Idiopathic Anaphylaxis: a Series of 335 Cases

Ditto, Anne Marie; Harris, Kathleen E.; Krasnick, Jane; Miller, Mark A.; Patterson, Roy

doi:10.1016/s1081-1206(10)63322-4

Cited by 88 publications

(51 citation statements)

References 20 publications

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“…A 2006 study of 601 cases of anaphylaxis in a tertiary referral center demonstrated a known cause in only 41% of cases [25]. Idiopathic anaphylaxis seems to be more prevalent in female patients and adults [26]. Atopic background was found in about half of the patient population.…”

Section: Clonal Mast Cells In Anaphylaxismentioning

confidence: 99%

Anaphylaxis and Mast Cell Disease: What Is the Risk?

Akin

2010

Curr Allergy Asthma Rep

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Mastocytosis is a proliferative disorder of the hematopoietic mast cell progenitor that results from expansion of a clone carrying the D816V c-kit mutation. Based on the dramatic increase in incidence of anaphylaxis in patients with mastocytosis, recent studies analyzed the presence of clonal mast cell markers, including D816V c-kit mutation, in patients with recurrent IgE- and non-IgE-mediated anaphylaxis. These studies demonstrated the presence of an aberrant mast cell clone in a significant proportion of patients with unexplained anaphylaxis, or anaphylaxis due to hymenoptera venom. Clonal mast cell disease should be suspected in particular in patients presenting with profound cardiovascular manifestations such as hypotension and syncope in the absence of urticaria.

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Section: Clonal Mast Cells In Anaphylaxismentioning

confidence: 99%

Anaphylaxis and Mast Cell Disease: What Is the Risk?

Akin

2010

Curr Allergy Asthma Rep

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“…8 It is generally agreed that anaphylaxis may occur with or without cutaneous signs, even though these latter signs are frequent and occur in 80-100% of cases. 8,11,13 In dogs, the main shock organ is the liver leading to GI signs such as vomiting and diarrhoea (over 90%). [14][15][16][17][18] Some GI changes may be due to direct histamine release from the intestine, but are mostly associated with mediator release directly from the liver, as shown in a study with dehepatized dogs.…”

Section: Introductionmentioning

confidence: 99%

Triggers, risk factors and clinico‐pathological features of urticaria in dogs – a prospective observational study of 24 cases

Rostaher¹,

Hofer‐Inteeworn

Kümmerle‐Fraune

et al. 2017

Advances in Veterinary Dermatology

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Background -Urticaria and anaphylaxis are frequently encountered in veterinary practice, but little is known about the causes and relative frequencies of these reactions.Hypothesis/Objectives -This study was designed to improve current knowledge on the triggers, risk factors and clinico-pathological features of urticaria.Animals -Twenty four dogs with signs of urticaria with or without anaphylaxis.Methods -The study included dogs with cutaneous immediate-type hypersensitivity reactions. The cases were grouped by clinical severity into either an urticaria or an anaphylaxis group. All treatments and diagnostic tests (haematology, biochemical profile, allergy investigation) were recorded. A causality algorithm for urticaria and anaphylaxis (ALUA) was designed to determine the probability of the identified triggers and cofactors. Disease incidence, breed, age and gender predispositions were evaluated statistically.Results -Sixteen of 24 urticaria cases were associated with anaphylaxis whilst 8 of 24 were confined to the skin. The annual hospital incidence was 0.12%. Females seemed to be over-represented (2.4:1) and most of the dog breeds were pure breed (22 of 24), with Rhodesian ridgeback, boxer, beagle, Jack Russell terrier, French bulldog and Vizslas over-represented. In addition to skin lesions, the most frequently and severely affected organ systems were the gastrointestinal and cardiovascular systems. The predominant blood abnormalities were elevated lipase and alanine aminotransferase values. Insects, food and drugs were the most commonly identified triggers.Conclusions -To the best of our knowledge, this is the first study describing the trigger factors and clinicopathological features of dogs with urticaria in veterinary medicine. Insects, food and drugs were the most frequently detected triggers.

