ライフサイエンスコーパス: anaphylaxis

1 at relative PGE(2) deficiency predisposes to anaphylaxis.

2 that EPIT specifically decrease IgE-mediated anaphylaxis.

3 No known therapies can prevent anaphylaxis.

4 alpha-tryptase and increased risk for severe anaphylaxis.

5 eactions (ARs) (7% in controls), including 1 anaphylaxis.

6 ectant that can cause IgE-mediated urticaria/anaphylaxis.

7 We did not find any data on food fatal anaphylaxis.

8 t allergies are the most important causes of anaphylaxis.

9 strated in a mouse model of passive systemic anaphylaxis.

10 hey may cause fulminant MC degranulation and anaphylaxis.

11 the most common cause of fatal food-related anaphylaxis.

12 ry group of clinical and research experts in anaphylaxis.

13 uld prevent IgE-mediated responses including anaphylaxis.

14 he food allergies, atopic eczema, asthma, to anaphylaxis.

15 Epinephrine is the first-line treatment for anaphylaxis.

16 of mast cell IgE and prevented IgE-mediated anaphylaxis.

17 ) was more frequently associated with severe anaphylaxis.

18 prophylactic therapy that reliably prevents anaphylaxis.

19 e used in a murine model of passive systemic anaphylaxis.

20 ry symptoms) or food-dependent NSAID-induced anaphylaxis.

21 C activation via EP2/EP4 and protect against anaphylaxis.

22 ean age, 43.0; 44% male) were diagnosed with anaphylaxis.

23 antation from donors with a history of fatal anaphylaxis.

24 o investigate the role of TWEAK/Fn14 axis in anaphylaxis.

25 ptake of food allergens is key to triggering anaphylaxis.

26 particular, in patients without a history of anaphylaxis.

27 which are the most common triggers of fatal anaphylaxis.

28 ial to prevent recurrent radiocontrast media anaphylaxis.

29 cantly protected against death during severe anaphylaxis.

30 e in regulating serum IgE level and allergic anaphylaxis.

31 ed as a function of the clinical severity of anaphylaxis.

32 harmacotherapy for uniphasic and/or biphasic anaphylaxis.

33 rameters, connected with high risk of severe anaphylaxis.

34 Foods are the commonest cause of anaphylaxis.

35 OX inhibitors are also frequent cofactors in anaphylaxis.

36 During up-dosing, 19.4% experienced anaphylaxis.

37 ersensitivity reaction clinically suggesting anaphylaxis.

38 ients with drug allergy, urticaria, HAE, and anaphylaxis.

39 alternative therapeutic target to ameliorate anaphylaxis.

40 lly linked to immediate hypersensitivity and anaphylaxis.

41 ts in the life-threatening allergic reaction anaphylaxis.

42 to monitor and treat IgE mast cell-mediated anaphylaxis.

43 nd likely activated the classical pathway of anaphylaxis.

44 ic options for modulating pseudo-allergy and anaphylaxis.

45 r intraperitoneal injection and assessed for anaphylaxis.

46 eat is a common food allergen that can cause anaphylaxis.

47 ng allergen immunotherapy without triggering anaphylaxis.

48 but not IgG, and prevents the initiation of anaphylaxis.

49 egranulation to attenuate pseudo-allergy and anaphylaxis.

50 Food allergy is the most common cause of anaphylaxis.

51 in an animal model of cutaneous and systemic anaphylaxis.

52 tive instruction and prevention of recurrent anaphylaxis.

53 at anaphylaxis are risk factors for biphasic anaphylaxis.

54 ics and their in vitro and in vivo impact on anaphylaxis.

55 at the injection site to reduce the risk of anaphylaxis.

56 tibody treatment and fully protected against anaphylaxis.

57 measures offered to patients who experienced anaphylaxis.

58 d for the manifestations of food allergy and anaphylaxis.

59 ng the most important food-related causes of anaphylaxis.

60 dministering asialylated IgE-markedly reduce anaphylaxis.

61 L-10 was not required for protection against anaphylaxis.

62 the diagnosis, management and prevention of anaphylaxis.

63 allergy is frequently associated with severe anaphylaxis.

64 cells and completely suppressed IgE-mediated anaphylaxis.

65 flammation at the injection site to systemic anaphylaxis.

