RESUMO
BACKGROUND: Previous work has shown that chronic rhinosinusitis (CRS) severity may be associated with particulate matter 2.5 (PM2.5 ) and black carbon (BC) in CRS patients without nasal polyps (CRSsNP). Data regarding occupational exposures, however, are lacking. We assessed the impact of PM2.5 , BC, as well as occupational airborne exposure on CRS disease severity. METHODS: Patients with CRS with nasal polyps (CRSwNP), CRSsNP, and aspirin-exacerbated respiratory disease (AERD) were identified from an institutionwide database. Spatial modeling from 37 pollutant monitoring sites in Allegheny County was used to estimate exposures. Patient occupations using the 2010 Standard Occupation Classification (SOC10) and airborne occupation exposures to vapors, gases, dusts, fumes, fibers and mists (VGDFFiM) or diesel fumes were recorded. Disease severity was measured by modified Lund-Mackay score (LMS), systemic corticosteroid therapy, and incidence of functional endoscopic sinus surgery (FESS). RESULTS: Two hundred thirty-four patients were included (CRSwNP, n = 113; CRSsNP, n = 96; AERD, n = 25). The prevalence of AERD among those with CRSwNP was 18%. Patients exposed to VGDFFiM or diesel fumes required higher steroid doses vs nonexposed patients (p = 0.015 and p = 0.03, respectively); patients with VGDFFiM levels >5% were more likely to undergo FESS vs nonexposed patients (p = 0.0378). There was no difference in PM2.5 and BC with regard to disease severity and FESS between CRSwNP, CRSsNP, and AERD patients. Steroid use was significantly higher in CRSwNP and AERD vs CRSsNP (p = 0.001). LMS was significantly higher in AERD as compared with CRSwNP and CRSsNP (p = 0.001). CONCLUSION: Occupational airborne exposure to VGDFFiM correlated with increased prevalence of FESS and need for corticosteroids in CRS patients. There was no difference in PM2.5 and BC levels and disease severity outcome measures between CRS subtypes in this subset.
Assuntos
Poluentes Ocupacionais do Ar/análise , Asma Induzida por Aspirina/epidemiologia , Doença Crônica/epidemiologia , Pólipos Nasais/epidemiologia , Rinite/epidemiologia , Sinusite/epidemiologia , Aerossóis/análise , Monitoramento Ambiental , Feminino , Gases/análise , Humanos , Masculino , Pessoa de Meia-Idade , Exposição Ocupacional/análise , Material Particulado/análise , Pennsylvania/epidemiologia , Prevalência , Índice de Gravidade de Doença , Emissões de Veículos/análiseRESUMO
Aspirin-exacerbated respiratory disease is a chronic and treatment-resistant disease, characterized by the presence of eosinophilic rhinosinusitis, nasal polyposis, bronchial asthma, and nonsteroidal anti-inflammatory drugs hypersensitivity. Alterations in arachidonic acid metabolism may induce an imbalance between pro-inflammatory and anti-inflammatory substances, expressed as an overproduction of cysteinyl leukotrienes and an underproduction of prostaglandin E2. Although eosinophils play a key role, recent studies have shown the importance of other cells and molecules in the development of the disease like mast cells, basophils, lymphocytes, platelets, neutrophils, macrophages, epithelial respiratory cells, IL-33 and thymic stromal lymphopoietin, making each of them promissory diagnostic and treatment targets. In this review, we summarize the most important clinical aspects of the disease, including the current topics about diagnosis and treatment, like provocation challenges and aspirin desensitization. We also discuss recent findings in the pathogenesis of the disease, as well as future trends in diagnosis and treatment, including monoclonal antibodies and a low salicylate diet as a treatment option.
Assuntos
Anti-Inflamatórios não Esteroides/efeitos adversos , Aspirina/efeitos adversos , Asma Induzida por Aspirina/imunologia , Asma/induzido quimicamente , Pólipos Nasais/induzido quimicamente , Doenças Respiratórias/induzido quimicamente , Rinite/induzido quimicamente , Sinusite/induzido quimicamente , Adulto , Anticorpos Monoclonais/uso terapêutico , Ácido Araquidônico/metabolismo , Asma/terapia , Asma Induzida por Aspirina/diagnóstico , Asma Induzida por Aspirina/epidemiologia , Asma Induzida por Aspirina/terapia , Cisteína/metabolismo , Citocinas/metabolismo , Dessensibilização Imunológica/métodos , Dinoprostona/metabolismo , Progressão da Doença , Síndrome de Hipersensibilidade a Medicamentos , Eosinófilos/metabolismo , Feminino , Humanos , Leucotrienos/metabolismo , Masculino , Mastócitos/metabolismo , Pólipos Nasais/terapia , Doenças Respiratórias/diagnóstico , Doenças Respiratórias/epidemiologia , Doenças Respiratórias/terapia , Rinite/terapia , Sinusite/terapia , Linfopoietina do Estroma do TimoRESUMO
AIM: To evaluate the association of three single nucleotide polymorphisms in TNF and one in LTA in Mexican patients with aspirin-exacerbated respiratory disease (AERD) and the correlation of those single nucleotide polymorphisms with serum levels of TNF-α. PATIENTS & METHODS: Case-control study including 133 patients with AERD, 135 patients with asthma (aspirin-tolerant asthmatics) and 182 healthy subjects. RESULTS: GA genotype of rs1800629 in TNF was found to be associated with the risk of developing AERD (p < 0.05; odds ratio = 2.36) and by dominant model (p < 0.05; odds ratio = 2.51). Furthermore, there was a difference in the serum levels between the aspirin-tolerant asthmatics group and the other groups (p < 0.001). CONCLUSION: The GA genotype of rs1800629 is associated with genetic susceptibility to AERD, but it does not correlate to protein serum levels.