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253

Orlandi et al.

TABLE V-2 Evidence for the definition of chronic rhinosinusitis Study Year LOE Study Design Study Groups

Conclusions

Kaper 150

2019

1

Systematic Review Consensus statements on CRSConsensus on endoscopic and computed tomography in the diagnosis of CRS.

Symptoms present for minimum of 12 weeks. Majority of international diagnosis rely on combination of symptoms and objective findings. Diagnosis of CRS based on 2 of CPODS symptoms for minimum of 12 weeks with objective evidence of inflammation.* Diagnosis of CRS based on 2 of CPODS symptoms for minimum of 12 weeks with objective evidence of inflammation.* Consistent adoption of “rhinosinusitis” vs “sinusitis” in the literature. Diagnosis of CRS based on 2 of CPODS symptoms for minimum of 12 weeks with objective evidence of inflammation.* Diagnosis of CRS based on 2 of CPODS symptoms for minimum of 12 weeks with objective evidence of inflammation.* Diagnosis of CRS based on sinonasal symptoms for minimum of 12 weeks with objective evidence of inflammation.*

Orlandi 1

2016

2

Systematic Review Patients with CRS

Rosenfeld 88

2015

2

Systematic Review Patients with CRS

Bachert 149

2014 2

Systematic Review Patients with CRS

Fokkens 31

2012

2

Systematic Review Patients with CRS

Meltzer 146

2004 3

Systematic Review Patients with CRS

Benninger 143 Strong history for diagnosis of CRS based on 2 major, 1 major plus 2 minor or purulence on nasal exam *Objective findings: positive nasal endoscopy (purulence, polyps, or edema) or positive imaging findings consisting of inflammation or mucosal changes within the sinuses 2003 3 Systematic Review Patients with CRS

cavities. 1 The challenge for every clinician is to charac terize and describe the clinical phenotype and endotype as well as possible, within the possibilities of diagnostic work-up in a routine clinical setting. 152 Given the mul titude of underlying etiologic factors, it is not surprising to find multiple phenotypes or mixtures of phenotypes inCRS. On the basis of history and nasal endoscopic and/or CT scan findings, CRS is generally divided into CRSsNP and CRSwNP. Apart from the latter 2 major clinical pheno types, other phenotypes relate to the variety of presenting symptoms in CRS patients and the presence or absence of concomitant bronchial disease. 26,153,154 Recognizable clin ical phenotypes include aspirin-exacerbated respiratory disease, fungal rhinosinusitis (RS), of which there are sev eral subtypes, and CRS associated with other systemic diseases including vasculitic, rheumatologic, and genetic processes. Also severity, level of control and response to treatment differ amongst CRS patients, which are all key determinants of the phenotype. 155 A wide range of inflammatory patterns may act together with mucociliary and/or structural abnormalities to give rise to the development of CRS. The multifactorial etiology

of CRS, involving genetic factors, environmental influ ences, occupational factors, infection, allergy, immune dysfunction, and systemic diseases, has led to definition of endotypes of disease. 154 CRS has been classified into different inflammatory clusters, including Th1 driven or neutrophilic inflammation, Th2 driven or eosinophilic inflammation, neurogenic, epithelial, and mixed endotypes. 156 In view of different clinical phenotypes and inflamma tory endotypes of CRS, this condition encompasses multi ple disease states of the sinonasal cavities. In a single CRS patient, pin-pointing the different etiologic factors respon sible for the development of the disease remains the chal lenge for the future. V.B.2 CRS: Endotyping Phenotypic stratification of CRS based on the pres ence (CRSwNP) or absence (CRSsNP) of nasal polyps may be overly simplistic for the purposes of treatment selection, as there is substantial inflammatory heterogene ity within each conventionally phenotyped category as