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World Allergy Forum: Non-Allergic Rhinitis and Polyposis

Nasal Polyposis: A Multifactorial disease

Ruby Pawankar

Nasal polyposis is a chronic inflammatory disease of the mucous membranes in the nose and paranasal sinuses presenting as pedunculated smooth, gelatinous, semitranslucent, round or pear shaped masses of inflamed mucosa prolapsing into the nose. Nasal polyposis is not a single disease entity, but, instead is a multifactorial disease often associated with asthma, and other respiratory diseases like cystic fibrosis, primary ciliary dyskinesia, and aspirin sensitivity.

In the general population the overall prevalence rate of nasal polyposis ranges from 1-4%. It is more common in adults than in children under 10 years of age except when associated with cystic fibrosis. It does not appear to be more common in atopics. The site of polyp origin is a particular narrow area in the upper part of the nose, lateral to the middle turbinate, and around the openings of the ethmoid and maxillary sinuses. This is a part where the mucous membranes come into close contact.

Polyps are characterized by massive tissue edema, resulting from a leakage of plasma through widened endothelial junctions in the blood vessels. The typical histological characteristics include edematous fluid with sparse fibrous cells, and few mucous glands with no innervation, squamous metaplasia of the surface epithelium, proliferation of stromal and epithelial elements and a thickening of the basement membrane.

Other characteristics of nasal polyps include the existence of different types of epithelium from respiratory pseudostratified to transitional epithelium and a lowered density of goblet cells. The cellular components comprise a variety of cells including eosinophils, mast cells, lymphocytes, neutrophils and plasma cells. Eosinophils are the dominant cell type except in cystic fibrosis which contain more neutrophils and relatively fewer eosinophils.

The underlying mechanisms of nasal polyposis are still largely unknown. Several hypotheses have been put forward including chronic infection, aspirin intolerance, alteration in aerodynamics with trapping of pollutants, epithelial disruptions, epithelial cell defects/ gene deletions (CFTR gene in cystic fibrosis), inhalant or food allergies.

Hereditary factors may also play an important role in the development of nasal polyposis in diseases like cystic fibrosis and ciliary dyskinesia, and this association was also reported in eosinophilic polyps. However, as stated by Settipane, local, mucosal and environmental factors may also be important in addition to a genetic predispostion.

Microscopic observations have revealed several characteristics of polyp disorder, but with some controversies. However, increased presence of inflammatory mediators are a prominent and common factor indicating that chronic persistent inflammation is undoubtedly a major factor in polyposis, irrespective of the etiology.

In majority of nasal polyps, eosinophils comprise more than 60% of the cell population, except in cystic fibrosis. There is also an increase in activated T cells (CD45RO+), with CD8+ T cells predominating over CD4+. Mast cells and plasma cells are also increased as compared to the normal nasal mucosa.

Increased expression and production of a variety of cytokines/ chemokines have been reported. Of special importance are GM-CSF, IL-3 and IL-5 crucial for eosinophil survival and activation. In fact, an increased expression of these cytokines has been reported in nasal polyps, which can result in prolonging the survival of the migrated eosinophils within the polyp tissue. Interestingly, a good correlation has been reported between the levels of GM-CSF/ IL-3/ IL-5 and the number of EG2+ cells in nasal polyps.

On the other hand, the levels of chemokines like RANTES and Eotaxin which are important for eosinophil migration (Eotaxin can also contribute to tissue damage ) are also increased in the nasal polyp tissue. IL-8, which is a known chemotactic factor for neutrophils is also increased in nasal polyp tissue. Again, pro-inflammatory cytokines like IL-1b and TNF-a are important in upregulating adhesion molecule expression in endothelial cells, a pre-requisite for cell migration into the tissue. In this context, it can be noted that an increased expression of TNF-a, VCAM-1 and ICAM-1 has been reported in nasal polyps.

A variety of cells like epithelial cells, fibroblasts, T cells, mast cells contribute as potent sources of the above mentioned cytokines / chemokines and thus can be instrumental in orchestrating eosinophil migration. However, eosinophils themselves are an important source of some of these cytokines / chemokines (IL-5, GM-CSF, TNF-a) and are thus capable of increasing their own survival, activation and migration in an autocrine manner.

