ライフサイエンスコーパス: angioedema

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

2 H) becomes clinically manifest as attacks of angioedema.

3 nt unlikely contribute to bradykinin-induced angioedema.

4 prone for local vascular leakage leading to angioedema.

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

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

7 the patient with NSAID-induced urticaria and angioedema.

8 the data and the resulting classification of angioedema.

9 a consensus conference aimed at classifying angioedema.

10 with different forms of bradykinin-mediated angioedema.

11 procedures and the presence of perioperative angioedema.

12 luated in other types of bradykinin-mediated angioedema.

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

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

15 difficult intubation, may precipitate severe angioedema.

16 ed by unpredictable and recurring attacks of angioedema.

17 concentrate in the management of hereditary angioedema.

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

19 placebo for treatment of an acute attack of angioedema.

20 t in the biology and treatment of hereditary angioedema.

21 , hyperkalemia, symptomatic hypotension, and angioedema.

22 hophysiology and the treatment of hereditary angioedema.

23 tor (C1INH) deficiency results in hereditary angioedema.

24 syndrome, hepatic dysfunction, and possibly angioedema.

25 ed drug to treat acute attacks of hereditary angioedema.

26 roved for treatment of attacks of hereditary angioedema.

27 suggested management of various subtypes of angioedema.

28 iotensin converting enzyme inhibitor-induced angioedema.

29 ed with decreased fear of suffocation due to angioedema.

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

31 nd to treat the swelling disorder hereditary angioedema.

32 severe H1-antihistamine-refractory CSU with angioedema.

33 sulting in adverse effects such as cough and angioedema.

34 mediate maculopapular exanthema or urticaria/angioedema.

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

36 taneous disease and NSAIDs-induced urticaria/angioedema.

37 eptor antagonist in ACE inhibitor-associated angioedema.

38 s of cerebral hemorrhagic transformation and angioedema.

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

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

41 [95%CI 1.35-2.38], I(2)=0%, high-certainty; angioedema: 2.25 [1.13-4.47], I(2)=0%, high-certainty; u

42 d least common reaction types were urticaria/angioedema (34.7%) and anaphylaxis (14.3%), respectively

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

44 ations in factor XII (FXII) cause hereditary angioedema, a life-threatening tissue swelling disease.

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

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

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

48 Like hereditary angioedema, acute IRI is also related to the uncontrolle

49 Recurrent angioedema (AE) is an important clinical problem in the

50 tion of patients carrying FXII-Lys/Arg309 to angioedema after trauma, and reveal a regulatory functio

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

52 e second one: single-NSAID-induced urticaria/angioedema/anaphylaxis and single-NSAID-induced delayed

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

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

55 t in various inflammatory diseases including angioedema and cancer.

56 in is a proinflammatory factor that mediates angioedema and inflammation in many diseases.

57 is a key player in some types of hereditary angioedema and is involved in septic shock, traumatic in

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

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

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

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

62 which selectively included CSU patients with angioedema and wheals.

63 notable advances in drug allergy, urticaria, angioedema, and anaphylaxis were reported in 2018.

64 in many cases, such as urticaria, flushing, angioedema, and anaphylaxis, are an expression of the bi

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

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

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

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

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

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

71 Hereditary angioedema attack history was collected at screening.

72 atment was accompanied by a reduction in the angioedema attack rate.

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

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

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

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

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

78 Angioedema attacks result from increased vascular permea

79 ular preconditioning' that may predispose to angioedema attacks.

80 re no biomarkers predicting the frequency of angioedema attacks.

81 sumed to provide clinical protection against angioedema attacks.

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

83 ptimal clinical efficacy in the treatment of angioedema attacks.

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

85 nduced), ACE-inhibitor intake and hereditary angioedema (both bradykinin-mediated).

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

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

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

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

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

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

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

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

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

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

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

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

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

99 This prompted us to develop such a tool, the Angioedema Control Test (AECT).

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

101 Predictors of perioperative angioedema could not be identified.

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

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

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

105 , hyperkalemia, symptomatic hypotension, and angioedema did not differ significantly between the two

106 , hyperkalemia, symptomatic hypotension, and angioedema did not differ significantly between the two

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

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

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

110 Hereditary angioedema due to C1 inhibitor deficiency is characteriz

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

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

113 Angioedema due to hereditary deficiency of C1 inhibitor

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

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

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

117 The absence of urticaria/angioedema during sting-induced anaphylaxis is indicativ

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

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

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

121 Patients with angioedema experience unpredictable attacks of tissue sw

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

123 Histaminergic angioedema generally presents with urticaria and/or prur

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

125 1-inhibitor, but individuals with hereditary angioedema (HAE) are deficient in C1-inhibitor and conse

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

127 monstrated efficacy in preventing hereditary angioedema (HAE) attacks in the phase 3 HELP Study.

