TY - JOUR T1 - Concurrent coxibs and anti-platelet therapy unmasks aspirin-exacerbated respiratory disease JF - European Respiratory Journal JO - Eur Respir J SP - 1418 LP - 1420 DO - 10.1183/09031936.00000612 VL - 42 IS - 5 AU - Irina Bobolea AU - Rosario Cabañas AU - Jesús Jurado-Palomo AU - Ana Fiandor AU - Santiago Quirce Y1 - 2013/11/01 UR - http://erj.ersjournals.com/content/42/5/1418.abstract N2 - To the Editor:Aspirin-exacerbated respiratory disease (AERD) is a clinical tetrad of chronic hypertrophic eosinophilic sinusitis, nasal polyps, asthma and sensitivity to any medication that inhibits cyclooxygenase (COX)-1, namely aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) [1].The final metabolites of the degradation of arachidonic acid via COX-1 pathway are thromboxanes, prostacyclin and prostaglandins (PG); the most crucial ones are PGE2 and PGD2. According to the classical “cyclooxygenase” hypothesis, inhibition of COX-1, but not COX-2, triggers various mechanisms leading to asthmatic and/or nasal symptoms in AERD patients. The central mechanism was regarded as the deprivation of PGE2 as a consequence of COX-1 inhibition, which would lead to an even more increased local and systemic generation of cysteinyl leukotrienes (LT). The overproduction of cysteinyl LT, due to upregulation of LTC4 synthase and/or cysteinyl LT receptors in the airways, the hallmark of the disease, occurs at baseline as well, although at a much lower degree than after aspirin/NSAIDs intake [2].After the introduction of the selective COX-2 inhibitors, casually referred to as coxibs, several well-designed studies reported the excellent safety profile of these new NSAIDs in patients with AERD [3, 4]. Nevertheless, shortly afterwards, as the use of coxibs extended, so did the number of case reports warning the clinicians that some AERD patients may not tolerate coxibs [5, 6]. In fact, all the position papers and updates on AERD evaluation and management recommend giving the first full dose of these … ER -