Relevant bibliographies by topics / Anaphylaxis

Academic literature on the topic 'Anaphylaxis'

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Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Anaphylaxis"

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Dogru, Mahmut, and Ilknur Bostanci. "Anaphylaxis and Advances in Anaphylaxis." Tuberculin Skin Test in Children 11, no. 2 (March 13, 2013): 43–53. http://dx.doi.org/10.5222/j.child.2011.043.

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Wong, H. C. George. "Factitious anaphylaxis and prevarication anaphylaxis." Journal of Allergy and Clinical Immunology 116, no. 3 (September 2005): 710. http://dx.doi.org/10.1016/j.jaci.2005.04.040.

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Herknerová, Magdalena. "Anaphylaxis." Medicína pro praxi 18, no. 2 (April 30, 2021): 92–96. http://dx.doi.org/10.36290/med.2021.015.

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Waibel, K. H. "Anaphylaxis." Pediatrics in Review 29, no. 8 (August 1, 2008): 255–63. http://dx.doi.org/10.1542/pir.29-8-255.

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Henderson, Nigel. "Anaphylaxis." Nursing Standard 12, no. 47 (August 12, 1998): 49–55. http://dx.doi.org/10.7748/ns.12.47.49.s49.

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Winbery, Stephen L., and Philip L. Lieberman. "ANAPHYLAXIS." Immunology and Allergy Clinics of North America 15, no. 3 (August 1995): 447–75. http://dx.doi.org/10.1016/s0889-8561(22)00757-3.

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Joanne, Hardy. "Anaphylaxis." Nursing Standard 22, no. 26 (March 5, 2008): 59. http://dx.doi.org/10.7748/ns.22.26.59.s49.

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Piper, Liz. "Anaphylaxis." Nursing Standard 22, no. 47 (July 30, 2008): 59. http://dx.doi.org/10.7748/ns.22.47.59.s45.

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Bartolomei, FJ, and T. Pearlstein. "Anaphylaxis." Journal of the American Podiatric Medical Association 80, no. 12 (December 1, 1990): 665. http://dx.doi.org/10.7547/87507315-80-12-665.

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Motosue, Megan S., James T. Li, and Ronna L. Campbell. "Anaphylaxis." Immunology and Allergy Clinics of North America 42, no. 1 (February 2022): 13–25. http://dx.doi.org/10.1016/j.iac.2021.09.010.

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Dissertations / Theses on the topic "Anaphylaxis"

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Harczy, Martha. "Lipid mediators in lung anaphylaxis." Mémoire, Université de Sherbrooke, 1988. http://hdl.handle.net/11143/11716.

