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Review
. 2019 May 29;48(1):23.
doi: 10.1186/s40463-019-0350-y.

Clinically relevant phenotypes in chronic rhinosinusitis

Affiliations
Review

Clinically relevant phenotypes in chronic rhinosinusitis

Jessica W Grayson et al. J Otolaryngol Head Neck Surg. .

Erratum in

Abstract

Background: Chronic rhinosinusitis (CRS) is a complex disease that incorporates many different conditions. Currently, primary CRS is considered a disease of broad airway inflammation, however, the previous classification of CRS with and without nasal polyposis fails to adequately classify patients based upon their etiology of illness. Our aim with this review is discuss the clinical presentation, radiology, endoscopy, histopathology, and treatment algorithm of three different phenotypes of primary CRS: central compartment atopic disease, eosinophilic CRS, and non-eosinophilic CRS.

Methods: A narrative review of a tertiary rhinology center's research themes and how they are applied to clinical protocols and practice was assessed.

Discussion: Diagnosis and treatment of upper and lower airway conditions become increasingly important as phenotypes and endotypes are being described. There are well-described therapies to treat the different phenotypes of CRS, based upon the presumed underlying cause of the inflammatory process. Research continues to shed more light on different endotypes and phenotypes of airway inflammation, however, clinical differentiation of CRS can be applied in clinic practice with three simple phenotypes of CRS. Understanding these different phenotypes and their etiologies allows for further management beyond the 'maximum medical therapy and then surgery' approach that has often been used in the management of CRS.

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Conflict of interest statement

RH is a consultant with Medtronic, Olympus and NeilMed pharmaceuticals. He has received research grant funding from Meda Pharmaceuticals and Stallergenes. He has been on the speakers’ bureau for BHR, Seqiris, Astra Zeneca, and Glaxo-Smith-Kline and Arthrocare. The remaining authors have no disclosures.

Figures

Fig. 1
Fig. 1
a – Middle turbinate edema present in CCAD or IgE drive airway inflammation; b – Middle meatus polyposis present in eCRS airway inflammation
Fig. 2
Fig. 2
a - Radiographic evidence of CCAD with central disease and peripheral clearing; b - “black halo”sign
Fig. 3
Fig. 3
a,b: Pre-operative CT images view of patient suffering from eCRS; c,d: Post-operative CT images of patient compliant on corticosteroid irrigations
Fig. 4
Fig. 4
Sample histopathology report
Fig. 5
Fig. 5
Widely opened sinus cavity view of a: middle meatus, b: sphenoethmoidectomy, c: draf 3/Lothrop cavity
Fig. 6
Fig. 6
a-c: Endoscopy images of a 70 yo male patient with non-eCRS referred for revision surgery, although some synechiae had formed, he had limited response to corticosteroid with diffuse airway symptoms suffering from non-eCRS following sinus surgery, but with persistent symptoms; d-f: Endoscopy images of same patient 3 months after initiation of macrolide therapy (Clarithromycin 250 mg daily)
Fig. 7
Fig. 7
CT images of patient suffering from non-eCRS airway inflammation compliant on topical therapy; a-c: Post-operative imaging, with persistent disease; d-f: After initiation of macrolide therapy for 3 months (Clarithromycin 250 mg daily)

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