ライフサイエンスコーパス: angioedema

1 nt unlikely contribute to bradykinin-induced angioedema.

2 iotensin converting enzyme inhibitor-induced angioedema.

3 O in bradykinin-induced extravasation and/or angioedema.

4 IUA), and single NSAID-induced urticaria and angioedema.

5 the patient with NSAID-induced urticaria and angioedema.

6 the data and the resulting classification of angioedema.

7 a consensus conference aimed at classifying angioedema.

8 ed with decreased fear of suffocation due to angioedema.

9 with different forms of bradykinin-mediated angioedema.

10 procedures and the presence of perioperative angioedema.

11 luated in other types of bradykinin-mediated angioedema.

12 ed in patients presenting with wheals and/or angioedema.

13 he management of patients with wheals and/or angioedema.

14 -to-resolution from ACE inhibitor-associated angioedema.

15 difficult intubation, may precipitate severe angioedema.

16 ed by unpredictable and recurring attacks of angioedema.

17 nd to treat the swelling disorder hereditary angioedema.

18 concentrate in the management of hereditary angioedema.

19 signs, most notably sepsis, anaphylaxis, and angioedema.

20 severe H1-antihistamine-refractory CSU with angioedema.

21 placebo for treatment of an acute attack of angioedema.

22 t in the biology and treatment of hereditary angioedema.

23 hophysiology and the treatment of hereditary angioedema.

24 tor (C1INH) deficiency results in hereditary angioedema.

25 syndrome, hepatic dysfunction, and possibly angioedema.

26 expressing this mutant protein has ever had angioedema.

27 ry third day to six patients with hereditary angioedema.

28 ntion and treatment of attacks of hereditary angioedema.

29 utant from a patient with type II hereditary angioedema.

30 sulting in adverse effects such as cough and angioedema.

31 gh-molecular-weight kininogen and attacks of angioedema.

32 roved for treatment of attacks of hereditary angioedema.

33 eptor antagonist in ACE inhibitor-associated angioedema.

34 s of cerebral hemorrhagic transformation and angioedema.

35 icacy end point was the number of attacks of angioedema.

36 suggested management of various subtypes of angioedema.

37 QoL), especially in patients with wheals and angioedema.

38 H) becomes clinically manifest as attacks of angioedema.

39 Among patients with urticaria/angioedema, 13 patients (3.9%) had a history of idiopath

40 ere assessed; 217 had histories of urticaria/angioedema, 50 of anaphylaxis, 26 of nonimmediate cutane

41 INE search was conducted with the MeSH terms angioedema, acquired angioedema, hereditary angioedema t

42 hing "A focused parameter update: Hereditary angioedema, acquired C1 inhibitor deficiency, and angiot

43 on age, gender, duration of CSU, presence of angioedema, activity (UAS at the time of blood sampling

44 nts, there were 16 outpatient recurrences of angioedema among 13 patients during 189 patient-years of

45 diate hypersensitivity reactions (urticaria, angioedema, anaphylaxis, and allergic rhinitis) that res

46 on, cost, and risk of side effects including angioedema and Alzheimer's disease.

47 ittle/no evidence was available on vibratory angioedema and aquagenic and contact urticaria.

48 in patients with acute attacks of hereditary angioedema and assessed the length of time to a clinical

49 t in various inflammatory diseases including angioedema and cancer.

50 spected when patients present with recurrent angioedema and low serum levels of C4 with normal levels

51 IgE antibody production leading to urticaria/angioedema and rarely to anaphylaxis.

52 nsteroidal anti-inflammatory drug-associated angioedema and serum sickness-like reactions, are more f

53 ans of both preventing attacks of hereditary angioedema and treating acute attacks.

54 xception of one patient who developed facial angioedema and two patients with > 20% drop in FEV1 (fol

55 which selectively included CSU patients with angioedema and wheals.

56 ANGPT1 impairment is associated with angioedema, and ANGPT1 variants can be the basis of HAE.

57 ficiency that is associated with thrombosis, angioedema, and emphysema.

58 accepted classification, different types of angioedema are not uniquely identified.

59 als, the patient should be diagnosed to have angioedema as a distinct disease.

60 nical evidence for their potential to induce angioedema as known already from blockers of the renin-a

61 potentially allergic diseases (anaphylaxis, angioedema, asthma, conjunctivitis, drug allergies, ecze

62 Hereditary angioedema attack history was collected at screening.

63 local activation process at the site of the angioedema attack.

64 pathomechanism and development of hereditary angioedema attacks in different patients.

