Nasal cavity, paranasal sinuses, nasopharynx
Inflammatory lesions
Allergic rhinosinusitis
Last author update: 1 April 2016
Last staff update: 2 March 2020
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PubMed Search: Allergic rhinosinusitis[TI]
Table of Contents
Definition / general | Terminology | Epidemiology | Sites | Pathophysiology | Etiology | Clinical features | Laboratory | Treatment | Microscopic (histologic) description | Cytology description | Differential diagnosis | Additional referencesCite this page: Sun J, Brandwein-Weber M. Allergic rhinosinusitis. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/nasalallergicrhinitis.html. Accessed April 19th, 2024.
Definition / general
- Common IgE mediated sinonasal hypersensitivity reaction provoked by reexposure to a specific antigen, including plant pollen, fungi, dust mites, animal allergens
- May be acute or chronic
- Also called hay fever
Terminology
- Also called type I IgE immunological rhinitis
- Acute allergic rhinosinusitis: develops 2 to 5 minutes after antigen-antibody exposure, reaching its peak about 15 minutes later
- Chronic allergic rhinosinusitis: lasts more than 6 weeks; includes aspirin exacerbated respiratory disease
Epidemiology
- 10 - 20% of the U.S. adult population (Hosp Pract (Off Ed) 1991; 26:105)
Sites
- Bilateral nasal cavity and paranasal sinuses
Pathophysiology
- IgE antibody binding and mast cells release various mediators (histamine, prostaglandins and leukotrienes) causing vasodilation, edema, eosinophilia, nasal congenstion, rhinorrhea, sneezing and itching
Etiology
- Type I IgE hypersensitive reaction to allergens, including pollen, animal dander, dust mites, mold spores and food
- Aspirin exacerbated respiratory disease (AERD, also known as Samter triad) refers to the syndrome of allergic nasal polyps with eosinophils, aspirin intolerance and bronchial asthma, which affects 4 - 10% of asthmatics
- AERD is due to inhibition of the cyclooxygenase pathway in sensitive individuals; this shunts metabolism of arachidonic acid to the 5-lipooxygenase pathway, leading to increased proinflammatory leukotrienes and decreased PGE2, a protective prostaglandin
Clinical features
- Rhinorrhea, sneezing, itching
Laboratory
- Stained smears of nasal secretion slow > 25% eosinophils
- Elevated total serum IgE
Treatment
- Avoidance of allergens, use of environmental controls, sublingual immunotherapy
Microscopic (histologic) description
- Mucous secretions have neutrophils and prominent eosinophils
Cytology description
- Stained smears of nasal secretion: > 25% eosinphils
Differential diagnosis
