Dramatic augmentation of a food allergy by acetylsalicylic acid

Paul, Eberhard; Gall, H.; Muller, I.; Möller, Ronald

doi:10.1067/mai.2000.105011

Cited by 15 publications

(16 citation statements)

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“…During the very early stages of the induction of oral tolerance, compromising the normal state of the intestinal environment, either by inhibiting the PGE 2 pathway with ibuprofen or by depleting the gut microbiota with oral antibiotics, resulted in a weakening of either the induction or the maintenance of oral tolerance to cow's milk proteins. Links between both treatment types and certain atopic diseases have already been suggested 9–13. However, no link has previously been made between the administration of NSAIDs or antibiotics and an increased risk of food allergy.…”

Section: Resultsmentioning

confidence: 99%

Commonly Used Drugs Impair Oral Tolerance in Mice

Pecquet

Prioult

Campbell

et al. 2004

Annals of the New York Academy of Sciences

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Section: Resultsmentioning

confidence: 99%

Commonly Used Drugs Impair Oral Tolerance in Mice

Pecquet

Prioult

Campbell

et al. 2004

Annals of the New York Academy of Sciences

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“…Severe urticarial reactions or anaphylaxis has been reported after aspirin has been taken with a specific food, but not separately 9 . Food‐dependent, exercise‐induced anaphylaxis (FDEIA) may be augmented by prior aspirin ingestion 10,11 .…”

Section: Aspirin As a Cofactor In Urticariamentioning

confidence: 99%

“…Severe urticarial reactions or anaphylaxis has been reported after aspirin has been taken with a specific food, but not separately. 9 Food-dependent, exercise-induced anaphylaxis (FDEIA) may be augmented by prior aspirin ingestion. 10,11 Aspirin with food alone may provoke anaphylaxis in some individuals with FDEIA (in other words, aspirin appears to substitute for exercise).…”

Section: Aspirin As a Cofactor In Urticariamentioning

confidence: 99%

Aspirin sensitivity and urticaria

Grattan

2003

Clinical and Experimental Dermatology

141

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The relationship of aspirin sensitivity to urticaria is complex. Aspirin sensitivity can cause acute urticaria in some individuals, aggravate pre-existing chronic urticaria in others or, rarely, act as a cofactor with food or exercise to provoke anaphylaxis. Individuals who react with urticaria appear to come from a different population to those who react with asthma, although there is some overlap. Aspirin-sensitive chronic urticaria patients may also react adversely to some food additives. The pharmacological mechanisms of aspirin-sensitive urticaria are not fully understood but probably involve diversion of arachidonic acid metabolism from prostaglandin to cysteinyl leukotriene formation leading to direct effects on blood vessels and delayed mast cell degranulation with release of histamine. Cross-reactivity amongst all nonsteroidal drugs is common in aspirin-aggravated chronic urticaria but appears not to occur with selective cyclo-oxygenase 2 inhibitors.

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“…11 Further, in another study almost half of LTP-induced anaphylaxis cases were related to cofactors, being NSAIDs involved in 36% of reactions. 9 The enhancing effect of NSAIDs in food anaphylaxis is well documented, 12, 13 and it extends beyond LTP to other common allergens such as shellfish, 14 sunflower seeds, 15 gliadin 16, 17 and peanut. 18 …”

Section: Introductionmentioning

confidence: 99%

Distinct transcriptome profiles differentiate nonsteroidal anti-inflammatory drug–dependent from nonsteroidal anti-inflammatory drug–independent food-induced anaphylaxis

Muñoz-Cano

Pascal

Bartra

et al. 2016

Journal of Allergy and Clinical Immunology

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Background Lipid transfer protein (LTP), an abundant protein in fruits, vegetables and nuts, is a common food allergen in Mediterranean areas causing diverse allergic reactions. Approximately 40% of food anaphylaxis induced by LTP require non-steroidal anti-inflammatory drugs (NSAIDs) as a triggering cofactor. Objective To better understand the determinants of NSAID-dependent (NSAID-LTP-A) and NSAID-independent LTP-anaphylaxis (LTP-A) Methods Selection of patients was based on a proven clinical history of NSAID-dependent or -independent anaphylaxis to LTP, positive skin prick test to LTP and serum LTP-IgE. Whole transcriptome (RNA-Seq) analysis of blood cells from 14 individuals with NSAID-LTP-A, 7 with LTP-A and 13 healthy controls was performed to identify distinct gene expression signatures. Results Expression of genes regulating gastrointestinal epithelium renewal was altered in both patient sets, particularly in LTP-A, who also presented gene expression profiles characteristic of an inflammatory syndrome. These included altered B cell pathways, increased neutrophil activation markers and elevated levels of reactive oxygen species. Increased expression of the IgG receptor (CD64) in LTP-A patients was mirrored by the presence of LTP-specific IgG1 and 3. Conversely, NSAID-LTP-A patients were characterized by reduced expression of IFN-γ-regulated genes and IFN-γ levels as well as up-regulated adenosine receptor 3 (ADORA3) expression and genes related to adenosine metabolism. Conclusions Gene ontology analysis suggests disturbances in gut epithelium homeostasis in both LTP-related anaphylaxis groups with potential integrity breaches in LTP-A that may explain their distinct inflammatory signature. Differential regulation in LTP-A and NSAID-LTP-A of the IFN-γ pathway, IgG receptors and ADORA3 may provide the pathogenic basis of their distinct responses.

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Dramatic augmentation of a food allergy by acetylsalicylic acid

Cited by 15 publications

References 0 publications

Commonly Used Drugs Impair Oral Tolerance in Mice

Commonly Used Drugs Impair Oral Tolerance in Mice

Aspirin sensitivity and urticaria

Distinct transcriptome profiles differentiate nonsteroidal anti-inflammatory drug–dependent from nonsteroidal anti-inflammatory drug–independent food-induced anaphylaxis

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