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Abstract: Arachidonic acid and PAF are released from the lungs during anaphyIaxis. The aim of this study is to describe the kinetics of the release of eicosanoids and to observe the effects of selected ihhibitors and a PAF antagonist on their release. Isolated lungs of previously sensitized animals were perfused via the pulmonary artery and challenged with ovalbumin. Prostaglandin E21 throraboxane B2, 6-keto prostaglandin F1? levels were determined in aliquots of effluents with radioimmunoassay and/or enzyme immunoassay techniques whereas leukotrienes B4 and D4 were measured by reverse-phase high performance liquid chromatography. In selected experiments 12-HHT and 12-keto HT were measured in the lung effluents. The peak release of eicosanoids from the lungs ensued approximately at 4-6 minutes after the initiation of anaphylactic shock. Perfusion of the lungs with aspirin, indomethacin decreased the formation of cyclooxygenase products and there was no significant change in the release of LTB4, LTD4. BW755C and ETYA at high concentrations reduced the release of all eicosanoids from the lungs as did high concentrations of FPL55712. An antagonist of PAF (BN52021) produced a dose dependent inhibition of prostaglandins, thromboxane and leukotrienes from the anaphylactic lungs. Perfusion of PAF in non-sensitized lungs produced a release of eicosanoids, however the magnitude of the release was negligible compared to that of the release in anaphylactic shock. A Vitamin E analog inhibited the release of LT-s while did not inhibit the release of PG-S and TxB2. These, results emphasize on the complex interactions regulating the synthesis of arachidonic acid metabolites and an indirect role of PAF has been suggested.||Résumé: L'acide arachidonique et le PAF sont libérés par le poumon durant le choc anaphylactique. Le but de la présente étude est d'analyser la cinétique de la libération d'eicosanoïdes, et d'observer les effets de plusieurs inhibiteurs et d'un antagonistes du PAF sur leur libération. Le poumon de cobaye sensibilisé a été perfusé via l'artère pulmonaire et stimulé avec l'ovalbumine. La prostaglandine E2, la thromboxane B2, la prostaglandine 6-ceto-F1? ont été déterminées dans les échantillons de l'effluent avec un essai radioimmunologique ou avec une technique d'essai immunologique enzymatique alors que les leucotriènes B4 et D4 ont été mesurées par chromatographie liquide à haute performance en phase inversée. Dans certaines expériences, le 12-HHT et le 12-ceto-HT ont été mesurés dans l'effluent pulmonaire. Le pic de libération des eicosanoïdes a été observé approximativement 4-6 minutes après le début du choc anaphylactique. La perfusion du poumon avec l'aspirine et l'indométacine a diminué la formation des produits de la cyclooxygénase et n'a pas modifié la libération de leucotriènes B4 et de leucotriènes D4. Le composé BW755C, le ETYA ainsi que le FPL55712 utilisés à fortes concentrations ont réduit la libération de tous les eicosanoïdes du poumon. L'antagoniste du PAF (BN52021) a produit une inhibition dose-dépendante de la libération de prostaglandines, de thromboxanes et de leucotriènes par le poumon anaphylactique. Lorsque les poumons de cobayes non-sensibilisés ont été traités avec des injections de PAF, nous avons noté la libération d'eicosanoïdes. Cependant, la libération d'eicosanoïdes stimulée avec ce médiateur lipidique était beaucoup moindre que celle observée au cours du choc anaphylactique. Un analogue de la vitamine E a inhibé la libération de leucotriènes alors qu'il n'a pas inhibé de libération de prostaglandines et de thromboxanes. Ces résultats mettent en évidence les interactions complexes qui interviennent au cours de la synthèse des métabolites de l'acide arachidonique et le rôle complexe du PAF dans les réactions d'hypersensibilité et inflammatoires.
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Hernández, Muñoz Luis Ulises. "Smartphone tools for anaphylaxis management." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5695/.

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Anaphylaxis is a severe life-threatening allergic condition which is increasing in prevalence and now affects more than 2% of UK children. Anaphylaxis management requires the avoidance of allergen triggers and preparation in readiness for an anaphylactic reaction. People with anaphylaxis and their carers carry Adrenaline Auto-Injectors which need to be administered immediately in the event of an anaphylactic reaction. But, unfortunately, many people often do not know how to use the injectors and fail to use them or fail to use them correctly. This is due in part to deficiencies in training and also to a lack of a system encouraging continuous practice and providing feedback on that practice. Pervasive healthcare research has demonstrated potential in supporting the management of chronic conditions such as diabetes. However, research into assistive technologies for the support of anaphylaxis management has been significantly neglected. Thesis results provide evidence of the potential that smartphone tools have to significantly improve adrenaline injection training skills and a positive influence on self-efficacy. In addition, the results provide insights into possible self-efficacy failings in traditional training and benefits of embedding self-efficacy theory into the design process. The thesis also shows that clinical staff expressed positive feedback after they were provided the technology for one week.
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Balbino, Bianca. "Characterizing the role of IgG antibodies in anaphylaxis." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS024.

