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J Quiralte-Castillo, M Del Robledo Ávila-Castellano, S Cimbollek, P Benaixa, S Leguisamo, K Baynova, M Labella, J Quiralte
BACKGROUND: Safer and less time consuming alternatives to single-blind placebo-controlled oral challenge (SBPCOC) in order to diagnose aspirin-exacerbated respiratory disease (AERD) have been searched for. Nasal challenges with different non-steroidal anti-inflammatory drugs and assessment methods have been developed. OBJECTIVE: Our objective was to evaluate the utility and safety of nasal ketorolac challenge (NKC) using an acoustic rhinomether in patients with suspected AERD Methods: Thirty-six patients with suspected AERD were included in the study...
October 19, 2016: Journal of Investigational Allergology & Clinical Immunology
Masamichi Yamashita
Aspirin is the oldest non-steroidal anti-inflammatory drug (NSAID), and it sometimes causes asthma-like symptoms known as aspirin-exacerbated respiratory disease (AERD), which can be serious. Unwanted effects of aspirin (aspirin intolerance) are also observed in patients with food-dependent exercise-induced anaphylaxis, a type I allergy disease, and aspirin-induced urticaria (AIU). However the target and the mechanism of the aspirin intolerance are still unknown. There is no animal or cellular model of AERD, because its pathophysiological mechanism is still unknown, but it is thought that inhibition of cyclooxygenase by causative agents lead to an increase of free arachidonic acid, which is metabolized into cysteinyl leukotrienes (cysLTs) that provoke airway smooth muscle constriction and asthma symptoms...
October 5, 2016: Current Drug Targets
Amber Dahlin, Scott T Weiss
Aspirin-exacerbated respiratory disease (AERD) severity and its clinical phenotypes are characterized by genetic variation within pathways for arachidonic acid metabolism, inflammation, and immune responses. Epigenetic effects, including DNA methylation and histone protein modification, contribute to regulation of many genes that contribute to inflammatory states in AERD. The development of noninvasive, predictive clinical tests using data from genetic, epigenetic, pharmacogenetic, and biomarker studies will improve precision medicine efforts for AERD and asthma treatment...
November 2016: Immunology and Allergy Clinics of North America
Andrew R Parker, Andrew G Ayars, Matthew C Altman, William R Henderson
Aspirin-exacerbated respiratory disease (AERD) is a syndrome of severe asthma and rhinosinusitis with nasal polyposis with exacerbations of baseline eosinophil-driven and mast cell-driven inflammation after nonsteroidal antiinflammatory drug ingestion. Although the underlying pathophysiology is poorly understood, dysregulation of the cyclooxygenase and 5-lipoxygenase pathways of arachidonic acid metabolism is thought to be key. Central features of AERD pathogenesis are overproduction of proinflammatory and bronchoconstrictor cysteinyl leukotrienes and prostaglandin (PG) D2 and inhibition of bronchoprotective and antiinflammatory PGE2...
November 2016: Immunology and Allergy Clinics of North America
Jennifer Hill, Trever Burnett, Rohit Katial
Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome characterized by severe persistent asthma, hyperplastic eosinophilic sinusitis with nasal polyps, and an intolerance to aspirin and other NSAIDs that preferentially inhibit COX-1. For more than 30 years, aspirin desensitization has proven to be of significant long-term benefit in carefully selected patients with AERD. Despite this, the exact mechanisms behind the therapeutic effects of aspirin desensitization remain poorly understood. In this article, we review the current understanding of the mechanisms of aspirin desensitization and discuss future areas of investigation...
November 2016: Immunology and Allergy Clinics of North America
John W Steinke, Spencer C Payne, Larry Borish
Aspirin-exacerbated respiratory disease (AERD) involves overexpression of proinflammatory mediators, including 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes. Mast cells and eosinophils have roles in mediating many of the observed effects. Increased levels of both interleukin-4 (IL-4) and interferon (IFN)-γ are present in the tissue of patients with AERD. Previous studies showed that IL-4 is primarily responsible for the upregulation of LTC4S by mast cells...
November 2016: Immunology and Allergy Clinics of North America
Jeremy D Waldram, Ronald A Simon
Aspirin-exacerbated respiratory disease (AERD) is characterized by chronic rhinosinusitis with nasal polyps, asthma, and reactions to cyclooxygenase-1-inhibiting drugs. This condition is often refractory to standard medical treatments and results in aggressive nasal polyposis that often requires multiple sinus surgeries. Aspirin desensitization followed by daily aspirin therapy is an important treatment option, and its efficacy has been validated in multiple research studies. Aspirin desensitization is not without risk, but specific protocols and recommendations exist to mitigate the risk...
