Hypersensitivity to aspirin: Common eicosanoid alterations in urticaria and asthma

Mastalerz, Lucyna; Setkowicz, Małgorzata; Sanak, Marek; Szczeklik, A

doi:10.1016/j.jaci.2003.12.323

Cited by 173 publications

(148 citation statements)

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“…According to this hypothesis, inhibition of cyclooxygenase by NSAIDs may lead to a decrease in protective prostaglandins production, leading to activation of mediator release from inflammatory cells in the skin. This hypothesis was further supported by observations that skin eruptions after oral aspirin challenge were accompanied by the release of eicosanoids similarly to patients with AERD (49,50).…”

Section: Pathomechanismsmentioning

confidence: 64%

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Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Kowalski

Makowska

Blanca³

et al. 2011

Allergy

380

348

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Following the first description of hypersensitivity reaction to aspirin (ASA) by Hirschberg in 1902, several types of hypersensitivity reactions to nonsteroidal anti-inflammatory drugs (NSAIDs) have been described. The NSAIDs-induced hypersensitivity reactions involve different mechanisms and present a wide range of clinical manifestations from anaphylaxis AbstractNonsteroidal anti-inflammatory drugs (NSAIDs) are responsible for 21-25% of reported adverse drug events which include immunological and nonimmunological hypersensitivity reactions. This study presents up-to-date information on pathomechanisms, clinical spectrum, diagnostic tools and management of hypersensitivity reactions to NSAIDs. Clinically, NSAID hypersensitivity is particularly manifested by bronchial asthma, rhinosinusitis, anaphylaxis or urticaria and variety of late cutaneous and organ-specific reactions. Diagnosis of hypersensitivity to a NSAID includes understanding of the underlying mechanism and is necessary for prevention and management. A stepwise approach to the diagnosis of hypersensitivity to NSAIDs is proposed, including clinical history, in vitro testing and/ or provocation test with a culprit or alternative drug depending on the type of the reaction. The diagnostic process should result in providing the patient with written information both on forbidden and on alternative drugs.

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Section: Pathomechanismsmentioning

confidence: 64%

“…Although measurements of sufidoleucotrienes from leucocytes and basophile activation tests have been proposed, there is no in vitro test approved for routine diagnosis of cutaneous type of NSAID hypersensitivity (49,55).…”

Section: Diagnosismentioning

confidence: 99%

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Kowalski

Makowska

Blanca³

et al. 2011

Allergy

380

348

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“…Although recent data suggest that abnormal arachidonate metabolism is a common finding in both AIA and aspirininduced urticaria [9][10][11], there have been very few studies to suggest a genetic predisposition to aspirin-induced urticaria for patients with aspirin hypersensitivity. In the present study, we speculated that the CysLTR1 and LTC4S genes might be useful for differentiating the two major phenotypes of aspirin hypersensitivity.…”

Section: Discussionmentioning

confidence: 99%

“…However, in contrast to AIA, the association of the cutaneous reaction with aspirin hypersensitivity has not been investigated. Up to 40% of patients with chronic urticaria exhibit increased wheal size and swelling after intake of aspirin [6,9], and it has been suggested that increased levels of CysLTs resulting from alterations in arachidonate metabolism may exacerbate latephase allergic reactions in AICU patients, as in AIA patients [9][10][11]. However, the pharmacologic effects of CysLT receptor antagonists on AICU patients have not been investigated.…”

Section: Introductionmentioning

confidence: 99%

Differential Contribution of the CysLTR1 Gene in Patients with Aspirin Hypersensitivity

et al. 2007

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In this study, we compared the roles of CysLT receptor type 1 (CysLTR1) and leukotriene C4 synthase (LTC4S) gene polymorphisms in two major aspirin-related allergic diseases, aspirin-intolerant asthma (AIA) and aspirin-induced chronic urticaria/angioedema (AICU). CysLTR1-634C>T and LTC4S-444A>C polymorphisms were genotyped and its functional effect on the promoter activity was compared. As in vivo functional study, changes of peripheral mRNA level of CysLTR1 were measured by real-time PCR before and after aspirin challenge. A significant association was found for the CysLTR1 promoter polymorphism and the AIA phenotype compared to AICU (P=0.015). In U937 cells, the variant genotype reporter construct showed significantly higher promoter activity than the common genotype (P < 0.05). The CysLTR1 mRNA levels increased significantly after aspirin challenge in AIA patients (P=0.013). In conclusion, the CysLTR1 polymorphism may contribute to develop to the AIA phenotype and be used as a genetic marker for differentiating two major aspirin hypersensitivity phenotypes.

