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The Relationship between the Upper and Lower Respiratory Tract
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Nigel K.F. Koo Ng, Gerald W. McGarry
Eosinophilic infiltration of the nasal mucosa has been demonstrated in patients with asthma irrespective of the presence of nasal symptoms,39 further supporting the hypothesis that asthma and rhinitis are clinical manifestations of the same disease. There is also a strong association between chronic rhinosinusitis and asthma, with a higher rate of nasal polyps in asthmatic patients compared to non-asthmatics.40 The triad of aspirin sensitivity, asthma and nasal polyps in aspirin-induced asthma is considered a separate clinical syndrome and found in about 10% to 15% of asthmatics.41
Investigating Possible Anaphylactio Deaths
Published in Julian L Burton, Guy Rutty, The Hospital Autopsy, 2010
Richard SH Pumphrey, Ian SD Roberts
Aspirin has been associated with both anaphylactic and anaphylactoid reactions. Aspirin-induced asthma (AIA) is a well-defined syndrome and is accompanied by nasal polyposis and sinusitis (Szczeklik and Stevenson, 1999). The mechanism is clearly related to the actions of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) on the cyclic oxygenases, COX1 and COX2. In those with aspirin-induced asthma, NSAIDs cause overproduction of cysteinyl leukotrienes, which in turn leads to asthma. However, fatal reactions to aspirin or NSAIDs may occur in those without AIA, and may have features of more typical anaphylactic reactions (Bosso et al., 1991). There is some evidence for IgE antibodies to aspirin (Zhu et al., 1992) and true anaphylaxis cannot be ruled out. Aspirin may be a cofactor for anaphylactic reactions. For example, a patient with positive allergy tests suggesting the possibility of allergy to carrots could tolerate carrot juice unless she had recently taken an aspirin tablet (Schöpf et al., 2000). Reactions such as this may be more common than has been reported because they are difficult to recognise and will commonly be interpreted as a reaction to aspirin.
Acute pain management in children
Published in Pamela E Macintyre, Suellen M Walker, David J Rowbotham, Clinical Pain Management, 2008
Patients with aspirin-induced asthma may be cross-sensitive to NSAIDs. Some caution has also been advised in the use of NSAIDs in the presence of respiratory wheeze in asthmatic patients. Diclofenac did not adversely affect respiratory function in a group of asthmatic children,77 and in studies of children with fever given paracetamol or ibuprofen, asthma morbidity was in fact relatively reduced by ibuprofen.78, 79 Risks of exacerbation of respiratory disease by NSAIDs in children may have been somewhat overemphasized. However, it has been suggested that NSAIDs be avoided in a small subgroup of adolescents with severe asthma and chronic rhinosinusitis with nasal polyposis who are likely to be more sensitive.80
Management of adult asthma and chronic rhinitis as one airway disease
Published in Expert Review of Respiratory Medicine, 2021
Angelica Tiotiu, Plamena Novakova, Guidos Guillermo, Jaime Correira de Sousa, Fulvio Braido
Drug-induced rhinitis could be an adverse event of systemic treatment (e.g. nonsteroidal anti-inflammatory drugs, beta-blockers, sedatives, antidepressants, oral contraceptives, drugs used to treat erectile dysfunction) or secondary to prolonged use of decongestive nasal therapy (rhinitis medicamentosa). For the rhinitis medicamentosa, the predominant symptom is nasal obstruction [1]. The presumed mechanism is the neuronal imbalance via mast cell activation through the Mas-related G-protein-coupled receptor X2 [120]. Usually, the arrest of offending treatments allows to improve outcomes [1]. The most recognized form of drug-induced rhinitis associated with asthma is due to the administration of aspirin or other nonsteroidal anti-inflammatory drugs. In about 10–15% of adults with asthma, an acute asthma attack could occur within 3 hours after the ingestion of aspirin or other nonsteroidal anti-inflammatory drugs, usually accompanied by profuse rhinorrhea, conjunctival congestion, periorbital edema and sometimes a scarlet flushing of the head and neck. This distinct clinical syndrome, called aspirin-induced asthma, is associated with an intense systemic and local (nasal and bronchial) eosinophilic inflammation combined with an overproduction of cysteinyl leukotrienes and other prostanoids. Despite the avoidance of aspirin and cross-reacting drugs, asthma could persist and associate a nasal polyposis development [2].
Effects of COX inhibitors on responsiveness of the tracheal tract to acetylcholine and histamine and their relationship with LTC4 and PGE2 levels of bronchoalveolar lavage fluid in allergic Guinea pigs
Published in Toxicology Mechanisms and Methods, 2020
Ali Rassouli, Hossein Keshavraz Tarikhi, Goudarz Sadeghi Sadeghi, Hadi Tabarraei, Farhang Sasani, Sepideh Ghaffari, Mohammad Amin Fayaz, A. Wallace Hayes
Due to their widespread availability, NSAIDs are used to reduce Aspirin-induced Asthma symptoms (Szczeklik 1997). However, it has been reported that some categories of NSAIDs can trigger the AIA response in patients (Dahlén et al. 1998). So far, however, no reports have compared the in vivo effects of such enzyme inhibitors involved in prostaglandins synthesis on airway responses or have assessed different aspirin-like NSAIDs on airway responsiveness. Since there are conflicting data currently available, this study was designed to evaluate the effects of this class of drugs on airway responsiveness as well as to investigate the effects of celecoxib (preferential COX-2 inhibitor) on the airways of guinea pigs.
Synthesis and structure–activity relationships for some novel diflapolin derivatives with benzimidazole subunit
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Lisa Vieider, Eva Zoeller, Erik Romp, Martin Schoenthaler, Victor Hernández-Olmos, Veronika Temml, Thomas Hasenoehrl, Daniela Schuster, Oliver Werz, Ulrike Garscha, Barbara Matuszczak
Moreover, it is well-known that crosstalk between the branches of AA cascade occurs. This crosstalk is especially evident when trying to inhibit one single branch.1 One of the early pieces of evidence on this subject is aspirin-induced asthma. It was discussed that the reaction is due to COX inhibition, since the free AA was shifted over to the 5-LOX pathway and converted to leukotrienes. 17 It should be mentioned that the system of crosstalk is not quite as easy to explain as that the AA strolls back and forth within the pathways. This inter-pathway crosstalk has not yet been sufficiently investigated and needs more detailed examination.18 Up to now, in most cases a single target has always been used to combat a certain disease. But in situations such as within the AA cascade, where it seems that one target alone cannot achieve much, the topic of polypharmacology comes into play. The advantage of multi target drugs (or designed multiple ligands DMLs) lies in the treatment of complex diseases such as inflammation, metabolic syndrome, and cancer. The possibility of reaching several targets with just one drug reduces the necessary dose and, as a result, fewer off-target side effects are to be expected.18 The number of FDA approved drugs in recent years shows the importance of this new approach for drug development. Below are some important examples of dual inhibitors within the AA cascade: a promising candidate is PTUPB, a dual sEH/COX-2 inhibitor—currently being studied in detail for bleomycin-induced pulmonary fibrosis.19 There are also various 5-LOX/sEH inhibitors, most of which were discovered via in-silico methods and are currently subject to further structural modifications. For example, the dual inhibitor KM55 inhibited the adhesion of leukocytes to endothelial cells by disturbing the leukocyte function.20