Identification of alpha‐gal sensitivity in patients with a diagnosis of idiopathic anaphylaxis

Carter, M. C.; Ruiz-Esteves, Karina; Workman, Lisa J.; Lieberman, Phil; Platts-Mills, Thomas A.E.; Metcalfe, Dean D.

doi:10.1111/all.13366

Cited by 61 publications

(37 citation statements)

References 19 publications

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“…More recently, van Nunen, Commins and others [18][19][20][21][22][23][24] have described a unique population with high titers of anti-gal IgE. Anti-gal IgE develops in a subset of people after an index exposure to gal.…”

Section: Prevalence Of Ige Anti-gal Antibodiesmentioning

confidence: 99%

“…The National Institute of Health (NIH) recently highlighted AGS and noted that it is often unrecognized or misdiagnosed 32 . For AGS patients, a tick bite can lead to a hypersensitivity reaction that characteristically manifests as anaphylaxis three to six hours after consumption of mammalian meat products, even in patients who previously tolerated red meat for their entire lives 20,22,33 .…”

Section: Prevalence Of Ige Anti-gal Antibodiesmentioning

confidence: 99%

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Alpha-gal syndrome: Implications for cardiovascular disease

Bianchi¹,

Walters²,

Fitch

et al. 2020

gcsp

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Alpha-gal syndrome (AGS) refers to a potentially life-threatening allergy to the molecule galactose-α1,3galactose (gal), which is expressed on most mammalian tissues but, importantly, is not expressed by humans. This syndrome can manifest as an allergic reaction to mammalian meat products, but other sources of mammalian tissue can also provoke an immune response, including injectable and implantable medical products. This syndrome has been linked to coronary atherosclerosis, and medical products that express gal are routinely used in cardiology and cardiac surgery. This article seeks to discuss potential implications of alpha syndrome as it relates to cardiovascular health and to heighten awareness in the cardiovascular community about this emerging public health issue. Prevalence of galactose-α1,3-galactoseMost mammalian species (including New World monkeys, cows, pigs, goats, horses, sheep, rabbits and mice) express the galactose-α1,3-galactose (gal) disaccharide sugar on cells and tissue surfaces 1-4 . Gal expression results from the catalytic activity of the α1,3-galactosyltransferase enzyme encoded by the glycoprotein α1,3galactosyltransferase gene (GGTA1) 1-3, 5 . Certain mammalian species, such as catarrhines (humans, apes, and Old World monkeys), do not have a functional GGTA1 gene 6-8 and correspondingly do not express gal 1, 3, 4 . Additionally, gal has been documented to be absent in fish, amphibians, reptiles, and birds 3,9,10 . The function of gal is unknown 3 , but it is clearly not essential for survival 1, 3 .

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Section: Prevalence Of Ige Anti-gal Antibodiesmentioning

confidence: 99%

Section: Prevalence Of Ige Anti-gal Antibodiesmentioning

confidence: 99%

Alpha-gal syndrome: Implications for cardiovascular disease

Bianchi¹,

Walters²,

Fitch

et al. 2020

gcsp

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“…Recently, it has been suggested that α‐gal might be also present in other animal species known to feed parasitically on mammals, and in particular, chiggers (mites of the Trombiculidae family at their larval stage) have been reported to be associated with sensitization to α‐gal and delayed allergy to red meat . Carter et al described, in a prospective study of 70 patients referred with a diagnosis of IA, six cases (9%) with sIgE to α‐gal. Two of these six patients experienced more severe clinical symptoms with a higher baseline serum tryptase and were subsequently found to have indolent systemic mastocytosis.…”

Section: Diagnostic Considerationsmentioning

confidence: 99%

“…Recently, it has been suggested that α-gal might be also present in other animal species known to feed parasitically on mammals, and in particular, chiggers (mites of the Trombiculidae family at their larval stage) have been reported to be associated with sensitization to α-gal and delayed allergy to red meat. 44 Carter et al 45…”

