Abstract

Background. The pathomechanism of rhinosinusitis associated with the use of non-steroidal anti-inflammatory drugs is complex and still not fully understood. They are now known to be associated with genetic predisposition and environmental triggers that lead to dysregulation of fatty acid and lipid metabolism, cell transmetabolism, and chronic inflammation in the airways.
 Aim: analysis of recent advances in the study of aspirin-associated respiratory disease (AERD), summarization of already known information about the pathomechanisms of the disease.
 Materials and methods. The analysis of literary sources included publications in the international electronic scientometric databases PubMed, Scopus, Web of Science by keywords for the period 2013-2023. 46 sources were selected for analysis, of which 24 were used that met the search criteria.
 Results. The results showed that researchers are actively studying the role of immunological factors, particularly IgG4 and IgE in the pathogenesis of the disease. IgG4 was detected in nasal polyp tissue and associated with poor postoperative outcome, which may indicate its important role in chronic sinusitis. In addition, cytokines such as thymic stromal lymphopoietin, IL-4, IL-10, IL-5, IL-13, and IL-33 have been detected in eosinophilic nasal polyps in patients with aspirin intolerance, suggesting their possible role in the development AERD.
 Conclusion. The cause of severe nasal polyposis in AERD has not been definitively determined. Further research may lead to the development of more personalized treatments. Dietary modification and development of new monoclonal antibody drugs lead to reduction of AERD symptoms and improvement of patients' quality of life.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call