November 2016: Immunology and Allergy Clinics of North America
Whitney W Stevens, Robert P Schleimer
Aspirin-Exacerbated Respiratory Disease (AERD) and Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) are both characterized by the presence of chronic sinonasal inflammation and nasal polyps. Unlike in CRSwNP, AERD patients develop respiratory reactions following ingestion of COX-1 inhibitors. AERD patients also, on average, have worse upper respiratory disease with increased sinonasal symptoms, mucosal inflammation and requirements for revision sinus surgery when compared to CRSwNP patients. While no single genetic factor has been identified in either CRSwNP or AERD to date, differences in the metabolism of arachidonic acid as well as innate immune cell activation may uniquely contribute to AERD pathogenesis...
November 2016: Immunology and Allergy Clinics of North America
Adam N Williams
Aspirin-exacerbated respiratory disease (AERD) is a distinct clinical condition characterized by chronic sinusitis with nasal polyps, asthma, and hypersensitivity reactions to nonsteroidal anti-inflammatory drugs (NSAIDs). Distinguishing AERD from other forms of chronic sinusitis, asthma, and NSAID reactivity has important clinical implications for management. The clinical history is helpful, but not adequate for confirming the diagnosis of AERD, in most cases. Diagnostic provocation challenge remains the only way to confirm or exclude the diagnosis of AERD...
November 2016: Immunology and Allergy Clinics of North America
Federica Porcaro, Antonio Di Marco, Renato Cutrera
Aspirin hypersensitivity associated with chronic rhinosinusitis-with or without nasal polyposis-and asthma resistant to conventional therapy defines the aspirin-exacerbated respiratory disease (AERD). We describe the case of a 15-year-old female patient with adverse reaction to aspirin, chronic rhinosinusitis, and severe asthma. She also experienced chronic idiopathic urticaria worsened by non-steroidal anti-inflammatory drug administration. AERD was diagnosed based on clinical history and symptoms. Given the poor responsiveness to standard therapy for respiratory and cutaneous symptoms, omalizumab was administered for 24 weeks with control of respiratory symptoms and short term improvement of cutaneous symptoms...
September 29, 2016: Pediatric Pulmonology
Jiun-Bo Chen, Louisa K James, Anna M Davies, Y-C Wu, Joanne Rimmer, Valerie J Lund, Jou-Han Chen, James M McDonnell, Yih-Chih Chan, George H Hutchins, Tse Wen Chang, Brian J Sutton, Harsha H Kariyawasam, Hannah J Gould
BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) is associated with local immunoglobulin hyperproduction and the presence of IgE antibodies against Staphylococcus aureus enterotoxins (SAEs). Aspirin-exacerbated respiratory disease (AERD) is a severe form of CRSwNP in which nearly all patients express anti-SAEs. OBJECTIVES: We aimed to understand antibodies reactive to SAEs and determine whether they recognize SAEs through their complementarity-determining regions (CDRs) or framework regions (FRs)...
September 19, 2016: Journal of Allergy and Clinical Immunology
Jessica Han Ying Tan, Anne Ann Ling Hsu
BACKGROUND: Patients with aspirin-exacerbated respiratory disease (AERD) also recently known as nonsteroidal anti-inflammatory drug (NSAID) exacerbated respiratory disease (NERD) must avoid aspirin and all other oral NSAIDs. The effect of topical NSAID (tNSAID), especially salicylates which are commonly present in topical medicated preparations, on asthma control of this phenotype is studied. METHODS: The study inclusion criteria were adults with: 1) NSAID hypersensitivity; 2) nasal polyposis/chronic rhinosinusitis; 3) not well-/poorly controlled asthma and 4) exposure to tNSAID...
September 2016: Respiratory Medicine
Katherine N Cahill, Christina B Johns, Jing Cui, Paige Wickner, David W Bates, Tanya M Laidlaw, Patrick E Beeler
BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is characterized by 3 clinical features: asthma, nasal polyposis, and respiratory reactions to cyclooxygenase-1 inhibitors (nonsteroidal anti-inflammatory drugs). Electronic health records (EHRs) contain information on each feature of this triad. OBJECTIVE: We sought to determine whether an informatics algorithm applied to the EHR could electronically identify patients with AERD. METHODS: We developed an informatics algorithm to search the EHRs of patients aged 18 years and older from the Partners Healthcare system over a 10-year period (2004-2014)...
July 25, 2016: Journal of Allergy and Clinical Immunology
Emine Güven Sakalar, Nuray Bayar Muluk, Murat Kar, Cemal Cingi
Aspirin-exacerbated respiratory disease (AERD) refers to the combination of asthma, chronic rhinosinusitis with nasal polyposis, and acute upper and lower respiratory tract reactions to the ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 inhibiting non-steroidal anti-inflammatory drugs. AERD affects 0.3-0.9 % of the general population. AERD generally occurs due to abnormalities in mediators and expression of arachidonic acid biosynthesis. Local IgE responses to staphylococcal enterotoxins may also be responsible for eosinophilic activation in the nasal polyp tissues of AERD patients...