65 refore we postulate an alternative model for angioedema attacks in patients with HAE, which assumes a

66 asma cascade systems, which results in acute angioedema attacks in patients with HAE.

67 ts with C1-INH-HAE experiencing more than 12 angioedema attacks per year were characterized by higher

68 Angioedema attacks result from increased vascular permea

69 sumed to provide clinical protection against angioedema attacks.

70 ducts are approved for the treatment of such angioedema attacks.

71 ptimal clinical efficacy in the treatment of angioedema attacks.

72 ular preconditioning' that may predispose to angioedema attacks.

73 re no biomarkers predicting the frequency of angioedema attacks.

74 rience with icatibant in eight patients with angioedema because of acquired C1-INH deficiency (AAE).

75 ibitor and had a first documented episode of angioedema between 1986 and 1992 were followed up for re

76 Number of angioedema-burdened days, time interval between successi

77 There was a threefold improvement in angioedema-burdened days/week with omalizumab (0.3) vs p

78 of patients with hypotension and nonserious angioedema but lower proportions with renal impairment,

79 seen in plasma from patients with hereditary angioedema but not plasma from healthy subjects.

80 fective not only in patients with hereditary angioedema, but also in a variety of other disease model

81 lasmin generation in all types of hereditary angioedema, but particularly hereditary angioedema with

82 ors are associated with an increased risk of angioedema, but the risk of recurrent angioedema if trea

83 Because attacks of hereditary angioedema can be related to infection and/or exposure t

84 ed here also provides an explanation for why angioedema can occur at multiple sites during an attack

85 e (ACE) inhibitors accounts for one third of angioedema cases in the emergency room; it is usually ma

86 ic events in female patients with hereditary angioedema caused by C1 inhibitor deficiency (HAE-C1-INH

87 atment including coniotomy or tracheotomy in angioedema caused by these drugs.

88 , solar urticaria, heat urticaria, vibratory angioedema, cholinergic urticaria, contact urticaria, an

89 Selected publications describing angioedema, clinical trials, diagnosis, management, and

90 of procedures, the presence of perioperative angioedema could not be excluded, leading to a maximum p

91 Predictors of perioperative angioedema could not be identified.

92 Patients with ACE inhibitor-associated angioedema (defined as swelling of lips, tongue, pharynx

93 mance outcome provided features suitable for angioedema diagnostic or follow-up.

94 ontact-phase activation and correlation with angioedema diagnostic requirements.

95 al anti-inflammatory drugs-induced urticaria/angioedema does not seem to precede the onset of CU over

96 iotensin-converting enzyme inhibitor-induced angioedema does not typically present with urticaria/wea

97 Hereditary angioedema due to C1 inhibitor deficiency (HAE-C1-INH) i

98 Hereditary angioedema due to C1 inhibitor deficiency is characteriz

99 geneous clinical manifestation of hereditary angioedema due to C1-INH deficiency (C1-INH-HAE) represe

100 ous attack (EA) in a patient with hereditary angioedema due to C1-INH deficiency to better understand

101 Angioedema due to hereditary deficiency of C1 inhibitor

102 s is insufficiently controlled in hereditary angioedema due to the deficiency of C1-inhibitor (C1-INH

103 patients with a first confirmed diagnosis of angioedema during 51 752 person-years of ACE inhibitor u

104 icacy was assessed by the rate of attacks of angioedema during a prespecified period (day 8 to day 50

105 levation of BST, (2) absence of urticaria or angioedema during anaphylaxis, (3) time interval of less

106 study, CSU patients (18-75 years) with >/=4 angioedema episodes during the 6 months before inclusion

107 dened days, time interval between successive angioedema episodes, disease activity, angioedema-specif

108 ients with greater disease activity and with angioedema experience greater HRQoL impairments.

109 Patients with angioedema experience unpredictable attacks of tissue sw

110 ved C1-INH has been used to treat hereditary angioedema for more than 30 years with excellent safety.

111 Histaminergic angioedema generally presents with urticaria and/or prur

112 diated angioedema, which includes hereditary angioedema (HAE types I, II and III), acquired C1-INH de

113 1-inhibitor, but individuals with hereditary angioedema (HAE) are deficient in C1-inhibitor and conse

114 Historically, treatment for hereditary angioedema (HAE) attacks has been administered by health

115 r antagonist, in the treatment of hereditary angioedema (HAE) attacks.

