RESUMO
We present a rare case of a young patient with chest pain whose ascending thoracic aortic aneurysm (TAA) was detected by point-of-care ultrasound (POCUS) leading to a successful surgical repair. POCUS identified a moderate pericardial effusion and an associated severely dilated ascending aorta. In this context, it is important to rule out aortic rupture and aortic dissection. We also discuss the epidemiology, complications, and management of TAAs as well as the role of cardiac POCUS in the diagnosis of thoracic aneurysmal disease.
Assuntos
Aneurisma da Aorta Torácica/diagnóstico por imagem , Dissecção Aórtica/diagnóstico por imagem , Derrame Pericárdico/diagnóstico por imagem , Sistemas Automatizados de Assistência Junto ao Leito , Ultrassonografia/métodos , Adulto , Dissecção Aórtica/fisiopatologia , Dissecção Aórtica/cirurgia , Aneurisma da Aorta Torácica/fisiopatologia , Aneurisma da Aorta Torácica/cirurgia , Dor no Peito/diagnóstico , Dor no Peito/etiologia , Diagnóstico Precoce , Ecocardiografia Transesofagiana/métodos , Serviço Hospitalar de Emergência , Feminino , Seguimentos , Humanos , Derrame Pericárdico/fisiopatologia , Derrame Pericárdico/cirurgia , Radiografia Torácica/métodos , Medição de Risco , Resultado do Tratamento , Procedimentos Cirúrgicos Vasculares/métodosRESUMO
The reason why particular inhaled Ags induce allergic sensitization while others lead to immune tolerance is unclear. Along with a genetic predisposition to atopy, intrinsic characteristics of these Ags must be important. A common characteristic of many allergens is that they either possess proteinase activity or are inhaled in particles rich in proteinases. Many allergens, such as house dust mite and cockroach allergens, have the potential to activate the proteinase-activated receptor (PAR)-2. In this study, we report that PAR-2 activation in the airways at the same time as exposure to inhaled Ags induces allergic sensitization, whereas exposure to Ag alone induces tolerance. BALB/c mice were administered OVA with a PAR-2 activating peptide intranasally. Upon allergen re-exposure mice developed airway inflammation and airway hyperresponsiveness, as well as OVA-specific T cells with a Th2 cytokine profile when restimulated with OVA in vitro. Conversely, mice given OVA alone or OVA with a PAR-2 control peptide developed tolerance. These tolerant mice did not develop airway inflammation or airway hyperresponsiveness, and developed OVA-specific T cells that secreted high levels of IL-10 when restimulated with OVA in vitro. Furthermore, pulmonary dendritic cell trafficking was altered in mice following intranasal PAR-2 activation. Finally, we showed that PAR-2-mediated allergic sensitization was TNF-dependent. Thus, PAR-2 activation in the airways could be a critical factor in the development of allergic sensitization following mucosal exposure to allergens with serine proteinase activity. Interfering with this pathway may prove to be useful for the prevention or treatment of allergic diseases.