August 18, 2016: European Archives of Oto-rhino-laryngology
Su-Kang Kong, Byung Soo Kim, Tae Gi Uhm, Hun Soo Chang, Jong Sook Park, Sung Woo Park, Choon-Sik Park, Il Yup Chung
Aspirin hypersensitivity is a hallmark of aspirin-exacerbated respiratory disease (AERD), a clinical syndrome characterized by the severe inflammation of the respiratory tract after ingestion of cyclooxygenase-1 inhibitors. We investigated the capacity of aspirin to induce interleukin-4 (IL-4) production in inflammatory cells relevant to AERD pathogenesis and examined the associated biochemical and molecular pathways. We also compared IL-4 production in peripheral blood mononuclear cells (PBMCs) from patients with AERD vs aspirin-tolerant asthma (ATA) upon exposure to aspirin...
2016: Experimental & Molecular Medicine
Ga-Young Ban, Kumsun Cho, Seung-Hyun Kim, Moon Kyung Yoon, Ji-Hye Kim, Hyun Young Lee, YooSeob Shin, Young-Min Ye, Joo-Youn Cho, Hae-Sim Park
BACKGROUND: To date, there has been no reliable in vitro test to diagnose aspirin-exacerbated respiratory disease (AERD). OBJECTIVE: To investigate potential diagnostic biomarkers for AERD using metabolomic analysis. METHODS: An untargeted profile of serum from asthmatics in the first cohort (group 1) comprising 45 AERD, 44 patients with aspirin-tolerant asthma (ATA), and 28 normal controls was developed using the UHPLC/Q-ToF MS system. Metabolites that discriminate AERD from ATA were quantified in both serum and urine, which were collected before (baseline) and after the lysine-aspirin bronchoprovocation test (Lys-ASA BPT)...
August 17, 2016: Clinical and Experimental Allergy: Journal of the British Society for Allergy and Clinical Immunology
Guanxiao Qi, Karlijn van Aerde, Ted Abel, Dirk Feldmeyer
Adenosine is considered to be a key regulator of sleep homeostasis by promoting slow-wave sleep through inhibition of the brain's arousal centers. However, little is known about the effect of adenosine on neuronal network activity at the cellular level in the neocortex. Here, we show that adenosine differentially modulates synaptic transmission between different types of neurons in cortical layer 4 (L4) through activation of pre- and/or postsynaptically located adenosine A1 receptors. In recurrent excitatory connections between L4 spiny neurons, adenosine suppresses synaptic transmission through activation of both pre- and postsynaptic A1 receptors...
August 13, 2016: Cerebral Cortex
N A T van der Maas, K van Aerde, L J Bont, M N Bekker, N Rots, H E de Melker
- In the first few months of life, newborns are vulnerable to infections.- Vaccination of the pregnant mother leads to transplacental antibody transfer, resulting in the best possible protection of the newborn.- Maternal vaccination has long been given for the prevention of tetanus in developing countries, and for the prevention of pertussis and influenza in developed countries, such as the United States, England and Belgium. These vaccinations give newborns good protection and, to date, no adverse effects are known for the foetus or the pregnancy...
2016: Nederlands Tijdschrift Voor Geneeskunde
Kai Fruth, Jan Gosepath
Aspirin exacerbated respiratory disease (AERD) has been defined as a non-steroidal anti-inflammatory drug (NSAID)-triggered hypersensitivity, non-allergic bronchial asthma and chronic rhinosinusitis (CRS) with nasal polyps. The underlying pathophysiology of AERD is not completely understood so far. An altered arachidonic acid metabolism and dysregulated enzyme activity are regarded to be causal. AERD is characterized by recalcitrant CRS with recurrent nasal polyps after sinus surgery, accompanied by difficult to treat bronchial asthma and adverse reaction after NSAID ingestion such as nasal blockage, itching, laryngospasm and severe asthma attacks...
2016: Advances in Oto-rhino-laryngology
Xin Feng, Madison K Ramsden, Julie Negri, Mary Grace Baker, Spencer C Payne, Larry Borish, John W Steinke
BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) differs from aspirin-tolerant disease in part because of eosinophilic tissue infiltration and overexpression of arachidonic acid metabolic pathway components that lead to enhanced secretion of cysteinyl leukotrienes and prostaglandin (PG) D2 observed constitutively and paradoxically in response to aspirin and other COX inhibitors. We have previously demonstrated the capacity of IFN-γ to drive cysteinyl leukotriene expression and response...
June 14, 2016: Journal of Allergy and Clinical Immunology
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