Section: Cofactor-dependent Anaphylaxismentioning

confidence: 99%

Idiopathic anaphylaxis

Bilò

Martini

Tontini

et al. 2019

Clin Experimental Allergy

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Idiopathic anaphylaxis (IA) or spontaneous anaphylaxis is a diagnosis of exclusion when no cause can be identified. The exact incidence and prevalence of IA are not known. The clinical manifestations of IA are similar to other known causes of anaphylaxis. A typical attack is usually acute in onset and can worsen over minutes to a few hours. The pathophysiology of IA has not yet been fully elucidated, although an IgE‐mediated pathway by hitherto unidentified trigger/s might be the main underlying mechanism. Elevated concentrations of urinary histamine and its metabolite, methylimidazole acetic acid, plasma histamine and serum tryptase have been reported, consistent with mast cell activation. There is some evidence that corticosteroids reduce the frequency and severity of episodes of IA, consistent with a steroid‐responsive condition. Important differential diagnoses of IA include galactose alpha‐1,3 galactose (a carbohydrate contained in red meat) allergy, pigeon tick bite (Argax reflexus), wheat‐dependent exercise‐induced anaphylaxis, Anisakis simplex allergy and mast cell disorders. Other differential diagnoses include “allergy‐mimics” such as asthma masquerading as anaphylaxis, undifferentiated somatoform disorder, panic attacks, globus hystericus, vocal cord dysfunction, scombroid poisoning, vasoactive amine intolerance, carcinoid syndrome and phaeochromocytoma. Acute treatment of IA is the same as for other forms of anaphylaxis. Long‐term management is individualized and dictated by frequency and severity of symptoms and involves treatment with H1 and H2 receptor blockers, leukotriene receptor antagonist and consideration for prolonged reducing courses of oral corticosteroids. Patients should possess an epinephrine autoinjector with an anaphylaxis self‐management plan. There are anecdotal reports regarding the use of omalizumab. For reasons that remain unclear, the prognosis of IA is generally favourable with appropriate treatment and patient education. If remission cannot be achieved, the diagnosis should be reconsidered.

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“…These patients did not experience any further anaphylactic episodes when red meat was removed from their diet. 26 In 131 participants, who reported adverse reactions to meat, and 26 control subjects, levels of alpha-gal sensitization correlate with high risk of red meat allergy. 27 Cutoff values are described for levels of sensitization to alpha-gal IgE and for the alpha-gal:total IgE ratio that is highly likely to result in clinically significant red meat allergy.…”

Section: Food Allerg En Smentioning

confidence: 99%

Food and drug allergy, and anaphylaxis in EAACI journals (2018)

Eigenmann

Akdiş²,

Bousquet

et al. 2019

Pediatric Allergy Immunology

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The European Academy of Allergy and Clinical Immunology (EAACI) supports three journals: "Allergy," "Pediatric Allergy and Immunology (PAI)," and "Clinical and Translational Allergy (CTA)." One of the major goals of EAACI is to support health promotion in which prevention of allergy and asthma plays a critical role and to disseminate the knowledge of allergy to all stakeholders including the EAACI junior members. This paper summarizes the achievements of 2018 in anaphylaxis, and food and drug allergy. Main topics that have been focused are anaphylaxis, mechanisms of food allergy (FA), epidemiology of FA, food allergens, diagnosis of FA, prevention and control of FA, FA immunotherapy, drug allergy, and political agenda. K E Y W O R D S allergy, anaphylaxis, Clinical and Translational Allergy, drug allergy, European Academy of Allergy and Clinical Immunology, food allergy, hypersensitivity, Pediatric Allergy and Immunology

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Identification of alpha‐gal sensitivity in patients with a diagnosis of idiopathic anaphylaxis

Cited by 61 publications

References 19 publications

Alpha-gal syndrome: Implications for cardiovascular disease

Alpha-gal syndrome: Implications for cardiovascular disease

Idiopathic anaphylaxis

Food and drug allergy, and anaphylaxis in EAACI journals (2018)

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