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L'anaphylaxie est la manifestation clinique la plus sévère de l’allergie. Il est couramment admis que chez l’homme, l’anaphylaxie est médiée par les anticorps de type IgE. Cependant, des données chez la souris indiquent que les IgG peuvent également contribuer à l’anaphylaxie. Le but de ma thèse a été de mieux comprendre comment les IgG induisent l’anaphylaxie. Dans un premier temps, nous avons démontré que les IgG murines induisent l’anaphylaxie en activant le récepteur FcγRIII à la surface des macrophages, ce qui aboutit à la libération de PAF. Nous avons ensuite voulu savoir si les IgG humaines peuvent également induire des chocs anaphylactiques. L’anticorps thérapeutique Omalizumab (IgG1 humanisée anti-IgE) induit des chocs anaphylactiques chez certains patients. Nous avons démontré que Omalizumab forme des complexes immuns qui peuvent activer les récepteurs FcγRs et induire des chocs anaphylactiques dans des souris exprimants les FcγRs humains (hFcγRKI). Nous avons ensuite développé une version mutante d’Omalizumab incapable de lier les FcγRs et démontré que cet anticorps bloque les IgE sans induire d’anaphylaxie. Finalement, nous avons développé un nouveau modèle humanisé d’anaphylaxie aux arachides dans lequel les souris hFcγRKI sont sensibilisées avec des IgG de patients allergiques aux arachiques. Nos données préliminaires indiquent que les IgG peuvent induire l’anaphylaxie dans ce modèle. De manière surprenante, l’anaphylaxie est augmentée dans des souris n’exprimant aucun FcγR. Nous étudions actuellement le(s) mécanisme(s) responsables de cet effet, et notamment l’implication de la voie du complément et le rôle du récepteur inhibiteur FcγRIIB
Anaphylaxis is a severe and potentially fatal allergic reaction. The current paradigm in humans states that anaphylaxis is triggered by allergen-specific IgE antibodies (Abs). Several reports in mice indicate that IgG Abs can also trigger anaphylaxis. The goal of my thesis was to better understand the pathways through which IgG mediate anaphylaxis. We first evaluated this in an adjuvant-free mouse model of active systemic anaphylaxis. We observed a contribution of the 'classical’ pathway mediated by IgE, FcγRI, mast cells and histamine. However, anaphylaxis was largely mediated by an ‘alternative’ pathway driven by IgG, FcγRIII, macrophages and PAF. We then examined whether human IgG can also trigger anaphylaxis. Omalizumab, an IgG1 anti-IgE mAb, has been reported to induce adverse events, including anaphylaxis. We found that Omalizumab forms immune complexes with IgE that engage FcγRs and induce both skin inflammation and anaphylaxis when injected into mice expressing all human FcγRs (hFcγRKI). We then developed an Fc-engineered version of Omalizumab which cannot bind FcγRs, and demonstrated that this Ab is as potent as Omalizumab at blocking IgE-mediated allergic reactions, but does not induce FcγR-mediated anaphylaxis. Finally, I describe ongoing work in a new model of peanut anaphylaxis in which hFcγRKI mice are sensitized with IgG from allergic subjects. Preliminary data indicate that these IgG induce anaphylaxis in this model; Surprisingly, anaphylaxis is increased in mice deficient for all FcγRs. We are now investigating the mechanism(s), in particular the implication of the complement pathway, and the role of the inhibitory receptor FcγRIIB
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Gillis, Caitlin. "Neutrophils in IgG- and endotoxin-induced systemic inflammation : protective or pathological agents ?" Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066279/document.

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Les neutrophiles contribuent à l'inflammation protectrice et pathologique. Ce projet de thèse consiste à déterminer le rôle des neutrophiles dans des modèles d'inflammation systémique graves et potentiellement mortelles, induite par le lipopolysaccharide (LPS, endotoxémie) ou par des complexes immuns antigène-anticorps (anaphylaxie). L'anaphylaxie est une réaction allergique qui peut être IgE- et/ou IgG-dépendante. L’endotoxémie est un modèle pertinent de l'inflammation au cours de maladies graves. Pour étudier les neutrophiles in vivo, nous avons utilisé un nouveau modèle murin de neutropénie inductible. Nous montrons que les neutrophiles et la Myélopéroxidase qu’ils produisent ont un rôle protecteur dans le choc endotoxique, indépendamment de l'environnement microbiologique. A l'inverse, les neutrophiles peuvent contribuer à l'anaphylaxie induite par les IgG chez la souris. Comme les récepteurs pour les IgG (FcγR) murins sont très différents des humains, nous avons développé un modèle de souris knock-in dans lequel les FcγR murins a été remplacé par les FcγR humains, activateurs et inhibiteur. Chez ces souris, nous montrons que des IgG humaines peuvent induire une anaphylaxie: le FcγRIIA a un rôle dominant, via l'activation des neutrophiles, et les médiateurs PAF et histamine. En parallèle, nous développons un modèle murin d’anaphylaxie à un curare, le Rocuronium, utilisé en clinique. Au même temps, dans une étude clinique, les résultats d’analyses des échantillons sanguins des patients suspectés d’avoir subi une anaphylaxie au curare soutien notre hypothèse de travail: que l’activation des neutrophiles par des IgG spécifiques est impliquée dans l'anaphylaxie humaine
Neutrophils are agents of protective and pathological inflammation. This thesis work aimed to determine the role of neutrophils during severe, potentially fatal models of systemic inflammation induced by lipopolysaccharide (LPS, endotoxemia) or by IgG immune complexes (anaphylaxis). Anaphylaxis is a severe allergic reaction that may proceed via IgE- or IgG-dependant pathways. Endotoxemia is a model relevant to inflammation during critical illness. To study neutrophils in vivo, we employed a new mouse model of inducible neutropenia. We found, surprisingly, that neutrophils and neutrophil-derived MPO protect against the severity of endotoxic shock, independently of the microbiological environment, suggesting that neutrophils limit inflammation during endotoxemia. Conversely, neutrophils can contribute to IgG-induced anaphylaxis in mice. As mice and human IgG receptors (FcγR) are very different, we developed a novel mouse strain in which targeted insertion of human FcγR into the murine loci recapitulated hFcγR expression. Herein, using these mice, this work demonstrates that anaphylaxis induced by hIgG proceeds within a native context of activating and inhibitory hFcγRs, and that neutrophil activation via FcγRIIA is a dominant pathological pathway, involving the mediators PAF and histamine. Finally, we describe ongoing development of a mouse model of anaphylaxis in response to Rocuronium, a curare-based neuromuscular blocking agent (NMBA). In addition, as part of a collaborative clinical study we analysed blood samples from patients suspected of NMBA-induced anaphylaxis, finding evidence for the activation of a neutrophil- and IgG-dependent axis during human anaphylaxis
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Wang, Yunguan. "Involvement of Complement in IgG2a-mediated Anaphylaxis." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1331300479.

