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a form of atopy characterized by an acute irritative inflammation of the mucous membranes of the eyes and upper respiratory passages accompanied by itching and profuse watery secretion, usually without temperature elevation, followed occasionally by bronchitis and asthma; the episode recurs annually at the same or nearly the same time of the year, in spring, summer, or late summer and autumn, caused by an allergic reaction to the pollen of trees, grasses, weeds, flowers, etc.
Synonym(s): allergic coryza
acute rhinitis caused by exposure to any allergen to which the person is hypersensitive.
allergic rhinitisAn inflammatory response in the nasal passages to allergens, which is the most common form of atopic-allergic disease, affecting 5–20% of the general population. Allergic rhinitis is initiated by exposure of the nasal mucosa to airborne antigens, evoking IgE production; upon repeated re-exposure to the allergen (e.g., ragweed pollen), histamine, leukotrienes C4, D4, E4, B4, PGD2, kinins, kininogen and serotonin are released.
Allergic rhinitis is the most widely used of a plethora of terms referring to the effect of allergens on the upper respiratory tract, in particular the nasopharynx. It is often related to environmental antigens—most commonly pollen—thus being known as seasonal allergic rhinitis (colloquially known as hay fever), and less often to “constant” allergens, in which case it is designated perennial allergic rhinitis.
Paroxysms of sneezing, nasal congestion, nasal and ocular pruritus, tearing, rhinorrhoea, anosmia, ageusia, postnasal drip (which may cause coughing), partial or total obstruction of airflow, throat clearing, and allergic periorbital hematomas (black eyes).
Skin testing with appropriate inhalant allergens is of greater use than measuring serum IgE.
Avoid allergens; antihistamines (especially H1-receptor antagonists); sympathomimetic amines; anticholinergics; corticosteroids; decongestants; cromolyn sodium; immunotherapy.
Unclear; possibly a hypersensitivity response to allergens in pollen, dander, mites, insects, mould spores, foods; most patients have circulating IgE antibodies that bind to high-affinity receptors on mast cells and basophils, and to low-affinity receptors on other cells, evoking release of inflammatory mediators.