128 evelopment for the prophylaxis of hereditary angioedema (HAE) attacks.

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

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

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

132 Hereditary angioedema (HAE) comprises HAE with C1-inhibitor deficie

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

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

135 Patients with hereditary angioedema (HAE) experience episodes of soft tissue swel

136 Patients with hereditary angioedema (HAE) have gained additional access to highly

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

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

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

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

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

142 Hereditary angioedema (HAE) is a rare genetic disorder primarily ca

143 Hereditary angioedema (HAE) is an autosomal dominant disease charac

144 Hereditary angioedema (HAE) is associated with recurrent, painful,

145 Hereditary angioedema (HAE) is characterized by unpredictable attac

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

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

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

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

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

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

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

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

154 provoke acute tissue swelling in hereditary angioedema (HAE).

155 of life (HRQoL) in patients with hereditary angioedema (HAE).

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

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

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

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

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

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

162 s was made in our understanding of recurrent angioedema in patients with normal laboratory results.

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

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

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

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

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

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

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

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

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

172 Angioedema induced by treatment with angiotensin-convert

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

174 Hereditary angioedema is a disabling, potentially fatal condition c

175 Recurrent angioedema is a frequent clinical problem characterized

176 Angioedema is a life-threatening syndrome with multiple

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

178 Angioedema is a potentially life-threatening occurrence

179 Angioedema is a result of increased vascular permeabilit

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

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

182 Isolated visceral angioedema is an extremely rare complication of angioten

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

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

185 Hereditary angioedema is characterized by recurrent and unpredictab

186 Angioedema is defined as localized and self-limiting ede

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

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

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

190 Hereditary angioedema is often misdiagnosed and poorly treated.

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

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

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

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

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

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

197 Angioedema may be mediated by histamine, bradykinin or o

198 Misdiagnosis of mucositis and angioedema may delay appropriate therapy.

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

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

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

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

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

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

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

206 on is available for NSAID-induced urticarial/angioedema (NIUA), despite it being the most frequent cl

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

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

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

210 NGPT1-HAE), kininogen 1 genes (KNG1-HAE), or angioedema of unknown origin (U-HAE).

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

212 %] in the tralokinumab every 2 weeks group), angioedema (one [1%] in the placebo group), and worsenin

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

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

215 with NECD and single-NSAID-induced urticaria/angioedema or anaphylaxis (SNIUAA) for comparison.

216 characterized by the development of wheals, angioedema or both in response to cold exposure.

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

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

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

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

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

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

223 Angioedema owing to hereditary deficiency of C1 inhibito

224 represents the most essential mechanism for angioedema patient protection.

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

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

227 Recurrent angioedema patients with chronic spontaneous urticaria o

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

229 ases including systemic lupus erythematosus, angioedema, pemphigus, bullous pemphigoid, and HS.

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

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

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

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

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

235 The Angioedema Quality of Life Questionnaire (AE-QoL) was ad

236 Angioedema Quality of Life Questionnaire is the first an

237 meaningful mean change from baseline in the angioedema-quality of life (AE-QoL) total score was show

238 ebilitating neuropathy and an unusually high angioedema rate.

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

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

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

242 When angioedema recurs without significant wheals, the patien

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

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

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

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

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

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

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

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

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

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

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

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

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

256 Antiestrogens can worsen angioedema symptoms.

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

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

259 state of diagnosis and management of various angioedema syndromes.

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

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

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

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

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

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

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

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

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

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

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

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

272 ypothesize that a kinin-dependent local lung angioedema via B1R and eventually B2R is an important fe

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

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

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

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

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

278 two patients with severe bradykinin-mediated angioedema were initially administered weekly subcutaneo

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

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

281 .5%}]), whereas higher incidence of rash and angioedema were reported for protocols with <6 doses esc

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

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

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

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

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

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

288 Hereditary angioedema with C1 inhibitor deficiency is characterized

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

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

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

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

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

294 0078) and was predicted by the occurrence of angioedema with first reaction (P = .01).

295 Hereditary angioedema with normal C1 esterase inhibitor and mutatio

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

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

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

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

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

301 ated a registry including different forms of angioedema without wheals.