66 iver and lung recipients developed grade III anaphylaxis.

67 hydrogenase inhibitor protected mice against anaphylaxis.

68 whom were female, participated; 22 (39%) had anaphylaxis.

69 dverse events such as infusion reactions and anaphylaxis.

70 e, and practical way to prevent IgE-mediated anaphylaxis.

71 ants receiving NAC [nausea and vomiting (3), anaphylaxis (1), pain at drip site (1)].

72 types were urticaria/angioedema (34.7%) and anaphylaxis (14.3%), respectively.

73 Of episodes, four (17%) presented with anaphylaxis, 14 (60%) presented with local reaction, and

74 Anaphylaxis, a life-threatening allergic reaction, is de

75 Anaphylaxis, a rare and potentially life-threatening hyp

76 acute allergic reactions, notably including anaphylaxis, a severe and potentially fatal IgE-dependen

77 gainst innocuous food antigens can result in anaphylaxis, a severe life-threatening consequence of al

78 Unspecified anaphylaxis accounted for 21%-28% of all cases, underlin

79 hese results, the patient was diagnosed with anaphylaxis after a sting by the ant.

80 We sought to describe reports of anaphylaxis after vaccination made to the Vaccine Advers

81 After diagnosis and treatment of anaphylaxis, all patients should be kept under observati

82 Main outcomes included anaphylaxis, allergic or adverse reactions, epinephrine

83 t reliable interventions to prevent biphasic anaphylaxis, although evidence supports a role for antih

84 Sera from 48 patients with anaphylaxis and 27 healthy subjects were analyzed for PG

85 We found a higher percentage of anaphylaxis and delayed onset of symptoms in the LTP-mon

86 y less able than divalent mAbs are to induce anaphylaxis and deplete mast cell and basophil IgE, but

87 ted as was its impact on mast cell-dependent anaphylaxis and food allergy phenotypes in vivo.

88 alpha mAbs more safely suppress IgE-mediated anaphylaxis and food allergy than divalent variants of t

89 nd were used to suppress murine IgE-mediated anaphylaxis and food allergy.

90 More information about anaphylaxis and its management from healthcare professio

91 (MC)-associated diseases, including allergy/anaphylaxis and neuroinflammatory pain disorders, exhibi

92 o data, mast cell-mediated passive cutaneous anaphylaxis and passive systemic anaphylaxis were reduce

93 with anaphylaxis should receive education on anaphylaxis and risk of recurrence, trigger avoidance, s

94 e: single-NSAID-induced urticaria/angioedema/anaphylaxis and single-NSAID-induced delayed reactions.

95 The epidemiology and triggers of anaphylaxis and the mechanisms underlying anaphylaxis we

96 accurately ascertaining the causes of fatal anaphylaxis and therefore in assigning the proper ICD-10

97 Severe anaphylaxis and/or the need for repeated doses of epinep

98 u p 3 sensitization, Tri a 19 sensitization, anaphylaxis, and any NSAID different from pyrazolones),

99 anut-specific IgE-mediated passive cutaneous anaphylaxis, and attenuated dansyl IgE-mediated systemic

100 mouse model, reducing IgE-mediated systemic anaphylaxis, and inhibits airway tryptase in Ascaris-sen

101 ns that are considered off-target, including anaphylaxis, and organ-specific and severe cutaneous adv

102 TWEAK levels were increased in patients with anaphylaxis, and plasma from those patients increased Fn

103 However, the actual number of deaths by anaphylaxis, and their related triggers, is probably und

104 reflexus), wheat-dependent exercise-induced anaphylaxis, Anisakis simplex allergy and mast cell diso

105 In the case of anaphylaxis appropriate supportive measures including th

106 Patients with a history of anaphylaxis are at risk of future anaphylactic reactions

107 hat address the immune component of allergic anaphylaxis are inadequate.

108 anifestations associated with food-triggered anaphylaxis are largely unexplored.

109 d for repeated doses of epinephrine to treat anaphylaxis are risk factors for biphasic anaphylaxis.

110 Epidemiological data on fatal anaphylaxis are underestimated worldwide.

111 such as urticaria, flushing, angioedema, and anaphylaxis, are an expression of the biological effects

112 cipants described their first experiences of anaphylaxis as frightening.

