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complete opacification (Fig. 10). Because AScA had sig- nificantly higher levels of CD4 1 cells than the control group, AScA mucosal inflammation is driven by T helper cells and most likely the Th2 process. Although Th2 mediated cytokines did not reach statistical difference in our study, IL4 and IL13 have been implicated in these IgE-associated atopic asthmatic patients. 12,13 The inflammation in AScA is usually not driven by infection, and therefore AScA patients respond better to oral steroids rather than antibiotics. The mucosal inflammation in these patients is so severe that they are likely to fail medical treatment and often require ESS to debulk the nasal polyps. Removing the nasal polyps decreases the local inflammation by eliminating the eo- sinophils and associated inflammatory mediators to the level where the mucosal inflammation can be controlled with postoperative medications. Another reason for ESS is to debulk the obstructive nasal polyps and open the sinuses so that topical medications, such as topical bude- sonide, can be delivered into the sinuses. Topical budesonide has been shown to improve patient sinus score and hyposmia in chronic eosinophilic sinusitis. 14 Another method to control the inflammation is immuno- therapy (sublingual and subcutaneous immunotherapy) that suppresses Th2-mediated response. 15 Immunomodu- lators using anti–IL4, anti-IL5, and anti-IL13 monoclonal antibodies are certainly options to be consid- ered and have been evaluated in the past. 12,16 Asthmatic Sinusitis Without Allergy The phenotype and histology of ASsA is similar to AScA and AERD, but ASsA is more comparable to AERD than ASsA. An interesting thought is that ASsA could be a precursor to AERD. Unlike AScA, ASsA patients usually do not have a history of pediatric aller- gic rhinitis or asthma. As stated earlier, AScA or unified airway CRS commonly has a history of pediatric allergic

Fig. 9. Flow chart demonstrating the cyclical pattern of chronic sinusitis.

allergy exacerbation could lead to mucosal swelling and thus the cyclical sinusitis pattern (Fig. 9). In these patients, they may respond to pharmacotherapy for the allergy component of their CRS.

Asthmatic Sinusitis With Allergy AScA represents the “unified airway” patients who have been described in the literature. 6 The unified air- way patients have sinusitis, allergic rhinitis, and asthma but no aspirin sensitivity and is mediated via an IgE Th2 inflammatory process. Upper respiratory tract stimulation affects the lower respiratory tract and vice versa in these patients. 11 The most plausible explanation for the connection between the upper and lower airways is circulation of activated eosinophils that are very high in AScA CRS polyps. Eosinophils are activated in the sinus mucosa due to exposure of stimulants in the nose. The activated eosinophils are transported to the lung via the circulatory system. These circulating eosinophils can then bind to the adhesion molecules in the pulmonary epithelial tissue. The activated eosinophils in the lower respiratory tract can then create a local inflammatory response in the lung. The amount of eosinophils in the nasal polyp appears to be a good histological marker or measure for intrinsic mucosal inflammation. This type of inflamma- tion should be called intrinsic mucosal inflammation because the airway mucosa develops an abnormal response to an irritant within the mucosa due to a genetic predilection. Other intrinsic mucosal inflamma- tory CRS subclasses are AFS and AERD. Intrinsic inflammatory CRS has abundant eosinophils in tissue samples. Hypercellularity of nasal polyps is also high in intrinsic inflammatory CRS. However, hypercellularity, which is also represented in CF, may not always be rep- resentative of an intrinsic inflammation. AScA patients commonly have a pediatric history of allergy or asthma. On nasal endoscopy, they have exten- sive nasal polyposis with little to no purulence. On CT findings, they have pansinusitis with complete or near

Fig. 10. Coronal computed tomography of the sinus demonstrat- ing pansinusitis with near-complete opacification of all the sinuses.

Han: Subclassification of Chronic Sinusitis

Laryngoscope 123: March 2013

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