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Fitzgerald, M. F. "The role of PAF-acether in guinea-pig anaphylaxis." Thesis, University of Sunderland, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378070.

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Li, Jamma. "In vitro testing in the evaluation of perioperative anaphylaxis." Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21355.

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Background Perioperative anaphylaxis is potentially life-threatening with an estimated incidence of 1:11,000 in Australia. The culprit agent is identified in 50-60% of cases. Neuromuscular blocking agents (NMBA) remain the leading cause. Standard evaluation in Australia comprises history, in vivo skin tests and in vitro specific IgE (sIgE) assays. Whilst drug provocation testing (DPT) to suspected NMBA culprits is the gold standard test for diagnosing or negating allergy, DPT is associated with significant risk particularly in this context. A few specialised international centres include an in vitro testing method known as basophil activation testing (BAT) as part of clinical assessment. BAT is a potentially useful in vitro test that is not commercially available in Australia or part of standard evaluation. Following diagnosis of NMBA anaphylaxis, identifying safe subsequent anaesthesia is critical. A patient with anaphylaxis to one NMBA may also have an allergic reaction to other NMBAs (cross-reactivity). Current standard practice in Australia to assess for cross-reactivity involves skin testing to other NMBAs available as there is significant risk with the use of DPT. Therefore, we sought to assess cross-reactivity by BAT, and examine its agreement with skin testing. Methods Our patient cohort was obtained from the Anaesthetic Allergy Clinic (AAC) at Royal North Shore Hospital, a service which receives referrals from the state of New South Wales for the evaluation of perioperative anaphylaxis, a severe allergic reaction during the perioperative period, which may be IgE or non-IgE mediated affecting at least one major organ system. All patients attending the AAC between May 2017 and July 2018, who received a NMBA during the perioperative episode qualified for the study. Patients received standard evaluation comprising clinical history, skin tests and specific IgE tests, including to morphine and pholcodine, plus BAT using CD63, CD203c and CD300a as surface activation markers. Results One-hundred-and-twenty patients were sequentially recruited from the AAC. Sixty-one patients were diagnosed with NMBA anaphylaxis and enrolled in the intervention arm. Fifty patients with a diagnosis other than NMBA anaphylaxis were enrolled in the control arm. A further nine patients had a clinical history suggestive of IgE-mediated anaphylaxis where no cause could be identified. BAT results were expressed as % upregulation above the negative control, and as a stimulation index (mean fluorescence index of stimulated sample divided by the negative control). We calculated cut-offs of 4.45% and 1.44 for CD63, and 8.80% and 1.49 for CD203c. Sensitivity using CD63 and CD203c was 77% with specificity 76%. A subgroup of 10 of 61 patients with NMBA anaphylaxis had no sensitisation on skin tests. BAT using CD63 and CD203c showed sensitisation in 6, and addition of CD300a to the testing strategy increased sensitisation to 9 patients. Cross-reactivity on skin testing was found in 31 of 61 patients with NMBA anaphylaxis. Sensitisation to a complete panel of NMBAs on skin testing and BAT only completely matched in 9 patients (15%). There was more sensitisation to pancuronium and cisatracurium on BAT (P<0.05). There was less sensitisation to rocuronium on BAT. Results of skin tests and BAT were comparable for vecuronium and suxamethonium (P<0.05). Conclusions BAT may a useful supplement to standard evaluation for diagnosing NMBA anaphylaxis in patients with suggestive histories but no sensitisation on skin tests. Ongoing study of this specific group of patients is required to clarify its utility in clinical practice. The potential role of BAT for identifying safe anaesthesia needs further evaluation. BAT detects a different cross-reactivity profile to skin tests. Negative skin testing and BAT may increase clinician confidence to perform DPT. We need further studies using DPT as well as follow-up of subsequent anaesthesia in our cohort to determine the clinical significance of BAT sensitisation.
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Lohman, Isabelle Carlotta 1948. "THE PRODUCTION AND PURIFICATION OF RABBIT SERUM IMMUNOGLOBULIN-E, AND THE ROLE OF IMMUNOGLOBULIN-E IN SYSTEMIC ANAPHYLAXIS." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/291183.