113 the medical records to analyze patients with anaphylaxis as the primary diagnosis who visited the eme

114 ons for persistent, refractory, and biphasic anaphylaxis, as well as for persistent and biphasic nona

115 scribe our experience of cases of refractory anaphylaxis at in-hospital challenge and propose a frame

116 used for first-line emergency management of anaphylaxis but little robust research has assessed its

117 ng number of adults are being diagnosed with anaphylaxis, but its impact on health-related quality of

118 omalizumab can induce skin inflammation and anaphylaxis by engaging FcgammaRs, and demonstrate that

119 weeks of EPIT significantly protects against anaphylaxis by promoting a faster recovery of challenged

120 ewarming and resolve within an hour and that anaphylaxis can occur.

121 hospital involving patients with history of anaphylaxis carrying an EAI.

122 ases in comparison with sex- and age-matched anaphylaxis cases triggered by other elicitors (non-VIA

123 We considered this case to be of anaphylaxis caused by koayu fish from Lake Biwa and spec

124 asps; therefore, we hypothesized that he had anaphylaxis caused by the insect's sting.

125 We previously demonstrated that IgE-mediated anaphylaxis could be safely prevented in wild-type BALB/

126 For accurate histamine measurements during anaphylaxis, DAO inhibition is essential to inhibit furt

127 ESULTS: From 2004 through 2016, 392 definite anaphylaxis deaths and 220 possible anaphylaxis deaths w

128 definite anaphylaxis deaths and 220 possible anaphylaxis deaths were recorded.

129 ich were divided into two classes: "Definite anaphylaxis deaths" and "Possible anaphylaxis deaths." R

130 Concerning possible anaphylaxis deaths, the most common cause was venom-stin

131 to identify all the ICD-10 codes related to anaphylaxis deaths, which were divided into two classes:

132 "Definite anaphylaxis deaths" and "Possible anaphylaxis deaths." RESULTS: From 2004 through 2016, 39

133 All children had anaphylaxis defined by objective symptoms in minimum two

134 t and WDEIA were the most frequent causes of anaphylaxis diagnosed in our department.

135 We herein examined cases of anaphylaxis diagnosed in our department.

136 inition are valid for immediately diagnosing anaphylaxis due to the very low certainty of evidence.

137 Although very rare, fatal anaphylaxis during in-hospital food challenge has been r

138 Anaphylaxis during oral food challenge is not uncommon a

139 Usability, adherence, anxiety and anaphylaxis episodes were evaluated as secondary endpoin

140 and histamine concentrations of four severe anaphylaxis events were determined at multiple serial ti

141 III were detected and no hypersensitivity or anaphylaxis events were reported up to 28 days after the

142 cells in vitro and IgE pharmacokinetics and anaphylaxis experiments in vivo.

143 assified into food-dependent exerciseinduced anaphylaxis (FDEIA) group and post-OIT-FDEIA group.

144 Food-induced anaphylaxis (FIA) is an IgE-dependent immune response th

145 Anaphylaxis following insect stings by this ant has been

146 s are main drivers of allergic reactions and anaphylaxis, for which prevalence is rapidly increasing.

147 The definition of anaphylaxis from NIAID/FAAN was the most commonly used.

148 cytosis (SM) and venom as well as idiopathic anaphylaxis from referral centers in Italy, Slovenia, an

149 The average mortality rate for definite anaphylaxis, from 2004 to 2016, was 0.51 per million pop

150 of Allergy and Clinical Immunology's (EAACI) anaphylaxis guideline.

151 Mice with PSA and active systemic anaphylaxis had increased Fn14 and TWEAK expression in l

152 Anaphylaxis has an adverse impact on the HRQoL of adults

153 g of the natural history and epidemiology of anaphylaxis, hindering clinical practice and research ef

154 sent an increased risk for Hymenoptera venom anaphylaxis (HVA).

155 Idiopathic anaphylaxis (IA) is a diagnosis of exclusion, thus takin

156 Idiopathic anaphylaxis (IA) or spontaneous anaphylaxis is a diagnos

157 to provide protection against cashew-induced anaphylaxis in a relevant mouse model.

158 zation to foods, scratching may promote food anaphylaxis in AD by expanding and activating intestinal

159 eanuts are most responsible for food-induced anaphylaxis in adults in developed countries.