Since TGF-b is an important cytokine responsible for inducing fibroblast proliferation, the increased stromal fibrosis seen in nasal polyps can be attributed to the increased in vivo expression of TGF-b in nasal polyps. Eosinophils are an important source of TGF-b indicating that eosinophils may be instrumental in inducing the stromal fibrosis. Still further, eosinophils can release a variety of toxic proteins like MBP and ECP which induce epithelial damage, as observed in nasal polyps.

Besides cytokines/chemokines, levels of other mediators like histamine, albumin, sCD23 and IgE in polyp tissue are significantly increased in nasal polyps. Levels of IgA, sIgA, IgE, IgG and IgM are also increased in polyp fluid and tissue. Only in those patients with associated allergy to inhalent allergens there is an increase in specific IgE in the polyp tissue. Of interest, is the strong correlation between the levels of IgE and EG2+ cells. In aspirin intolerant asthmatics, there is an increased release of peptido-Leukotrienes and lower release of PGE2 from the nasal polyp tissue and peripheral blood cells.

Association with asthma
The association on nasal polyposis with asthma is well recognized ranging from 7-20%. The association of nasal polyposis, bronchial asthma, and aspirin sensitivity has also been well recognized. Usually, such a triad starts off with vasomotor rhinitis associated with profuse rhinorrhea, followed by severe nasal congestion, development of nasal polyposis, bronchial asthma and finally aspirin sensitivity. Patients with aspirin sensitivity have an increased incidence of recurrence of nasal polyps.

Role of Atopy

Although atopy may not be a direct cause of nasal polyposis, associated allergy has been found to be a cause of recurrence of nasal polyps (based on skin tests 66%). Furthermore, the incidence of nasal polyps is higher in non-atopic asthmatics and rhinitics than atopic rhinitics and asthmatics. Also, an increased degranulation of stromal rather than intraepithelial mast cells in nasal polyps does not favor inhalant allergy as a cause. In this context, it is of interest that bacterial infection can lead to IgE-sensitization and increase in bacteria specific IgE and a shift to a Th2 type cytokine profile. On the other hand, increased levels of IL-4, IL-13, IgE and IgE receptor (FceRI) expression as well as IgE-dependent mediator release could be seen from nasal polyp mast cells of atopics.

Clinical Features

Primary symptoms of nasal polyposis are nasal blockage, congestion, hyposmia or anosmia and if associated with chronic sinusitis a purulent nasal discharge. Secondary symptoms comprise post nasal drip, rhinorrhea, facial pain, headache, sleep disturbance and lowered quality of life. Diagnosis can be made by history, clinical examination, radiography, nasal endoscopy and additional tests for allergy, aspirin sensitivity, bacteriology, and pulmonary function tests.

The treatment is targeted to increase the osteal patency, increase drainage, reduce inflammatory exudate, and improve sense of smell and quality of life. The mainstay of treatment of nasal polyposis are intranasal steroids, which can reduce the polyp size, inflammatory exudate and also the incidence of recurrence, as well as increase nasal airway patency. Surgery is important in that it can increase osteal patency, reduce inflammatory exudate and increase drainage. Therefore, in severe cases, combined treatment with surgery and steroids is recommended. Antibiotics are important to treat the infection. However, in cases of associated atopy or aspirin sensitivity, desensitization is also necessary.


In conclusion, it is important to remember that there is no single etiological factor that is responsible for the development of nasal polyposis, but that inflammation still remains to be the central major factor in all nasal polyps. Activation of epithelial cells, mast cells, and macrophages by various factors (bacteria, virus, allergens, altered AA metabolism, altered aerodynamics) results in the release of inflammatory mediators.

This cytokine-chemokine cascade results in increased inflammatory cell infiltration (predominantly eosinoiphils). The migrated eosinophils can in turn further enhance the inflammatory process by contributing to stromal fibrosis, epithelial damage, increased interstitial edema, and increased extracellular matrix production. Thus a network of interactions between structural cells and inflammatory cells within the polyp microenvironment can lead to this chronic state of inflammation and the subsequent growth and persistence of nasal polyps.


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