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Dunn, Anita Marie 1956. "The role of neutrophils in systemic anaphylaxis in the rabbit." Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/276960.

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The objective of this study was to determine whether neutrophils play a significant role in anaphylaxis or in the response to the anaphylactic mediator platelet activating factor (PAF) in the rabbit. Vinblastine and anti-neutrophil antibodies were compared as neutrophil depleting agents, and 0.35 mg/kg vinblastine was selected as optimal for efficiency and specificity of depletion. Anaphylaxis was induced in sensitized rabbits by intravenous antigen challenge. Neutrophil depletion to 399 ± 101 cells/mm³ blood (14 ± 3%) did not significantly inhibit the physiologic and hematologic events associated with anaphylaxis except tachycardia. However, vinblastine pretreatment significantly reduced tachycardia and the right ventricular pressure increase and abolished the increase in pulmonary resistance caused by intravenous PAF. We conclude that although neutrophils do not play a significant role in IgE-anaphylaxis, they are important in the PAF-induced increases in right ventricular pressure and pulmonary resistance. PAF may not be a major mediator of these two physiologic alterations in IgE-anaphylaxis.
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Rastogi, Shruti. "The Role of Prostaglandin E2 in causing susceptibility towards Anaphylaxis." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21632.

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Die Ausbildung und der Schweregrad einer Anaphylaxie kann durch verschiedene Co-Faktoren beeinflusst werden. Zu diesen zählen die nichtsteroidalen Antiphlogistika (NSAIDs), die ihre Wirkung über die Inhibition der COX entfalten. Wie NSAIDs den Schweregrad der Anaphylaxie beeinflussen, ist bisher nicht genau bekannt. Interessanterweise zeigen Anaphylaxie-Patienten mit einer NSAID-Hypersensibilität niedrige Konzentrationen des regulatorischen Prostaglandins E2 (PGE2). Zudem zeigen ASA-tolerante und –intolerante Asthma-Patienten variable anaphylaktische Sensitivitäten. Anhand der vorliegenden Arbeit sollte untersucht werden, ob sich eine PGE2-Dysregulation auf die Ausbildung und den Schweregrad der Anaphylaxie auswirkt und ob diese durch genetische Prädispositionen gefördert werden kann. Dazu wurden zunächst die PGE2 Konzentration im Serum von ANA-Patienten und gesunden Individuen gemessen. ANA-Patienten zeigten reduzierte PGE2 Level, die invers mit dem Schweregrad der ANA korrelierten. Unterstützend weisen zwei in der Allergieforschung häufig verwendete Mauslinien, Balb/c und C57BL/6, unterschiedliche PGE2 Level auf, die wiederum invers mit dem ANA-Schweregrad korrelierten. Eine Stabilisierung der PGE2 Konzentration mittels eines pharmakologischen Inhibitors der Hydroxyprostaglandin-Dehydrogenase (15-PGDH-I) in vivo führte zu einer Verbesserung des ANA Schweregrades. Um in diesem Zusammenhang den Einfluss von ASA und PGE2 besser zu verstehen, wurde das Model der systemisch passiven ANA im Mausmodel eingesetzt. ASA verschlimmerte den Schweregrad der ANA durch die Inhibition der COX1/2. PGE2 konnte diese Verschlimmerung über die EP Rezeptoren 2, 3 und 4 reduzieren. Um die zugrundeliegenden Mechanismen der Wirkweise von exogenem PGE2 und EP-Agonisten besser zu verstehen, wurden diese Zusammenhänge in murinen und humanen Mastzellen untersucht. PGE2 reduzierte die Schwere der ANA durch Inhibition der Mastzell-Aktivität in diesem System über die Rezeptoren EP2 und EP4. Anhand der vorliegenden Arbeit konnte gezeigt werden, dass bereits homöostatische PGE2 Konzentrationen die Aktivität der Mastzelle verändern und vor einer schweren ANA schützen. Zudem kann der Grad der ANA und der Einfluss des PGE2 auf die Mastzellantwort durch genetische Prädisposition beeinflusst werden. Die pharmakologische Stabilisierung des PGE2 könnte daher eine vielversprechende, therapeutische wie auch vorbeugende Strategie zur Behandlung risikoreicher ANA- Patienten sein.