160 E production by B cells and passive systemic anaphylaxis in an in vivo mouse model, ligelizumab is le

161 Orally induced anaphylaxis in CC027/GeniUnc mice was correlated with se

162 The reported incidence of anaphylaxis in children varied widely.

163 able morbidity and is the commonest cause of anaphylaxis in children.

164 ere demographic risk factors associated with anaphylaxis in children.

165 and attenuated dansyl IgE-mediated systemic anaphylaxis in human FcepsilonRIalpha transgenic mice.

166 Relative deficiency of PGE(2) predisposes to anaphylaxis in humans and mice, whereas PGE(2) stabiliza

167 ta suggest that BTKis may be able to prevent anaphylaxis in humans by inhibiting FcepsilonRI-mediated

168 Risk for severe anaphylaxis in humans is associated with inherited diffe

169 d associated impact of tryptase genotypes on anaphylaxis in humans.

170 dulthood, 2) reduced severity of MC-mediated anaphylaxis in males is linked with the naturally high l

171 During severe anaphylaxis in mastocytosis patients, DAO is likely rele

172 eated IgE could not induce passive cutaneous anaphylaxis in mouse ears.

173 thout conformational epitopes did not induce anaphylaxis in peanut-sensitized mice.

174 present in plasma after induction of severe anaphylaxis in rats, guinea pigs, and rabbits.

175 idelines for clinically recognizing systemic anaphylaxis in real time, regardless of whether allergen

176 E attenuates effector-cell degranulation and anaphylaxis in several functional models of allergic dis

177 mediated activation of mast cells, prevented anaphylaxis in Tg mice with mast cells expressing human

178 b completely prevented moderate IgE-mediated anaphylaxis in these mice and also significantly protect

179 IgE causes anaphylaxis in type I hypersensitivity diseases by activ

180 a new paradigm for understanding severity in anaphylaxis, in which poor outcomes may occur as a resul

181 Increasing total or food-induced anaphylaxis incidence over time was reported by 19 studi

182 Anaphylaxis includes mast cell (MC) activation, but less

183 a change of behaviour in patients at risk of anaphylaxis, increasing satisfaction, improving adherenc

184 terations in the PGE(2) system contribute to anaphylaxis independently of COX inhibitor intake is unc

185 Here, we present a case study of anaphylaxis induced by three uronium coupling agents, HA

186 ma, dermatological diseases, food allergies, anaphylaxis, insect venom, and drug allergy.

187 Idiopathic anaphylaxis (IA) or spontaneous anaphylaxis is a diagnosis of exclusion when no cause ca

188 Anaphylaxis is a life-threatening allergic reaction caus

189 Immunoglobulin E (IgE)-mediated anaphylaxis is a potentially fatal condition in which al

190 Anaphylaxis is a potentially life-threatening condition

191 Anaphylaxis is a severe allergic reaction that can be le

192 Anaphylaxis is a severe, potentially fatal, systemic all

193 Anaphylaxis is a severe, systemic hypersensitivity react

194 Anaphylaxis is an acute, potential life-threatening syst

195 Anaphylaxis is classically mediated by allergen cross-li

196 Identifying the differences in phenotypes of anaphylaxis is crucial for future management guidelines

197 of urticaria/angioedema during sting-induced anaphylaxis is indicative of a severe reaction, serum tr

198 Anaphylaxis is recognized mainly through clinical criter

199 in plasma from mastocytosis patients during anaphylaxis is severely compromised compared to DAO from

200 , there could be a NSAIDH overdiagnosis when anaphylaxis is the clinical manifestation.

201 tions leading to mast cell degranulation and anaphylaxis is unclear.

202 training for laypeople may slightly improve anaphylaxis knowledge and competence in using autoinject

203 nic L sigmodontis infection protects against anaphylaxis, likely due to reduction in mast cell number

204 sufficient evidence about the impact of most anaphylaxis management and prevention strategies.

205 d to determine whether patient behaviour and anaphylaxis management improve with its use.

206 nst the native molecule and also explain how anaphylaxis may occur in individuals who lacked specific

207 s accompanied by down-regulation of systemic anaphylaxis mediators such as histamine and mast cell pr

208 llergen rapid desensitization and suppressed anaphylaxis more rapidly than omalizumab or ligelizumab.

