Allergic rhinitis is a chronic nasal disease caused by an allergic reaction of the nasal mucosa. It is very common, with a prevalence of 6.7%. It can develop into bronchial asthma in at least 30% of patients. It can be divided into two categories: perennial and seasonal, the latter being chytridiomycosis. Allergic rhinitis is generally referred to as perennial allergic rhinitis. The cause is mainly exogenous inhalation factors, most commonly house dust, cotton dust, grain dust, bedding dust, including bushels of lint, animal dander, poultry feathers, various kinds of smoke, insect scales, etc.; a few foods with special odors, such as onion, ginger, garlic, curry, pepper, chili pepper, certain fragrant fruits, can constitute a trigger; other still have humidity, cold air and certain chemical gases. After the allergen is inhaled into the nasal cavity, the corresponding IgE antibodies are produced under the nasal mucosa and bind to the IgE receptors on the surface of the surrounding mast cells, and the patient is in a sensitized state. When the same allergen is inhaled again, the antigen-antibody combination and activation of mast cells cause the release of a large number of mediators, resulting in vasodilation of the nasal mucosa, increased permeability, massive exudation, increased glandular secretion and inflammatory infiltration mainly by eosinophils. In terms of immune response, allergic rhinitis is an IgE antibody-mediated inflammatory response. When the body is exposed to an allergen, the body produces IgE antibodies, which attach to the surface of tissue mast cells and basophils, leaving the body in a sensitized state. When the body is exposed to the same allergen again, these allergens will combine with IgE antibodies to cause degranulation of mast cells and basophils, releasing histamine, leukotrienes and other biogenic mediators, which act on the corresponding tissues to cause allergic reactions.