a reduction in the number of attacks (about 90%). After ending hormonal replacement therapy, three of eight women became symptom-free. Three women with exacerbation of HAE-FXII during intake of quinapril or enalapril had no further HAE-FXII attacks after discontinuation of those drugs. Eleven women were treated with pdC1-INH for 143 facial attacks. The duration of the treated facial attacks (mean: 26.6 h; SD: 10.1 h) was significantly shorter than that of the previous 88 untreated facial attacks in the same women (mean: 64.1 h; SD: 28.0 h; P < 0.01). The mean reduction in attack frequency was 99.8% under progestins after discontinuing eOC (16 women), 93.8% under tranexamic acid (four women), and 100% under danazol (three women). For patients with HAE-FXII, various treatment options are available which completely or at least partially reduce the number or duration of attacks.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1612
[Cu] Class update date: 170106
[Lr] Last revision date:170106
[St] Status:In-Process
[do] DOI:10.1111/all.13076

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[PMID]: 27871580
[Au] Autor:Yu SK; Callum J; Alam A
[Ad] Address:Department of Anesthesia, University of Toronto, Toronto, ON M4N 3M5, Canada.
[Ti] Title:C1-esterase inhibitor for short-term prophylaxis in a patient with hereditary angioedema with normal C1 inhibitor function.
[So] Source:J Clin Anesth;35:488-491, 2016 Dec.
[Is] ISSN:1873-4529
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hereditary angioedema with normal C1-esterase inhibitor (HAE-nC1INH) perioperative is a rare condition which could have potential disastrous ramifications for the anesthesiologist in the perioperative period. However, there is limited evidence and/or guidelines on the optimal way to manage these patients. We present the case of a patient with HAE-nC1INH who was successfully managed in the perioperative period with plasma derived C1-esterase inhibitor (pdC1INH). A 29-year-old woman with a diagnosis of HAE-nC1INH presented to the preoperative consultation in preparation for an upcoming total thyroidectomy. She had a 14-year history of ongoing lip and facial edema sometimes necessitating emergency department visitation. Close consultation with her immunologist, transfusion medicine specialists, and anesthesia care providers allowed for a preoperative plan to provide the patient adequate prophylaxis. Both pdC1INH and tranexamic acid were given preoperatively. The patient underwent surgery with no complications. A multidisciplinary team of clinical immunologists, transfusion medicine specialists, and anesthesiologists facilitated the successful perioperative management of a patient with HAE-nC1INH; pdC1INH may a suitable prophylactic perioperative therapy for this rare patient population.
[Mh] MeSH terms primary: Angioedemas, Hereditary/surgery
Complement C1 Inhibitor Protein/therapeutic use
Complement Inactivating Agents/therapeutic use
Postoperative Complications/prevention & control
[Mh] MeSH terms secundary: Adult
Angioedemas, Hereditary/complications
Antifibrinolytic Agents/therapeutic use
Complement C1 Inactivator Proteins/physiology
Female
Humans
Preoperative Care/methods
Thyroidectomy
Tranexamic Acid/therapeutic use
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Antifibrinolytic Agents); 0 (Complement C1 Inactivator Proteins); 0 (Complement C1 Inhibitor Protein); 0 (Complement Inactivating Agents); 0 (SERPING1 protein, human); 6T84R30KC1 (Tranexamic Acid)
[Em] Entry month:1709
[Cu] Class update date: 170901
[Lr] Last revision date:170901
[Js] Journal subset:IM
[Da] Date of entry for processing:161123
[St] Status:MEDLINE

  6 / 93 MEDLINE  
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[PMID]: 27116602
[Au] Autor:Germenis AE; Speletas M
[Ad] Address:Department of Immunology and Histocompatibility, School of Medicine, University of Thessaly, 3, Panepistimiou Street, Biopolis, 41500, Larissa, Greece. agermen@med.uth.gr.
[Ti] Title:Genetics of Hereditary Angioedema Revisited.
[So] Source:Clin Rev Allergy Immunol;51(2):170-82, 2016 Oct.
[Is] ISSN:1559-0267
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Contemporary genetic research has provided evidences that angioedema represents a diverse family of disorders related to kinin metabolism, with a much greater genetic complexity than was initially considered. Convincing data have also recently been published indicating that the clinical heterogeneity of hereditary angioedema due to C1 inhibitor deficiency (classified as C1-INH-HAE) could be attributed at least in part, either to the type of SERPING1 mutations or to mutations in genes encoding for enzymes involved in the metabolism and function of bradykinin. Alterations detected in at least one more gene (F12) are nowadays considered responsible for 25 % of cases of hereditary angioedema with normal C1-INH (type III hereditary angioedema (HAE), nlC1-INH-HAE). Interesting data derived from genetic approaches of non-hereditary angioedemas indicate that other immune pathways might be implicated in the pathogenesis of HAE. More than 125 years after the recognition of the hereditary nature of HAE by Osler, the heterogeneity of clinical expressions, the genetics of this disorder, and the genotype-phenotype relationships, still presents a challenge that will be discussed in this review. Large scale, in-depth genetic studies are expected not only to answer these emerging questions but also to further elucidate many of the unmet aspects of angioedema pathogenesis. Uncovering genetic biomarkers affecting the severity of the disease and/or the effectiveness of the various treatment modalities might lead to the prevention of attacks and the optimization of C1-INH-HAE management that is expected to provide a valuable benefit to the sufferers of angioedema.
[Mh] MeSH terms primary: Angioedemas, Hereditary/genetics
Genetic Association Studies
[Mh] MeSH terms secundary: Alleles
Amino Acid Substitution
Angioedemas, Hereditary/immunology
Angioedemas, Hereditary/metabolism
Angiotensin-Converting Enzyme Inhibitors
Autoimmune Diseases/immunology
Autoimmune Diseases/metabolism
Autoimmunity
Complement C1 Inactivator Proteins/chemistry
Complement C1 Inactivator Proteins/genetics
Complement C1 Inhibitor Protein/chemistry
Complement C1 Inhibitor Protein/genetics
Factor XII/genetics
Genetic Heterogeneity
Humans
Kinins/metabolism
Mutation
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Complement C1 Inactivator Proteins); 0 (Complement C1 Inhibitor Protein); 0 (Kinins); 0 (SERPING1 protein, human); 9001-30-3 (Factor XII)
[Em] Entry month:1702
[Cu] Class update date: 171107
[Lr] Last revision date:171107
[Js] Journal subset:IM
[Da] Date of entry for processing:160427
[St] Status:MEDLINE
[do] DOI:10.1007/s12016-016-8543-x