209 The aims of the study are to determine the anaphylaxis mortality rate in Italy and its associations

210 ase level is associated with severe systemic anaphylaxis, most notably caused by Hymenoptera envenoma

211 < .05) and more prevalent in both idiopathic anaphylaxis (n = 8 of 47; [17%; P = .006]) and SM (n = 1

212 Seven episodes of anaphylaxis occurred during the study, all in patients w

213 odic consultations, and 16 patients recurred anaphylaxis of the diagnosis.

214 m of this study was to explore the impact of anaphylaxis on HRQoL of newly diagnosed adults.

215 ar edema induced by either passive cutaneous anaphylaxis or direct challenge with histamine, a major

216 eutic strategies to target mast cells during anaphylaxis or other allergic diseases.

217 e Brighton Collaboration case definition for anaphylaxis or received a physician's diagnosis.

218 Forty-four patients with anaphylaxis or urticaria upon CHX exposure and positive

219 Utilizing rodent models of MC-mediated anaphylaxis, our data here reveal that, 1) compared with

220 standardize the terminology used to describe anaphylaxis outcomes and serve as the foundation for fut

221 onsensus definitions for clinically relevant anaphylaxis outcomes by utilizing a multidisciplinary gr

222 The use of inconsistent definitions for anaphylaxis outcomes limits our understanding of the nat

223 Thirteen out of 237 (5.5%) SAR/anaphylaxis patients were triggered by Ana o 3.

224 us sensitized AD model and passive cutaneous anaphylaxis (PCA) model on VAD and vitamin A supplementa

225 -risk history includes patients who have had anaphylaxis, positive penicillin skin testing, recurrent

226 ability and mouse models of passive systemic anaphylaxis (PSA) and active systemic anaphylaxis were a

227 Although 75.5% of children with peanut anaphylaxis reached a maintenance dose of 0.25-5 g, only

228 the age of seven, he experienced an unknown anaphylaxis reaction twice.

229 In all four cases, the anaphylaxis reactions were amenable to treatment with lo

230 y in mice leads to enhanced passive systemic anaphylaxis, reflected by increased drop in body tempera

231 llenges to be able to manage cases of severe anaphylaxis refractory to intramuscular adrenaline, and

232 who all experienced severe life-threatening anaphylaxis, refractory to intramuscular adrenaline trea

233 Using data from the European Anaphylaxis Registry (12,874 cases), we identified 3,612

234 Data from the Anaphylaxis Registry were analyzed to identify secondary

235 de, (2) respiratory or cutaneous symptoms or anaphylaxis related to NSAID, (3) positive skin prick te

236 This is the first study of anaphylaxis-related mortality coming from an official da

237 HalphaT was associated with grade IV venom anaphylaxis (relative risk = 2.0; P < .05) and more prev

238 associated with increased risk for systemic anaphylaxis (relative risk = 9.5; P = .007).

239 s and the implication for the elicitation of anaphylaxis remains to be elucidated.

240 from the milk ladder; no patient experienced anaphylaxis requiring treatment with intramuscular adren

241 ysis, including history of hypersensitivity (anaphylaxis, respiratory allergies, and drug allergies)

242 drogenized female MCs results in MC-mediated anaphylaxis response that reflects the MC sex and not ho

243 Peanut-specific IgE titers and anaphylaxis responses were significantly blunted in Tfr

244 Characterization of anaphylaxis revealed that FcER1 and mast cells were requ

245 possess an epinephrine autoinjector with an anaphylaxis self-management plan.

246 Associated anaphylaxis severity (Mueller scale) was subsequently ex

247 as assessed, and culprit allergen source and anaphylaxis severity grade were established.

248 nel members regarding the need to develop an anaphylaxis severity grading system.

249 ncluding research aimed at development of an anaphylaxis severity grading system.

250 All patients with anaphylaxis should receive education on anaphylaxis and

251 elt a strong need to have control over their anaphylaxis so that it did not take over their lives.

252 ly important, but a lack of understanding of anaphylaxis sometimes hindered that support.