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“…Indeed, these patients had experienced laryngeal or pharyngeal edema or ''massive tongue edema''. Perhaps, most persuasively, in this series of 335 patients, upper airway obstruction occurred in 210 (63%) patients (Ditto et al, 1996). However, skin and mucosal symptoms and signs are absent or unrecognized in 10% to 20% of all anaphylactic episodes (Simons, 2010).…”

Section: Clinical Presentationmentioning

confidence: 72%

“…Dyspnea, which may have included oropharyngeal or laryngeal swelling, was noted in 59.7% of patients (Thong et al, 2005). In patients with idiopathic anaphylaxis, 335 patients, ages 5 to 83, were categorized based on whether the acute episode was generalized (urticaria or angioedema with bronchospasm, hypotension, syncope, or gastrointestinal symptoms with or without upper airway obstruction) or angioedema (urticaria or angioedema with upper airway compromise without other systemic symptoms such as shock) (Ditto et al, 1996). From the 335 patients, 201 (60%) were classified as IA-G and 119 (35.5%) were designated as IA-A.…”

Section: Clinical Presentationmentioning

confidence: 99%

Anaphylaxis: Etiology, Clinical Manifestations, Diagnosis and Management

Gelincik¹,

Büyüköztürk²

2012

Allergic Diseases - Highlights in the Clinic, Mechanisms and Treatment

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Anaphylaxis: Etiology, Clinical Manifestations, Diagnosis and Management 169 Animal modelsStudies with murine models demonstrate 2 pathways of systemic anaphylaxis: one mediated by IgE, FcεRI, mast cells, histamine, and platelet-activating factor (PAF), and the other mediated by IgG, FcγRIII, macrophages, and PAF. The former pathway requires much less antibody and antigen than the latter. As a result, IgG antibody can block IgE-mediated anaphylaxis induced by small quantities of antigen without mediating FcγRIII-dependent anaphylaxis (Finkelman et al., 2005). The IgE pathway is most likely responsible for most human anaphylaxis, which generally involves small amounts of antibody and antigen; similarities in the murine and human immune systems suggest that the IgG pathway might mediate disease in persons repeatedly exposed to large quantities of antigen. Antigen cross-linking of antigen specific IgE bound to mast cell FcεRI stimulates mast cell degranulation, with the rapid release of histamine and serotonin and the synthesis and secretion of platelet activation factor (PAF) and leukotrienes. These mediators act on target cells to increase vascular permeability which cause depletion of intravascular volume. The resulting decrease in vital organ perfusion is the primary cause of the symptoms that characterize murine anaphylaxis (Finkelman et al., 2005). The other pathway in mouse is Ig-E independent pathway. As contrary of clasical pathway, at first immunized and antigen challenged mice had anaphylaxis despite the absence of mast cells, FcεRI and IgE. This pathway is also complement independent but requires IgG antibody, macrophages, Fc RIII and PAF. Regardless which pathway takes place, mouse anaphylaxis occurs in very short time and displays similar symptoms. Potentially important differences between mouse and human anaphylaxis are proposed as follows: 1. Mouse IgG has some ability to activate mast cells, an effect that is not shared by any human IgG isotype, 2. IgE binds weakly to murine, but not human low-affinity Fc Rs, 3. Human but not mouse macrophages, Langerhans cells and dendritic cells can express FcεRI, and 4. Human platelets, B cells and natural killer cells, and neutrophils express low affinity IgG receptor (Fc RIIA, Fc RIIC, and Fc RIIIB, respectively) that are not expressed in mouse (Finkelman et al., 2005). Less antibody and antigen are required to trigger IgE dependent anaphylaxis then IgG mediated anaphylaxis. IgG and IgA blocking antibodies inhibit the ability of small quantities of antigen to induce IgE dependent anaphylaxis by neutralizing antigen before it can cross link mast cell associated IgE. IgG antibodies also inhibit IgE-dependent anaphylaxis by mediating an interaction between FcεRI and Fc RIIb on mast cells. In mice the predominant determinants that influence whether IgE dependent anaphylaxis is induced appear to be the quantity of antigen specific IgG antibody produced and the quantity of antigen used to challenge immunized mice. This suggests that IgG antibodies, in addition to me...

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Idiopathic Anaphylaxis: a Series of 335 Cases

Cited by 88 publications

References 20 publications

Anaphylaxis and Mast Cell Disease: What Is the Risk?

Anaphylaxis and Mast Cell Disease: What Is the Risk?

Triggers, risk factors and clinico‐pathological features of urticaria in dogs – a prospective observational study of 24 cases

Anaphylaxis: Etiology, Clinical Manifestations, Diagnosis and Management

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