The clinical outcome of anaphylaxis (ANA) can be affected by several co-factors. Non-steroidal anti-inflammatory drugs (NSAIDs) are well-known co-factors of ANA acting via COX-inhibition. The NSAIDs-mediated mechanisms altering the severity of ANA are not well-defined. It is reported that patients of ASA (NSAID)-hypersensitivity show low levels of the regulatory prostaglandin E2 (PGE2). Moreover, the effectiveness of PGE2 administration in such patients suggests a critical role of PGE2 in ASA hypersensitivity. In addition, patients of ASA-tolerant and ASA-intolerant asthma show variable ANA sensitivities suggesting a role of genetic variation in susceptibility. The aim of this thesis was to study whether and how PGE2 dysregulation predisposes to ANA and whether genetic pre-dispositions affect the PGE2 system and therefore ANA susceptibility. First, sera from ANA patients and healthy individuals were analyzed for PGE2 levels. ANA patients were characterized by reduced PGE2 levels which inversely correlated with the severity of ANA. This disparity was confirmed by differential PGE2 levels between Balb/c and BL/6 strains, two genetic mouse strains frequently employed in allergy research. PGE2 levels in these mice were again inversely related with the severity of ANA. Results were confirmed by in vivo PGE2 stabilization using 15-hydroxyprostaglandin dehydrogenase inhibitor (15-PGDH-I). Pharmacological PGE2 stabilization ameliorated ANA severity in mice. A passive systemic ANA (PSA) model was applied to study the impact of ASA on ANA severity and the role of PGE2 in this context. ASA aggravated ANA by inhibiting COX-1/COX-2, while PGE2 reduced the aggravation through EP receptors 2, 3 and 4. To delineate the underlying mechanisms, murine and human mast cells were used to study the impact of exogenous PGE2 and EP agonists. PGE2 attenuated ANA severity by inhibiting MC activation through EP2 and EP4 receptors and interfering with MC signaling. In summary, this thesis demonstrates that homeostatic levels of PGE2 modulate MC activation and protect against ANA severity. The impact of PGE2 on MC responses and ANA susceptibility is governed by genetic variation. Pharmacological stabilization of PGE2 may prove to be a therapeutic or preventive strategy in the management of high-risk ANA patients.
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Books on the topic "Anaphylaxis"

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Bock, Gregory, and Jamie Goode, eds. Anaphylaxis. Chichester, UK: John Wiley & Sons, Ltd, 2004. http://dx.doi.org/10.1002/0470861193.

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Ellis, Anne K., ed. Anaphylaxis. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8.

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Gregory, Bock, Goode Jamie, and Novartis Foundation, eds. Anaphylaxis. Chichester: John Wiley & Sons, 2004.

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F, Kemp Stephen, ed. Anaphylaxis. Philadelphia: Saunders, 2001.

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(Firm), S. Karger, ed. Anaphylaxis. Basel: Karger, 2010.

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Cingi, Cemal, and Nuray Bayar Muluk. Quick Guide to Anaphylaxis. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33639-4.

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Castells, Mariana C., ed. Anaphylaxis and Hypersensitivity Reactions. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-951-2.

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Bridgit, Dimond, ed. Anaphylaxis: A practical guide. Edinburgh: Butterworth-Heinemann, 2004.

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1941-, Schocket Alan L., ed. Clinical management of urticaria and anaphylaxis. New York: M. Dekker, 1993.

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Nursing, Royal College of, ed. Anaphylaxis: Guidance for nurses, midwives and health visitors. London: TheRoyal College of Nursing, 1995.

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Book chapters on the topic "Anaphylaxis"

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French, Shannon, and Anne K. Ellis. "Introduction to Anaphylaxis Essentials." In Anaphylaxis, 1–10. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_1.

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Ellis, Anne K. "Resources for Anaphylaxis." In Anaphylaxis, 123–25. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_10.

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Stukus, David R. "Early Recognition of Anaphylaxis in High Risk Settings." In Anaphylaxis, 11–28. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_2.