253 Anaphylaxis susceptibility was sometimes increased by tr

254 elease assay and the human passive cutaneous anaphylaxis test were utilized to study the absorption k

255 lieve to be a novel humanized mouse model of anaphylaxis that does not require marrow ablation or hum

256 (+) germinal center B cells, serum IgG1, and anaphylaxis that was mediated by the alternative pathway

257 hip between alpha-Gal cases and cases of IFA anaphylaxis that were closely related to the territory o

258 EAK/Fn14 interaction could be efficacious in anaphylaxis therapy.

259 nd IgE can induce both skin inflammation and anaphylaxis through engagement of IgG receptors (Fcgamma

260 ystemic allergen absorption is important for anaphylaxis through the gastrointestinal tract.

261 role of ectoparasites in the development of anaphylaxis to food and medication in patients at risk o

262 tier of the survey included questions about anaphylaxis to imported fire ants (IFAs).

263 ical case of a patient with extremely severe anaphylaxis to paper wasp venom.

264 igation and management of patients reporting anaphylaxis to suspected bites must therefore be pragmat

265 completely different to previously described anaphylaxis to tick saliva.

266 It is important for patients with anaphylaxis to undergo allergy testing after discharge f

267 anisms that control IgE activity and prevent anaphylaxis under normal conditions are still enigmatic.

268 lergy-mimics" such as asthma masquerading as anaphylaxis, undifferentiated somatoform disorder, panic

269 He was diagnosed with anaphylaxis upon visiting our emergency department.

270 of cystinuria, identification of penicillin anaphylaxis, urea, bilirubin, biomarkers related to huma

271 excellent responses during passive systemic anaphylaxis using human IgE to selectively evoke human m

272 Venom-induced anaphylaxis (VIA) is a common, potentially life-threaten

273 Patient-based protection from anaphylaxis was 76% (4/17) in cMCD vs. 100% in controls

274 IgE-mediated passive anaphylaxis was blunted in mice treated with omeprazole

275 The absence of skin symptoms during anaphylaxis was correlated with baseline serum tryptase

276 Anaphylaxis was induced by intravenous injection of anti

277 Moreover, anaphylaxis was less frequent in patients with profilin

278 Definite fatal anaphylaxis was mostly due to the use of medications (73

279 A sublethal model of anaphylaxis was used, in which BALB/c mice were sensitiz

280 As complement is activated in food-induced anaphylaxis, we aimed to assess the role of C5a in disea

281 r PGE(2) levels and higher susceptibility to anaphylaxis were also found in C57BL/6 mice vis-a-vis in

282 stemic anaphylaxis (PSA) and active systemic anaphylaxis were applied to wild-type (WT), TWEAK- and F

283 The trigger of the anaphylaxis were assessed; the most popular trigger was

284 Patients with anaphylaxis were characterized by markedly reduced PGE(2

285 of anaphylaxis and the mechanisms underlying anaphylaxis were elucidated further.

286 guidelines, clinical diagnostic criteria for anaphylaxis were found in 76 patients and lacking in 26.

287 lant Donor-Registry, 3 cases (0.5%) of fatal anaphylaxis were identified, 2 because of peanut and 1 o

288 to systemic allergic reaction (SAR) and food anaphylaxis were recruited.

289 e cutaneous anaphylaxis and passive systemic anaphylaxis were reduced in NHERF1(+/-) mice and mast ce

290 Almost 82% of patients with severe Ana o 3 anaphylaxis were sensitized only to this component and h

291 nge, the clinical symptoms of peanut-induced anaphylaxis were significantly lower in the microneedle

292 ents felt more involved in the management of anaphylaxis when using the medical device.

293 proven to be IgE-independent acute systemic anaphylaxis, which may due to IgG immune complex trigger

294 dose to mice with typical susceptibility to anaphylaxis, while a rapid desensitization approach safe

295 holoBLG prevented allergic sensitization and anaphylaxis, while sustaining regulatory T cells.

296 We report a case of anaphylaxis with hypoallergenic cochineal onset in a sch

297 used to assess its role in murine models of anaphylaxis with WT (wild-type) and IgE(-/-) (IgE-defici

298 nents as the triggers responsible for severe anaphylaxis, with regard to characteristics and associat

299 ne of the most common food triggers of fatal anaphylaxis worldwide although peanut allergy affects on

300 allergy ranks among the top three causes of anaphylaxis worldwide, and approximately one-quarter of