Tryptase and histamine release during aspirin-induced respiratory reactions

Bosso, John V.; Schwartz, Lawrence B.; Stevenson, Donald D.

doi:10.1016/0091-6749(91)90238-j

Cited by 108 publications

(55 citation statements)

References 19 publications

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“…Several reports suggest an increased production and the release of sLTs already at backgound levels, but even more following the exposure to NSAIDs in hypersensitive patients. Although eosinophils are increased in NSAID hypersensitivity and are known as generators of sLTs, the involvement of local mast cells has been frequently implied [11,12,13,14,15,16,17,18,19,20,21]. However, up to now, with one possible exception [62], there has been no direct evidence that blood basophils were also participating in the NSAID hypersensitivity syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…It has been proposed 28 years ago [7,8,9,10] that the reaction results from the inhibition of cyclooxygenase (COX) by ASA-like drugs in the airways or in the skin of hypersensitive patients. This basic COX theory has recently been restricted to the inhibition of the COX-1 enzyme, which diminishes the production of prostaglandin E 2 (PGE 2 ), normally acting as a ‘brake’ on the production of sulfidoleukotrienes (sLTs, alias cysteinyl-leukotrienes) LTC 4 , LTD 4 and LTE 4 and the release of other mediators by mast cells [11,12,13,14,15,16]. sLTs are major mediators of clinical symptoms in hypersensitivity reactions to ASA/NSAIDs [17, 18].…”

Section: Introductionmentioning

confidence: 99%

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A New Combined Test with Flowcytometric Basophil Activation and Determination of Sulfidoleukotrienes Is Useful for in vitro Diagnosis of Hypersensitivity to Aspirin and other Nonsteroidal Anti-Inflammatory Drugs

Sánz

Gamboa

Weck

2005

Int Arch Allergy Immunol

105

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Background: We assessed whether nonsteroidal anti-inflammatory drugs (NSAIDs) may provoke blood basophil activation in vitro in aspirin- and NSAID-hypersensitive patients, as detected by a flowcytometric technique using the CD63 marker – flowcytometric basophil activation test (FAST) assay – in addition to the sulfidoleukotriene (sLT) release – the cellular allergen stimulation test (CAST). Methods: Sixty aspirin- and/or NSAID-hypersensitive patients were studied. Thirty control patients without history and negative provocation challenge were also included. The percentage of activated basophils after in vitro stimulation with NSAIDs at 3 different concentrations was evaluated by an anti-CD63 phycoerythrin conjugate (FAST assay) and the amount of sLTs released in the cell supernatant by ELISA (CAST assay). Results: For aspirin, the FAST indicated a sensitivity of 41.7%, a specificity of 100%, a positive predictive value of 100% and a negative predictive value of 99.4%; for paracetamol 11.7 and 100%, for metamizol 15 and 100%, for diclofenac 43.3 and 93.3%, and for naproxen 54.8 and 74.1%. Many patients showed positive tests to more than 1 NSAID. When considering the first 4 NSAIDs, the global sensitivity increased to 66.7%, while the specificity remained at 93.3%. The addition of the CAST results still increased the sensitivity up to 73.3%, but with a decrease of the specificity to 71.4%. Conclusions: The FAST shows a high percentage of positive reactions, which may reach 60–70% when 4 NSAIDs are tested and even 88% when the test is performed within 1 month of the last clinical drug exposure and reaction. The test has a high specificity above 90%. The addition of sLT determinations yields additional information in a few isolated cases. It is suggested that this test, when properly used, may help avoid some cumbersome and dangerous provocation challenges.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A New Combined Test with Flowcytometric Basophil Activation and Determination of Sulfidoleukotrienes Is Useful for in vitro Diagnosis of Hypersensitivity to Aspirin and other Nonsteroidal Anti-Inflammatory Drugs

Sánz

Gamboa

Weck

2005

Int Arch Allergy Immunol

105

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“…One theory proposes that aspirin leads directly to an unspecific, IgE-independent activation of mast cells and eosinophils [21][22][23]. Studies that reported an increase in the blood levels of histamine and tryptase [24], and an increase of histamine and leukotriene C4 in nasal lavage [25] after aspirin-provocation supported this theory. A second theory is based on the mode of action of NSAIDs that inhibit the cyclooxygenase, leading to an increased degradation of arachidonic acid by 5-lipoxygenase and an increased production of LTs [26,27] and numerous studies correspond to this theory [28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Aspirin-sensitive rhinitis-associated changes in upper airway innervation