116 Hereditary angioedema (HAE) caused by a deficiency of functional C1

117 Hereditary angioedema (HAE) caused by C1-inhibitor (C1-INH) deficie

118 ommended management of attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor (C1-INH) d

119 Hereditary angioedema (HAE) due to C1 inhibitor deficiency manifest

120 or XII (FXII) are associated with hereditary angioedema (HAE) in the presence of normal C1 esterase i

121 Hereditary angioedema (HAE) is a disease characterized by recurrent

122 Hereditary angioedema (HAE) is a heterozygous deficiency of first c

123 Hereditary angioedema (HAE) is a rare genetic disease characterized

124 Hereditary angioedema (HAE) is a rare genetic disease usually cause

125 Hereditary angioedema (HAE) is characterized by unpredictable attac

126 Hereditary angioedema (HAE) types I and II were then tested.

127 ed treatment for acute attacks of hereditary angioedema (HAE) with C1-inhibitor (C1-INH) deficiency.

128 Hereditary angioedema (HAE) with normal C1 inhibitor (C1Inh) associ

129 Hereditary angioedema (HAE) with normal C1-INH (HAEnCI) may be link

130 ency of C1-INH is associated with hereditary angioedema (HAE), an autosomal inherited disease charact

131 Hereditary angioedema (HAE), caused by deficiency in C1-inhibitor (

132 e management and understanding of hereditary angioedema (HAE), while integrating insights into pediat

133 nder development for treatment of hereditary angioedema (HAE).

134 ement of patients with chronic urticaria and angioedema has been prepared by the Standards of Care Co

135 ients who are double-positive for wheals and angioedema has not been systematically studied.

136 ted with the MeSH terms angioedema, acquired angioedema, hereditary angioedema type III, and angioten

137 isk of angioedema, but the risk of recurrent angioedema if treatment is continued is not known.

138 converting enzyme (ACE) inhibitor-associated angioedema in 1 study of European patients.

139 defined as the exacerbation of wheals and/or angioedema in patients with a history of chronic spontan

140 The risk of perioperative angioedema in patients with HAE type I or II without pro

141 ith recurrent wheals and bradykinin-mediated angioedema in patients with recurrent swellings.

142 yze symptom presentation of gastrointestinal angioedema in pediatric and adult HAE patients.

143 The absence of urticaria or angioedema in severe reactions to Hymenoptera stings wit

144 Angioedema in the previous 12 months was reported by 66%

145 editary angioedema or ACE-inhibitor-mediated angioedema including variations in bradykinin type 2 rec

146 r in transplant recipients, the incidence of angioedema increases significantly.

147 nifested as rhinitis and asthma or urticaria/angioedema induced by cross-reacting nonsteroidal anti-i

148 The majority of angioedema induced by DPP IV inhibitors occurs during co

149 ing contrast, the molecular pathways causing angioedema induced by neprilysin inhibitors, that is, sa

150 Angioedema induced by treatment with angiotensin-convert

151 hat emerged during treatment were attacks of angioedema, injection-site pain, and headache.

152 Hereditary angioedema is a disabling, potentially fatal condition c

153 Recurrent angioedema is a frequent clinical problem characterized

154 Angioedema is a life-threatening syndrome with multiple

155 Hereditary angioedema is a potentially life-threatening disorder, b

156 Angioedema is a potentially life-threatening occurrence

157 Angioedema is a result of increased vascular permeabilit

158 PURPOSE OF REVIEW: Angioedema is a serious complication of renin-angiotensi

159 Hereditary angioedema is an autosomal-dominant deficiency of C1 inh

160 Isolated visceral angioedema is an extremely rare complication of angioten

161 Absence of urticaria/angioedema is an indicator of severe anaphylaxis and pos

162 ition of complement proteases, suggests that angioedema is caused by bradykinin generated from contac

163 Angioedema is defined as localized and self-limiting ede

164 Although angioedema is induced by bradykinin, the function and ac

165 These data support the hypothesis that angioedema is mediated by bradykinin via Bk2R.

166 nomenon of isolated ACEI-associated visceral angioedema is necessary given the increasing use of thes

167 Hereditary angioedema is often misdiagnosed and poorly treated.

168 C1INH) for on-demand treatment of hereditary angioedema is purified from milk of transgenic rabbits.

169 The absence of urticaria/angioedema is significantly related to BST elevation (P

170 role of this mutation in the pathogenesis of angioedema is unclear.

