SOME VIEWS ON THE ASPIRIN‐HYPERSENSITIVE ALLERGY GROUP<sup>1</sup>

Salén, Ernst B.; Arner, B

doi:10.1111/j.1398-9995.1948.tb03302.x

Cited by 18 publications

(4 citation statements)

References 8 publications

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“…Several investigations performed at this particular time (11,12,19) and subsequent studies have confirmed that aspirin-intolerant subjects with asthma have increased urinary excretion of cysteinyl-leukotrienes (20,21). On the basis of the well-established association between eosinophils and aspirin-intolerant asthma (22)(23)(24), and the indications that circulating eosinophils have an enhanced capacity to generate leukotrienes (25), the findings would seem to fit with the hypothesis that the eosinophils are one major source of the baseline production of leukotrienes.…”

Section: Leukotrienes As Mediators Of Persistent Airway Obstruction Imentioning

confidence: 83%

Treatment of Aspirin-intolerant Asthma with Antileukotrienes

Dahlén

2000

Am J Respir Crit Care Med

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Section: Leukotrienes As Mediators Of Persistent Airway Obstruction Imentioning

confidence: 83%

Treatment of Aspirin-intolerant Asthma with Antileukotrienes

Dahlén

2000

Am J Respir Crit Care Med

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“…A clinically salient and often early recognised feature of AIA is an increase in blood eosinophils [1,9]. This particular cell is known to have an efficient pathway for the biosynthesis of CysLTs [10], and we recently observed that activated sputum cells derived from subjects with AIA produced increased levels of CysLTs ex vivo that correlated with sputum eosinophil counts [11].…”

Section: Introductionmentioning

confidence: 97%

The Influence of Aspirin on Release of Eoxin C4, Leukotriene C4 and 15-HETE, in Eosinophilic Granulocytes Isolated from Patients with Asthma

James

Daham

Backman

et al. 2013

Int Arch Allergy Immunol

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Background: The effect of aspirin on the release of key arachidonic acid metabolites in activated eosinophils from subjects with aspirin-intolerant asthma (AIA) has not been investigated previously, despite the characteristic eosinophilia in AIA. Methods: Peripheral blood eosinophils were isolated from four groups of subjects: healthy volunteers (HV; n = 8), mild asthma (MA; n = 8), severe asthma (SA; n = 9) and AIA (n = 7). In the absence or presence of lysine-aspirin, eosinophils were stimulated with arachidonic acid or calcium ionophore to trigger the 15-lipoxygenase-1 (15-LO) and 5-lipoxygenase (5-LO) pathways, respectively. 15(S)-hydroxy-eicosatetraenoic acid (15-HETE) and eoxin C₄ (EXC₄) were measured as 15-LO products and leukotriene (LT)C₄ as a product of the 5-LO pathway. Results: Activated eosinophils from patients with SA and AIA produced approximately five times more 15-HETE than eosinophils from HV or MA patients. In the presence of lysine-aspirin, eosinophils from AIA, MA and SA patients generated higher levels of 15-HETE than in the absence of lysine-aspirin. Furthermore, in the presence of lysine-aspirin, formation of EXC₄ was also significantly increased in eosinophils from AIA patients, and LTC₄ synthesis was increased both in AIA and SA patients. Conclusions: Taken together, this study shows an increased release of the recently discovered lipid mediator EXC₄, as well as the main indicator of 15-LO activity, 15-HETE, in activated eosinophils from severe and aspirin-intolerant asthmatics, and also elevated EXC₄ and LTC₄ formation in eosinophils from AIA patients after cellular activation in the presence of lysine-aspirin. The findings support a pathophysiological role of the 15-LO pathway in SA and AIA.

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“…Salen and Arner 9 Walton and Randle 10 Giraldo et al 11 Falliers 12 Chafee & Settipane 7 Settipane et al 8 veyed, and the inclusion or exclusion of a pure nasal response without a decrease in pulmonary function. Based only on a history of adverse reactions to aspirin, Chafee and Settipane 1 found that the prevalence among allergic asthmatics was 4.3% and among those with allergic rhinitis, 0.7%.…”

Section: Investigatorsmentioning

confidence: 99%