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“…The exact mechanism of aspirin-induced urticaria and angioedema is unknown, 28 but the difference between patients who develop AERD and those who develop urticaria is not explained easily by metabolic differences in the production of different eicosanoids. 29 To date, there have been no publications regarding the incidence and reaction profile of aspirin or NSAID hypersensitivity among Asian children but, interestingly, 5-lipoxygenase-related genetic markers associated strongly with AERD in a Korean population 19,20 were not found to be significant in a study performed in the United States. 30 In our population, 2.7% of pediatric patients admitted to the Kendang Kerbau Children's Hospital in Singapore reported histories of ADRs, mostly cutaneous.…”

mentioning

confidence: 99%

Early Presentation With Angioedema and Urticaria in Cross-reactive Hypersensitivity to Nonsteroidal Antiinflammatory Drugs Among Young, Asian, Atopic Children

et al. 2005

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ABSTRACT. Objective. Nonsteroidal antiinflammatory drugs (NSAIDs), mainly ibuprofen, are used extensively among children as analgesic and antipyretic agents. Our initial survey in the Kendang Kerbau Children's Hospital in Singapore showed NSAIDs to be the second most common adverse drug reaction-causing medications among children of Asian descent. We attempted to characterize the clinical and epidemiologic profile of NSAID reactions in this group of patients.Methods. A retrospective case series from a hospitalbased pediatric drug allergy clinic was studied. A diagnosis of NSAID hypersensitivity was made with a modified oral provocation test. Atopy was evaluated clinically and tested with a standard panel of skin-prick tests. We excluded from analysis patients with any unprovoked episodes of urticaria and/or angioedema, patients <1 year of age, and patients who refused a diagnostic challenge test.Results. Between March 1, 2003, and February 28, 2004, 24 patients, including 14 male patients (58%) and 18 Chinese patients (75%), with a mean age of 7.4 years (range: 1.4 -14.4 years), were diagnosed as having crossreactive NSAID hypersensitivity. A family history consistent with NSAID hypersensitivity was elicited for 17% of patients. None of the patients reported any episodes of angioedema/urticaria unrelated to NSAIDs. The median cumulative reaction-eliciting dose was 7.1 mg/kg. Facial angioedema developed for all patients (100%) and generalized urticaria for 38% of challenged patients, irrespective of age. There was no circulatory compromise, but respiratory symptoms of tachypnea, wheezing, and/or cough were documented for 42% of patients. A cross-reactive hypersensitivity response to acetaminophen was documented for 46% of our patients through their history and for 25% through diagnostic challenge. Compared with patients with suspected adverse drug reactions to antibiotics, patients in the NSAID group were older (7.4 vs 4.8 years) and more likely to have a diagnosis of asthma (odds ratio: 7.5; 95% confidence interval: 3.1-19).Conclusions. Early presentations of facial angioedema and urticaria are key features of dose-and potency-dependent, cross-reactive reactions to NSAIDs in a subpopulation of young, Asian, atopic children. Significant overlap with acetaminophen hypersensitivity, especially among very young patients, for whom the use of a cyclooxygenase-2-specific medication may not be feasible, severely limits options for medical antipyretic treatment. A spirin and other nonsteroidal antiinflammatory drugs (NSAIDs) are a widely used group of medications whose mechanism of action involves inhibition of prostaglandin production through blockade of the cyclooxygenase (COX) enzymes known as COX-1 and COX-2. This blockade also results in the shunting of arachidonic acid metabolism toward the 5-lipoxygenase pathway, resulting in increased production and release of cysteinyl leukotrienes.Acetaminophen, the most ubiquitously used antipyretic medication for children worldwide, is an "old" medication whose mechanism of a...

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Hypersensitivity to aspirin: Common eicosanoid alterations in urticaria and asthma

Abstract: CIU with aspirin sensitivity is characterized by the eicosanoid alterations, which are similar to those present in aspirin-induced asthma.

Cited by 173 publications

References 39 publications

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Differential Contribution of the CysLTR1 Gene in Patients with Aspirin Hypersensitivity

Early Presentation With Angioedema and Urticaria in Cross-reactive Hypersensitivity to Nonsteroidal Antiinflammatory Drugs Among Young, Asian, Atopic Children

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