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[PMID]: 27012020
[Au] Autor:Moreno AS; Maia LS; Palhas PB; Dias MM; Muglia VF; Castelli EC; Bork K; Arruda LK
[Ti] Title:Genetic Analysis as a Practical Tool for Diagnosis of Hereditary Angioedema With Normal C1 Inhibitor: A Case Report.
[So] Source:J Investig Allergol Clin Immunol;26(1):57-9, 2016.
[Is] ISSN:1018-9068
[Cp] Country of publication:Spain
[La] Language:eng
[Mh] MeSH terms primary: DNA Mutational Analysis
Factor XII/genetics
Genetic Testing/methods
Hereditary Angioedema Type III/genetics
Mutation
[Mh] MeSH terms secundary: Adult
Female
Genetic Markers
Genetic Predisposition to Disease
Hereditary Angioedema Type III/blood
Hereditary Angioedema Type III/diagnosis
Hereditary Angioedema Type III/immunology
Hereditary Angioedema Type III/therapy
Humans
Phenotype
Predictive Value of Tests
Risk Factors
Tomography, X-Ray Computed
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Genetic Markers); 9001-30-3 (Factor XII)
[Em] Entry month:1604
[Cu] Class update date: 160325
[Lr] Last revision date:160325
[Js] Journal subset:IM
[Da] Date of entry for processing:160326
[St] Status:MEDLINE

  8 / 93 MEDLINE  
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PubMed Central Full text
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[PMID]: 26605293
[Au] Autor:Worm M; Köhler EC; Panda R; Long A; Butler LM; Stavrou EX; Nickel KF; Fuchs TA; Renné T
[Ad] Address:1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden
[Ti] Title:The factor XIIa blocking antibody 3F7: a safe anticoagulant with anti-inflammatory activities.
[So] Source:Ann Transl Med;3(17):247, 2015 Oct.
[Is] ISSN:2305-5839
[Cp] Country of publication:China
[La] Language:eng
[Ab] Abstract:The plasma protein factor XII (FXII) is the initiating protease of the procoagulant and proinflammatory contact system. FXII activates both the bradykinin (BK) producing kallikrein-kinin system and the intrinsic pathway of coagulation. Contact with negatively charged surfaces induces auto-activation of zymogen FXII that results in activated FXII (FXIIa). Various in vivo activators of FXII have been identified including heparin, misfolded protein aggregates, nucleic acids and polyphosphate. Murine models have established a central role of FXII in arterial and venous thromboembolic diseases. Despite the central function of FXII in pathologic thrombosis, its deficiency does not impair hemostasis in animals or humans. The selective role of FXIIa in thrombosis, but not hemostasis, offers an exciting novel strategy for safe anticoagulation based on interference with FXIIa. We have generated the recombinant fully human FXIIa-blocking antibody 3F7, which abolished FXIIa enzymatic activity and prevented thrombosis in a cardiopulmonary bypass system in large animals, in the absence of increased therapy-associated bleeding. Furthermore, 3F7 also interfered with BK-driven edema in the severe swelling disorder hereditary angioedema (HAE) type III. Taken together, targeting FXIIa with 3F7 appears to be a promising approach to treat edema disorders and thrombosis.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1511
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Da] Date of entry for processing:151126
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.3978/j.issn.2305-5839.2015.09.07