171 In patients with hereditary angioedema, kallikrein and bradykinin formation can occu

172 After the episode of angioedema, lifetime discontinuation of all renin-angiot

173 genic insights, for example, into urticaria, angioedema, mastocytosis, led to the development of new

174 Angioedema may be mediated by histamine, bradykinin or o

175 Misdiagnosis of mucositis and angioedema may delay appropriate therapy.

176 o, reduced the rate of attacks of hereditary angioedema (mean difference with 40 IU, -2.42 attacks pe

177 Multiple NSAID-induced urticaria/angioedema (MNSAID-UA) is an entity well differentiated

178 o aspirin included urticaria (n=177, 53.6%), angioedema (n=69, 20.9%), asthma (n=65, 19.7%), and anap

179 In subjects with hereditary angioedema, nanofiltered C1 inhibitor concentrate shorte

180 vity reactions, with NSAID-induced urticaria/angioedema (NIUA) being the most frequent clinical entit

181 persensitivity with NSAIDs-induced urticaria/angioedema (NIUA) the most common phenotype.

182 dal anti-inflammatory drug-induced urticaria/angioedema (NIUA), and single NSAID-induced urticaria an

183 first known case of ACEI-associated visceral angioedema occurring in a liver transplant recipient who

184 except for three, experienced an unequivocal angioedema of the lips as a positive reaction in SBPCPT.

185 igned patients who had ACE-inhibitor-induced angioedema of the upper aerodigestive tract to treatment

186 ncreases local vasopermeability and mediates angioedema on interaction with BK receptor 2 on the endo

187 %] in the tralokinumab every 2 weeks group), angioedema (one [1%] in the placebo group), and worsenin

188 In the losartan group, one (1%) patient had angioedema, one (1%) had deterioration of renal function

189 hich trigger and/or contribute to hereditary angioedema or ACE-inhibitor-mediated angioedema includin

190 e common plasma leakage syndromes, including angioedema or systemic anaphylaxis.

191 eing investigated for recurrent anaphylaxis, angioedema, or acute urticaria underwent spirometry, exh

192 rized by the recurrence of transient wheals, angioedema, or both for more than 6 weeks.

193 caria (CSU) is defined as persistent wheals, angioedema, or both lasting for >6 weeks due to known or

194 cell-driven disease, presenting with wheals, angioedema, or both.

195 disorder characterized by recurrent wheals, angioedema, or both.

196 Angioedema owing to hereditary deficiency of C1 inhibito

197 represents the most essential mechanism for angioedema patient protection.

198 A type I hereditary angioedema patient was recently described in whom the C1

199 ssess changes of QoL impairment in recurrent angioedema patients over time, including changes due to

200 One hundred and ten angioedema patients took part in the validation of AE-Qo

201 Recurrent angioedema patients with chronic spontaneous urticaria o

202 uality of life (QoL) impairment in recurrent angioedema patients.

203 imary end point was the number of attacks of angioedema per period, with each subject acting as his o

204 ith systemic lupus erythematosus but without angioedema previously was shown to have diminished inhib

205 At baseline, the mean (SD) total Angioedema QoL (AE-QoL; 56.2 [18.7] and 59.9 [19.2]) and

206 ed and included in the final instrument, the Angioedema QoL Questionnaire (AE-QoL).

207 The Angioedema Quality of Life Questionnaire (AE-QoL) has re

208 Angioedema Quality of Life Questionnaire is the first an

209 ebilitating neuropathy and an unusually high angioedema rate.

210 ammatory drug (NSAID)-induced urticarial and angioedema reactions are among the most commonly encount

211 Recurrent angioedema (RecA) is a frequent clinical problem charact

212 dema results in a markedly increased rate of angioedema recurrence with serious morbidity.

213 When angioedema recurs without significant wheals, the patien

214 utosomal dominant disorder type I hereditary angioedema, reduced levels of C1 inhibitor may be due in

215 ic spontaneous urticaria (CSU) patients with angioedema refractory to high doses of H1 -antihistamine

216 lts as well as all other applied anchors for angioedema-related QoL impairment and disease activity.

217 Angioedema-related QoL, skin-related QoL impairment, and

218 the contact activation system for hereditary angioedema-related vascular permeability.

219 Hereditary angioedema results from a congenital deficiency of funct

220 Continuing use of ACE inhibitors in spite of angioedema results in a markedly increased rate of angio

221 ents taking ACE inhibitors who had recurrent angioedema revealed that physicians attributed angioedem

222 ng in C1 inhibitor deficiency as well as the angioedema seen with ACE inhibitors and may contribute t

223 Therefore, the risk of angioedema should always be considered, especially in am

224 to the drug (single NSAID-induced urticaria/angioedema, SNIUA), and (iii) controls who tolerated NSA

225 ssive angioedema episodes, disease activity, angioedema-specific and overall QoL impairment were seco

226 Omalizumab significantly improved angioedema-specific QoL (P < 0.001).

227 a Quality of Life Questionnaire is the first angioedema-specific QoL questionnaire.

