Nasal Polyps: Epidemiology, Pathology, Immunology, and Treatment

Abstract

Nasal polyps frequently are associated with aspirin intolerance, intrinsic asthma. Young's syndrome, cystic fibrosis, and Kartagener's syndrome. Children 16 years or younger with nasal polyps should be evaluated for cystic fibrosis. Nasal polyps are frequently bilateral, multiple, freely movable, and pale-gray and arise from the middle meatus of the nose. Histologically, they classically have pseudostratified ciliated columnar epithelium, thickening of the epithelial basement membrane, high stromal eosinophil count, mucin with neutral pH, few glands, and essentially no nerve endings. Cells consist of a mixture of lymphocytes, plasma cells, and eosinophils. Polyps from patients with Young's syndrome, Kartagener's syndrome, and cystic fibrosis have predominately neutrophils with insignificant eosinophils. Chemical mediators found in nasal polyps are as follows: histamine, serotonin, leukotrienes [(SRS-A or LTC4, LTD4, LTE4), LTB4], ECF-A, norepinephrine, kinins, TAME-esterase, and possibly PGD2. There is more histamine in nasal polyps than in normal nasal mucosa, and norepinephrine is present in greater concentration in the base of nasal polyps than in normal mucosa. The concentrations of IgA and IgE and, in some cases, IgG and IgM are greater in polyp fluid than in serum. IgE-mediated disease is not the cause of nasal polyps, but when present, may contribute to episodes of exacerbation. Despite medical or surgical management, a significant number of nasal polyps are recurrent. For treatment, systemic corticosteroids should be tried before surgical polypectomy. Polypectomy does not increase the risk of developing asthma or making asthma worse. At the present time, the pathogenesis of polyp formation is unknown.