Background: Despite the frequent presence of clinical symptoms such as sneezing and itching, elevated histamine and IgE in extracellular polyp fluids, tissue eosinophilia, and degranulated mast cells, allergy is not considered an important cause of nasal polyposis.
Objective: To investigate the prevalence of immediate skin reactivity to airborne allergens in patients with nasal polyposis.
Methods: Sixty-eight patients with nasal polyposis and 36 controls with chronic sinusitis were submitted to skin prick tests (SPTs) with a large series of seasonal and perennial airborne allergens including: grass, mugwort, ragweed, pellitory, plantain, birch, hazel, olive, cypress, house dust mites, cat and dog dander, and thirteen molds (Alternaria, Aspergillus, Cladosporium, Penicillium, Candida, Trichophyton, Fusarium, Curvularia, Botrytis, Pullularia, Rhizopus, Mucor, Helminthosporium).
Results: Forty-three of 68 (63%) patients with nasal polyposis versus 6 of 35 (17%) controls were positive on SPT with airborne allergens (P < .001). A comparison with 1,128 subjects with respiratory allergy seen from 1996 to 1999 showed a markedly higher prevalence of sensitivity to Candida albicans (19 of 43 [44%] vs 8 of 1,128 [1%]; P < .001) and to house dust mites (12 of 43 [28%] vs 154 of 1,128 [14%]; P < .05) among allergic patients with polyps. Altogether, 30 of 43 (70%) patients versus 215 of 1,128 (19%) controls were sensitive to at least one perennial airborne allergen (ie, mold, mite, or animal dander) on SPT (P < .001); in contrast, 26 of 43 (60%) patients versus 942 of 1,128 (84%) controls were sensitive to seasonal airborne allergens (P < .005). A review of the clinical histories of SPT-positive patients revealed the presence of obstructive rhinitis and chronic rhinorrhea only in most cases, whereas acute symptoms, such as sneezing and itching, were reported only by a minority of subjects.
Conclusions: A clinically slight respiratory allergy, particularly to perennial airborne allergens, might play a relevant role in the pathogenesis of nasal polyposis, probably through the induction of a long-lasting inflammation of the nasal mucosa.