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Allergic rhinitis - Causes and pathogenesis
Last reviewed: 04.07.2025

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Causes of allergic rhinitis
The triggers for the development of allergic rhinitis are mainly airborne allergens. The most common "household" allergens are: house dust mite secretions, animal saliva and dander, insects and plant allergens. The main "external" allergens include plant pollen and mold fungi.
There is also occupational allergic rhinitis, which is most often accompanied by damage to the lower respiratory tract and is the responsibility of occupational pathologists.
In addition to airborne allergens, the disease may be caused by taking acetylsalicylic acid and other nonsteroidal anti-inflammatory drugs. In this case, rhinitis is considered a component of the "aspirin triad".
The role of heredity in the development of atopic allergy is generally recognized. This is proven by pedigree data, observations of twins, statistical studies among the population of different countries, as well as immunogenetic and molecular cytogenetic methods.
Pathogenesis of allergic rhinitis
Allergens, entering the nasal cavity with air, partially settle on the ciliated epithelium and, entering into local contact, sensitize the body. When they re-enter the sensitized mucous membrane, an IgE-dependent allergic reaction occurs. Allergic rhinitis is characterized by inflammatory infiltration of the mucous membrane of the nasal cavity by various cells.
In patients with persistent allergic rhinitis, the degree of contact with allergens varies throughout the year, and at certain times it can be very low. However, even in the absence of symptoms, these patients have been shown to have inflammation of the nasal mucosa: the so-called "minimal persistent inflammation". The manifestations of persistent rhinitis are considered to be the result of a complex interaction of allergy triggers and an ongoing inflammatory response.
Non-specific nasal hyperreactivity is one of the main features of allergic rhinitis. It is characterized by an increased response to non-allergic irritants that cause sneezing, nasal congestion and/or rhinorrhea. Against this background, the effect of allergens on the nasal mucosa causes more pronounced clinical manifestations of rhinitis. Nasal hyperreactivity is considered a significant factor, the presence of which should always be taken into account in the diagnosis and treatment of allergic rhinitis. Studying the mechanisms of disease development creates the basis for rational treatment, which involves influencing the complex inflammatory response, and not only the symptoms of allergy.
Relationship with bronchial asthma
Studies confirm the presence of a direct link between allergic rhinitis and bronchial asthma: allergic inflammation of the mucous membrane of the nose and bronchi plays a major role in the pathogenesis of these diseases. At the same time, the same cells and mediators participate in the formation of the inflammatory focus in the mucous membrane of the nose and bronchi. A provocative bronchial test with a specific allergen in patients with allergic rhinitis leads to the occurrence of an asthmatic response involving cells and proinflammatory mediators in the mucous membrane of the nasal passages, and provocative tests on the mucous membrane of the nose in turn cause inflammation in the bronchi.
These findings support the “single airway” concept, which demonstrates a close relationship between allergic rhinitis and asthma and suggests that the inflammatory response can be maintained and enhanced by interrelated mechanisms.
In this regard, patients with persistent allergic rhinitis should be examined for bronchial asthma. In turn, in patients with bronchial asthma, attention should be paid to the diagnosis of allergic rhinitis. Treatment should be aimed at eliminating the pathology of both the upper and lower respiratory tract.