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Hammond, Catherine, and Jay Lieberman. "Management of Anaphylaxis Refractory to Standard First Line Therapy." In Anaphylaxis, 29–42. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_3.

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Alqurashi, Waleed. "Biphasic Anaphylaxis: Epidemiology, Predictors, and Management." In Anaphylaxis, 43–60. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_4.

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Aberumand, Babak, and Anne K. Ellis. "Exercise-Induced Anaphylaxis." In Anaphylaxis, 61–67. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_5.

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Banta, Erin, and Marcella Aquino. "In-Office Preparedness for Anaphylaxis." In Anaphylaxis, 69–83. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_6.

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Upton, Julia E. M. "Masqueraders of Anaphylaxis." In Anaphylaxis, 85–100. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_7.

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Ramsey, Nicole B., and Julie Wang. "Anaphylaxis Education: For Patients, Daycares, Schools, and Colleges." In Anaphylaxis, 101–14. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_8.

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Winders, Tonya, and Stanley Fineman. "Advocacy for Anaphylaxis." In Anaphylaxis, 115–22. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43205-8_9.

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Conference papers on the topic "Anaphylaxis"

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Lakner, T., M. Cuevas, and M. Frank. "Emergency treatment of anaphylaxis." In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1710837.

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Levent, Ayşenur, Cansu Altuntaş, Yelda Türkmenoğlu, Birol Öztürk, and Adem Karbuz. "246 Allergy or Anaphylaxis?" In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.246.

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Starkel, S., S. Wilson, R. Plambeck, R. Mertens, and M. Malesker. "Anaphylaxis Following Rocuronium Administration." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2629.

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Abdelghany, Y., J. Resnyk, A. Nadi Khalil, A. Zimrin, and J. J. Rose. "A Case of Anaphylaxis Associated Thrombocytopenia." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5290.

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Schwartz, David G., Abdelouahab Bellou, Luis Garcia-Castrillo, Antonella Muraro, and Nikolaos G. Papadopoulos. "Towards chronic emergency response communities for anaphylaxis." In 2014 IEEE International Conference on Information Reuse and Integration (IRI). IEEE, 2014. http://dx.doi.org/10.1109/iri.2014.7051878.

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Bilal, M. I., B. Prayson, A. Nasrullah, M. Simpson, and S. Sangli. "A Rare Case of Dalbavancin Induced Anaphylaxis." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3066.

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Hota, Gopabandhu, Abhilash Nandy, Kshitiz Goel, Dishank Yadav, Saumo Pal, and Ankush Roy. "An Adaptive Anaphylaxis Detection and Emergency Response System." In 2019 IEEE 32nd International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2019. http://dx.doi.org/10.1109/cbms.2019.00019.

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Kotb, Youssef, Dina Khattab, Omar Ibrahim, Amir Haroun, Fares Fawzi, and Mohamed Serry. "Subcutaneous Remote Auto-Injector for Smartwatch Monitored Anaphylaxis." In 2022 IEEE Sensors. IEEE, 2022. http://dx.doi.org/10.1109/sensors52175.2022.9967364.

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Jain, T., M. Choudhary, and P. Grover. "Severe Lactic Acidosis Following Epinephrine Use in Anaphylaxis." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a3413.

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Nic Aodha Bhuí, B., J. Buckley, M. Mokoka, and B. MacNeill. "63 Polymorphic VT following anaphylaxis to COVID-19 vaccination." In Irish Cardiac Society Annual Scientific Meeting & AGM, October 6th – 8th 2022, Radisson Hotel, Little Island, Cork Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-ics.63.

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Reports on the topic "Anaphylaxis"

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Pühringer, Vanessa, Bernd Jilma, and Harald Herkner. Population-based incidence of all-cause anaphylaxis and its development over time: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0047.

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Gidengil, Courtney, Matthew Bidwell Goetz, Margaret Maglione, Sydne J. Newberry, Peggy Chen, Kelsey O’Hollaren, Nabeel Qureshi, et al. Safety of Vaccines Used for Routine Immunization in the United States: An Update. Agency for Healthcare Research and Quality (AHRQ), May 2021. http://dx.doi.org/10.23970/ahrqepccer244.