228 The For Angioedema Subcutaneous Treatment (FAST)-2, a phase III,

229 Patient-reported data on urticaria and angioedema symptoms, HRQoL, and work productivity and ac

230 Antiestrogens can worsen angioedema symptoms.

231 The mechanistic understanding of angioedema syndromes has improved in recent years, and n

232 ophysiology, classification and treatment of angioedema syndromes, with an emphasis on the novel phar

233 state of diagnosis and management of various angioedema syndromes.

234 is, food allergies, urticaria, nonhereditary angioedema, systemic anaphylaxis, and allergic conjuncti

235 trial involving 22 subjects with hereditary angioedema that compared prophylactic twice-weekly injec

236 In patients with hereditary angioedema, the prophylactic use of a subcutaneous C1 in

237 Among patients with ACE-inhibitor-induced angioedema, the time to complete resolution of edema was

238 ensin-converting enzyme inhibitor-associated angioedema." This is a complete and comprehensive docume

239 underlies diseases as diverse as cirrhosis, angioedema, thrombosis and dementia.

240 gioedema revealed that physicians attributed angioedema to a number of causes not related to ACE inhi

241 nts with more than two episodes of urticaria/angioedema to a single NSAID with good tolerance to a st

242 Hereditary angioedema type III (HAEIII) is a rare inherited swellin

243 angioedema, acquired angioedema, hereditary angioedema type III, and angiotensin converting enzyme i

244 Hereditary angioedema types I and II are caused by a functional def

245 nts with moderate-to-severe CSU symptoms and angioedema unresponsive to high doses of antihistamine t

246 nduced acute skin reactions manifesting with angioedema, urticaria, or both have been distinguished:

247 her SBT levels (P = .03) but only rarely had angioedema/urticaria associated with hypotension (P = .0

248 reaction characteristics (isolated urticaria/angioedema vs other presentations), baseline egg-specifi

249 The median time to first recurrence of angioedema was 57-63 days with omalizumab and <5 days wi

250 The rate of angioedema was much higher in users of ACE inhibitors wi

251 The incidence of asphyxiation due to angioedema was similar for HAE-FXII and HAE-unknown.

252 es of acquired and three types of hereditary angioedema were identified as separate forms from the an

253 Urticaria and angioedema were not reported as symptoms in 40.7% and 34

254 chronic spontaneous urticaria or hereditary angioedema were repeatedly asked to complete the AE-QoL

255 .5%}]), whereas higher incidence of rash and angioedema were reported for protocols with <6 doses esc

256 Bradykinin-mediated angioedema, which includes hereditary angioedema (HAE ty

257 y for C1INH deficiency results in hereditary angioedema, which is mediated by bradykinin.

258 n patients with type I or type II hereditary angioedema who had had four or more attacks in a consecu

259 Hereditary angioedema with a mutation in the PLG gene is a novel ty

260 us documents published to date on hereditary angioedema with C1 inhibitor deficiency (C1-INH-HAE) hav

261 Hereditary angioedema with C1 inhibitor deficiency (C1-INH-HAE) is

262 Hereditary angioedema with C1 inhibitor deficiency is characterized

263 n of lanadelumab to patients with hereditary angioedema with C1 inhibitor deficiency reduced cleavage

264 ogen in plasma from patients with hereditary angioedema with C1 inhibitor deficiency to levels approa

265 Patients with hereditary angioedema with C1 inhibitor deficiency were randomly as

266 ial for prophylactic treatment of hereditary angioedema with C1 inhibitor deficiency.

267 with other NSAIDs, and the last patient had angioedema with different NSAIDs.

268 Hereditary angioedema with normal C1 esterase inhibitor and mutatio

269 Hereditary angioedema with normal C1 inhibitor levels (HAE-N) is as

270 tary angioedema, but particularly hereditary angioedema with normal C1 inhibitor with a factor XII mu

271 Hereditary angioedema with normal C1-INH may be linked to specific

272 y of the disease remains unknown (hereditary angioedema with yet unknown genetic defect [U-HAE]).

273 The rate of documented angioedema without prophylaxis across all procedures was