Physiopathology and genetics in aspirin-exacerbated respiratory disease

Pavón-Romero, Gandhi F.; Ramírez-Jiménez, Fernando; Roldán-Alvarez, Marco Alejandro; Terán, Luis M.; Falfán-Valencia, Ramcés

doi:10.1080/01902148.2017.1358776

Cited by 15 publications

(10 citation statements)

References 46 publications

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“…For example, aspirin-exacerbated respiratory disease (asthma, nasal polyps and aspirin sensitivity: Samter's triad) was recognized to be familial in the 1950s; it is associated with genetic abnormalities, usually in the production or action of cysteinyl leukotrienes. 26 Another pharmacodynamic susceptibility recognized in the 1950s was haemolytic anaemia with oxidizing agents. The resistance of haemoglobin in red blood cells to oxidation depends on the function of glucose-6-phospate dehydrogenase (G6PD), the key enzyme in the generation of reduced glutathione.…”

Section: Genetic Factorsmentioning

confidence: 99%

Susceptibility to adverse drug reactions

Ferner

Aronson

2019

Brit J Clinical Pharma

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The pharmacological effects of a drug depend on its concentration at the site of action, and therefore on the concentration in blood and on the dose. The relationship between the concentration or dose and the corresponding effect can usually be represented mathematically as a rectangular hyperbola; when effect is plotted against log concentration or log dose, the curve is sigmoidal.Inevitably, the effect size and the doses causing benefit and harm will differ among individuals, since they are biological phenomena: some individuals are more likely than others to suffer harm at any given dose. Some harmful effects can occur at much lower doses than those used in therapeutics; that is, the log dose–response curve for harm lies far to the left of the log dose–response curve for benefit. Those who suffer such reactions are hypersusceptible. When the dose–response curves for harm and therapeutic effect are in the same range, dose cannot separate the harmful effects from the therapeutic effects, and adverse reactions are collateral. Toxic effects occur when harmful doses are above the doses needed for benefit.In this review we consider factors that influence a subject's susceptibility to adverse drug reactions. Determinants of susceptibility include Immunological, Genetic, demographic (Age and Sex), Physiological and Exogenous factors (drug–drug interactions, for example), and Diseases and disorders such as renal failure, giving the mnemonic I GASPED. Some susceptibility factors are discrete (for example, all‐or‐none) and some are continuous; susceptibility can therefore be discrete or continuous; and the factors can interact to determine a person's overall susceptibility to harm.

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Section: Genetic Factorsmentioning

confidence: 99%

Susceptibility to adverse drug reactions

Ferner

Aronson

2019

Brit J Clinical Pharma

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“…Another adverse effect of aspirin is to exacerbate respiratory disease, including asthma and chronic rhinosinusitis with nasosinusal polyposis . Mechanistically, the development of aspirin‐exacerbated respiratory disease involves aberrated eicosanoid metabolisms and activated eosinophils, mast cells, and platelets .…”

Section: Adverse Effects Of Aspirinmentioning

confidence: 99%

Complex roles of the old drug aspirin in cancer chemoprevention and therapy

Hua

Zhang

Kong

et al. 2018

Medicinal Research Reviews

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The nonsteroidal anti-inflammatory agent aspirin is widely used for preventing and treating cardiovascular and cerebrovascular diseases. In addition, epidemiologic evidences reveal that aspirin may prevent a variety of human cancers, while data on the association between aspirin and some kinds of cancer are conflicting. Preclinical studies and clinical trials also reveal the therapeutic effect of aspirin on cancer. Although cyclooxygenase is a well-known target of aspirin, recent studies uncover other targets of aspirin and its metabolites, such as AMP-activated protein kinase, cyclin-dependent kinase, heparanase, and histone. Accumulating evidence demonstrate that aspirin may act in different cell types, such as epithelial cell, tumor cell, endothelial cell, platelet, and immune cell. Therefore, aspirin acts on diverse hallmarks of cancer, such as sustained tumor growth, metastasis, angiogenesis, inflammation, and immune evasion. In this review, we focus on recent progress in the use of aspirin for cancer chemoprevention and therapy, and integratively analyze the mechanisms underlying the anticancer effects of aspirin and its metabolites. We also discuss mechanisms of aspirin resistance and describe some derivatives of aspirin, which aim to overcome the adverse effects of aspirin.

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“…The physiopathology is unclear yet, principally is oriented in a didactic way to the mechanism of action of NSAID, blockage of the cyclooxygenase pathway deriving the metabolic substrate from arachidonic acid (AA) to the lipoxygenase pathway, with subsequent overproduction of leukotrienes (LTC4, LTD4, and LTE4) that induce typical symptoms of N-ERD such as nasal constipation and bronchospasm before intake of NSAID [3]. Recently, other mechanisms have been integrated, such as epithelial damage mediated by thymic stromal lymphopoietin with activation of the innate type 2 immune system [4,5] and the role of enterotoxins of Staphylococcus aureus in airway inflammation [6].…”

Section: Introductionmentioning

confidence: 99%

IL10 rs1800872 Is Associated with Non-Steroidal Anti-Inflammatory Drugs Exacerbated Respiratory Disease in Mexican-Mestizo Patients

et al. 2020

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Non-steroidal anti-inflammatory drugs (NSAID) exacerbated respiratory disease (N-ERD) is a disease integrated by asthma, nasal polyps, and hypersensitivity to non-steroidal anti-inflammatory drugs (NSAID). Genetic association studies have explored single nucleotide polymorphisms (SNPs) in genes involved in theoretical pathophysiological mechanisms, but most of these lack replication of findings in second populations. Our objective was to evaluate the association of SNPs in candidate genomic regions described in Asian and European subjects with N-ERD in Mexican-mestizo patients. We designed a replicative study in two stages. We included 381 SNPs selected by fine mapping of associated genes in a microarray, which were tested in three groups: N-ERD (N), asthma (A), and control group (CG); by means of GoldenGate array, positive results by genetic models were validated in the second stage in another population through qPCR with the same methodology. In the allelic model, we identified 11 SNPs in N vs. CG comparison, and five in N vs. A and A vs. CG, respectively. By genetics models, all SNPs in PPARG, rs13239058 in TBXAS1, and rs1554286 and rs1800872 in IL10 were associated in both models. In the second stage, only rs1800872CC showed an association in the dominant model comparing N vs. GC, p = 0.004, OR = 0.44. In conclusion, rs1800872 in IL10 was the only associated with N-ERD in Mexican-mestizo patients.

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Physiopathology and genetics in aspirin-exacerbated respiratory disease

Cited by 15 publications

References 46 publications

Susceptibility to adverse drug reactions

Susceptibility to adverse drug reactions

Complex roles of the old drug aspirin in cancer chemoprevention and therapy

IL10 rs1800872 Is Associated with Non-Steroidal Anti-Inflammatory Drugs Exacerbated Respiratory Disease in Mexican-Mestizo Patients

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