Groneberg

Heppt²,

Welker³

et al. 2003

Eur Respir J

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Aspirin-sensitive rhinitis is the manifestation of aspirin intolerance in the upper respiratory tract. The disease represents a pseudoallergy against aspirin or related nonsteroidal anti-inflammatory drugs. As a major immunomodulatory role for airway innervation has been proposed in airway inflammatory diseases, the present study assessed changes in human nasal mucosa innervation in patients with aspirinsensitive rhinitis in comparison to a control group.Immunohistochemistry for protein gene product 9.5, tachykinins, calcitonin generelated peptide, vasoactive intestinal peptide (VIP) and neuropeptide tyrosine was performed on cryostats sections of nasal mucosa and neuropeptide containing nerves were examined independently using a score grading.In comparison to the control, the aspirin-sensitive rhinitis group had a significant increase of VIP-like immunoreactivity in mucosal nerve fibres. In contrast to constant numbers of mast cells, highly significant increases in the numbers of eosinophils were found in the group of aspirin-sensitive rhinitis patients.In summary, the present quantification of neuropeptide-immunoreactivity of mucosal nerves demonstrated differences in the human nasal mucosa innervation between nonrhinitic and aspirin-sensitive rhinitic individuals. These differences may reflect a pathophysiological role of upper airway innervation in pseudoallergic reactions. Eur Respir J 2003; 22: 986-991.

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“…Suggestions of aspirin-induced activation of platelets from patients with AIA [27] have not been replicated [18]. Moreover, despite in vivo evidence that mast cell activation occurs during aspirin-induced bronchoconstriction [9,10,11,28,29,30,31,32], Wang et al [33] could not trigger activation of blood-derived mast cells from subjects with AIA by ex vivo exposure to aspirin. The present study therefore gives support to the concept that aspirin/NSAID intolerance is a unique and not yet completely understood in vivo reaction in which presumably many cells interact in a complex fashion that, however, requires contact with the target tissue in the airways.…”

Section: Discussionmentioning

confidence: 99%

Challenge of Isolated Sputum Cells Supports in vivo Origin of Intolerance Reaction to Aspirin/Non-Steroidal Anti-Inflammatory Drugs in Asthma

Higashi¹,

Kumlin²,

Higashi³

et al. 2012

Int Arch Allergy Immunol

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Background: There is no in vitro test to diagnose aspirin-intolerant asthma (AIA). The aim of this study was to test if challenge with aspirin of sputum cells from subjects with AIA triggers the release of cysteinyl leukotrienes (CysLTs), known to be mediators of bronchoconstriction in AIA. Methods: Sputum induction was performed at baseline and at another visit 2 h after a lysine-aspirin bronchoprovocation in 10 subjects with AIA and 9 subjects with aspirin-tolerant asthma (ATA). The isolated sputum cells were incubated for ex vivo challenge. Results: Release of CysLTs by sputum cells from patients with AIA was not induced by lysine-aspirin ex vivo, neither when cells were collected at baseline nor in sputum cells recovered after lysine-aspirin-induced bronchoconstriction, whereas release of CysLTs from sputum cells was triggered by an ionophore on both occasions. However, the CysLT levels elicited by the ionophore were higher in the AIA group both at baseline (AIA vs. ATA: 3.3 vs. 1.6 ng/million cells; p < 0.05) and after the lysine-aspirin bronchoprovocation (3.9 vs. 1.7 ng/million cells; p < 0.05). This difference in the amount of CysLTs released between the groups appeared to be related to the number of eosinophils. Conclusions: Intolerance to aspirin could not be triggered in sputum cells isolated from subjects with AIA. Together with the previous inability to demonstrate intolerance to non-steroidal anti-inflammatory drugs in isolated blood cells, these results support the requirement of tissue-resident cells in the adverse reaction. However, ex vivo stimulation of sputum cells may be developed into a new test of capacity for LT release in inflammatory cells recovered from airways.

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Tryptase and histamine release during aspirin-induced respiratory reactions

Cited by 108 publications

References 19 publications

A New Combined Test with Flowcytometric Basophil Activation and Determination of Sulfidoleukotrienes Is Useful for in vitro Diagnosis of Hypersensitivity to Aspirin and other Nonsteroidal Anti-Inflammatory Drugs

A New Combined Test with Flowcytometric Basophil Activation and Determination of Sulfidoleukotrienes Is Useful for in vitro Diagnosis of Hypersensitivity to Aspirin and other Nonsteroidal Anti-Inflammatory Drugs

Aspirin-sensitive rhinitis-associated changes in upper airway innervation

Challenge of Isolated Sputum Cells Supports in vivo Origin of Intolerance Reaction to Aspirin/Non-Steroidal Anti-Inflammatory Drugs in Asthma

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