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[PMID]: 26502460
[Au] Autor:Malbrán E; Fernández Romero D; Juri MC; Larrauri BJ; Malbrán A
[Ad] Address:Unidad de Alergia, Asma e Inmunología Clínica, Buenos Aires, Argentina. E-mail: elomalbran@hotmail.com.
[Ti] Title:Epidemiology of angioedema without wheals in an allergy and immunology center.
[So] Source:Medicina (B Aires);75(5):273-6, 2015.
[Is] ISSN:0025-7680
[Cp] Country of publication:Argentina
[La] Language:eng
[Ab] Abstract:We describe the diagnostic epidemiology, the clinical course, the family history and the response to treatment of patients with angioedema without wheals (AWW) at an Allergy and Immunology Clinical Center. We reviewed the case records of all patients at our office from January 1997 to April 2013. We recorded sex, age, age at onset of symptoms, family history of angioedema, number of visits to the office, type of angioedema, and response to treatment from those patients with angioedema without wheals. We classified angioedema according to its pathophysiology. We also describe those patients with angioedema mimics. From a total of 17,823 new patients, 303 had a presumptive diagnosis of angioedema without wheals. Twenty-three patients had an angioedema mimic. Forty percent were male and 60% were female. Average age at first visit was 40.6. Average number of visits was 2.4. Fifty-seven patients referred a family history. We attributed idiopathic angioedema to 55.7% of patients, 24.3% were drug related, 15.7% were due to C1 inhibitor deficiency, 2.1% were drug related+idiopathic angioedema, 1.4% were type III and 0.7% had exercise-induced angioedema. Ninety six percent of 53 evaluable idiopathic angioedema patients referred a benefit with anti-histamine therapy. AWW was a rare cause of consultation. Most of our patients had anti H1 responsive idiopathic angioedema and none had allergic angioedema. Women cases prevailed over men's. Family history and average age of onset of symptoms were different among the different types of angioedema.
[Mh] MeSH terms primary: Angioedema/diagnosis
Angioedema/epidemiology
Histamine H1 Antagonists/therapeutic use
Rare Diseases/epidemiology
Tertiary Care Centers/statistics & numerical data
[Mh] MeSH terms secundary: Adolescent
Adult
Age of Onset
Aged
Aged, 80 and over
Ambulatory Care/statistics & numerical data
Angioedema/classification
Angioedema/drug therapy
Angioedemas, Hereditary/epidemiology
Child
Child, Preschool
Diagnosis, Differential
Family Health
Female
Humans
Male
Middle Aged
Prevalence
Rare Diseases/diagnosis
Rare Diseases/drug therapy
Retrospective Studies
Sex Factors
Symptom Assessment/statistics & numerical data
Urticaria/epidemiology
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Histamine H1 Antagonists)
[Em] Entry month:1604
[Cu] Class update date: 151027
[Lr] Last revision date:151027
[Js] Journal subset:IM
[Da] Date of entry for processing:151027
[St] Status:MEDLINE

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[PMID]: 26193639
[Au] Autor:Björkqvist J; de Maat S; Lewandrowski U; Di Gennaro A; Oschatz C; Schönig K; Nöthen MM; Drouet C; Braley H; Nolte MW; Sickmann A; Panousis C; Maas C; Renné T
[Ti] Title:Defective glycosylation of coagulation factor XII underlies hereditary angioedema type III.
[So] Source:J Clin Invest;125(8):3132-46, 2015 Aug 03.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hereditary angioedema type III (HAEIII) is a rare inherited swelling disorder that is associated with point mutations in the gene encoding the plasma protease factor XII (FXII). Here, we demonstrate that HAEIII-associated mutant FXII, derived either from HAEIII patients or recombinantly produced, is defective in mucin-type Thr309-linked glycosylation. Loss of glycosylation led to increased contact-mediated autoactivation of zymogen FXII, resulting in excessive activation of the bradykinin-forming kallikrein-kinin pathway. In contrast, both FXII-driven coagulation and the ability of C1-esterase inhibitor to bind and inhibit activated FXII were not affected by the mutation. Intravital laser-scanning microscopy revealed that, compared with control animals, both F12-/- mice reconstituted with recombinant mutant forms of FXII and humanized HAEIII mouse models with inducible liver-specific expression of Thr309Lys-mutated FXII exhibited increased contact-driven microvascular leakage. An FXII-neutralizing antibody abolished bradykinin generation in HAEIII patient plasma and blunted edema in HAEIII mice. Together, the results of this study characterize the mechanism of HAEIII and establish FXII inhibition as a potential therapeutic strategy to interfere with excessive vascular leakage in HAEIII and potentially alleviate edema due to other causes.
[Mh] MeSH terms primary: Blood Coagulation
Factor XII/metabolism
Hereditary Angioedema Type III/metabolism
Mutation, Missense
[Mh] MeSH terms secundary: Adult
Amino Acid Substitution
Animals
Antibodies, Neutralizing/pharmacology
Bradykinin/genetics
Bradykinin/metabolism
Disease Models, Animal
Factor XII/genetics
Female
Glycosylation/drug effects
Hereditary Angioedema Type III/drug therapy
Hereditary Angioedema Type III/genetics
Hereditary Angioedema Type III/pathology
Humans
Mice
Mice, Knockout
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antibodies, Neutralizing); 9001-30-3 (Factor XII); S8TIM42R2W (Bradykinin)
[Em] Entry month:1510
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:150721
[St] Status:MEDLINE


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