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Objective. To conduct a systematic review of the literature on the safety of vaccines recommended for routine immunization in the United States, updating the 2014 Agency for Healthcare Research and Quality (AHRQ) report on the topic. Data sources. We searched MEDLINE®, Embase®, CINAHL®, Cochrane CENTRAL, Web of Science, and Scopus through November 9, 2020, building on the prior 2014 report; reviewed existing reviews, trial registries, and supplemental material submitted to AHRQ; and consulted with experts. Review methods. This report addressed three Key Questions (KQs) on the safety of vaccines currently in use in the United States and included in the Centers for Disease Control and Prevention’s (CDC) recommended immunization schedules for adults (KQ1), children and adolescents (KQ2), and pregnant women (KQ3). The systematic review was supported by a Technical Expert Panel that identified key adverse events of particular concern. Two reviewers independently screened publications; data were extracted by an experienced subject matter expert. Studies of vaccines that used a comparator and reported the presence or absence of adverse events were eligible. We documented observed rates and assessed the relative risks for key adverse events. We assessed the strength of evidence (SoE) across the existing findings from the prior 2014 report and the new evidence from this update. The systematic review is registered in PROSPERO (CRD42020180089). Results. A large body of evidence is available to evaluate adverse events following vaccination. Of 56,608 reviewed citations, 189 studies met inclusion criteria for this update, adding to data in the prior 2014 report, for a total of 338 included studies reported in 518 publications. Regarding vaccines recommended for adults (KQ1), we found either no new evidence of increased risk for key adverse events with varied SoE or insufficient evidence in this update, including for newer vaccines such as recombinant influenza vaccine, adjuvanted inactivated influenza vaccine, and recombinant adjuvanted zoster vaccine. The prior 2014 report noted a signal for anaphylaxis for hepatitis B vaccines in adults with yeast allergy and for tetanus, diphtheria, and acellular pertussis vaccines. Regarding vaccines recommended for children and adolescents (KQ2), we found either no new evidence of increased risk for key adverse events with varied SoE or insufficient evidence, including for newer vaccines such as 9-valent human papillomavirus vaccine and meningococcal B vaccine. The prior 2014 report noted signals for rare adverse events—such as anaphylaxis, idiopathic thrombocytopenic purpura, and febrile seizures—with some childhood vaccines. Regarding vaccines recommended for pregnant women (KQ3), we found no evidence of increased risk for key adverse events with varied SoE among either pregnant women or their infants following administration of tetanus, diphtheria, and acellular pertussis vaccines during pregnancy. Conclusion. Across this large body of research, we found no new evidence of increased risk since the prior 2014 report for key adverse events following administration of vaccines that are routinely recommended. Signals from the prior report remain unchanged for rare adverse events, which include anaphylaxis in adults and children, and febrile seizures and idiopathic thrombocytopenic purpura in children. There is no evidence of increased risk of adverse events for vaccines currently recommended in pregnant women. There remains insufficient evidence to draw conclusions about some rare potential adverse events.
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Grundy, Helen H., Lucy C. Brown, Mark Sykes, M. Rosario Romero, and Dominic Anderson. Review of allergen analytical testing methodologies. Food Standards Agency, September 2023. http://dx.doi.org/10.46756/sci.fsa.noe660.

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The Food Information Regulation (FIR) states that accurate and understandable allergen information needs to be supplied to consumers for the 14 priority allergens. Food allergies affects between 1-2% of the UK population, with some allergens responsible for hospital admissions with anaphylaxis. Food businesses have a legal responsibility to provide food that is safe, which means declaring allergens present as ingredients and warning consumers about their potential unintended presence due to cross-contact. A system needs to be implemented for testing allergens in foods, responding to incidents, and manage risks to protect consumers. This review was prepared to inform FSA on the current state of the art of allergen testing methodologies and the remaining challenges. This project combined a critical literature review of testing methods with assessments of allergen proficiency testing data, consultation with stakeholders from the food industry, and consultation with industry experts regarding multiplex methodologies and the harmonisation of methods in an unbiased review of the current status of testing capabilities for the 14 EU-retained regulated food allergens. Gaps in testing capabilities were highlighted in order to inform future direction, including a lack of transparent public data for the performance and applicability of commercial test kits. Cross-reactivities of kits were also highlighted along with the need for development of fast and accurate point-of-use tests to support food production. A review of allergen proficiency testing data revealed gaps in testing capabilities and variations between the outputs of different test kits when testing for the same allergen. This review critically compares current testing methods to progress towards a suitable harmonised testing protocol that facilitates allergen risk management, and to mitigate limitations and evidence gaps. Suitable workflows outlining recommended testing protocols are presented for priority allergens to provide a resource for compliant testing and incident management. Estimations of the cost of setting up new testing laboratories to support allergen workflows are also included in addition to detailing the cost of testing by established laboratories.
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