xRead - Nasal Obstruction (September 2024) Full Articles

20426984, 2021, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1002/alr.22741 by Stanford University, Wiley Online Library on [01/07/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

219

Orlandi et al.

TABLE I-2 Diagnostic criteria for diagnosis of CRS Greater than or equal to 12 weeks of: Two or more of the following symptoms: Nasal discharge (rhinorrhea or post-nasal drip) Nasal obstruction or congestion Hyposmia Facial pressure or pain Cough (in Pediatric CRS) AND One or more of the following objective findings:

Evidence of inflammation on nasal endoscopy or computed tomography Evidence of purulence coming from paranasal sinuses or ostiomeatal complex AND CRS is divided in to CRSsNP or CRSwNP based on the presence or absence of nasal polyps

In Europe, the prevalence for CRS symptoms have been reported to range from 6.9% to 27.1%. 14 In China, a survey of 10,636 participants in 7 cities reported a prevalence rang ing from 4.8% to 9.7% depending on the city. 15 Billing codes have also been analyzed as a proxy for the incidence of CRS. In a Canadian population-based analysis of Interna tional Classification of Disease, 9 th Revision (ICD-9) codes, the incidence of CRS was found to be 2.3-2.7 per 1000 people. 16 A similar analysis of ICD-9 codes in Pennsylva nia found the average incidence of CRSsNP to be 1048 ± 48 per 100,000 person-years. 17 Recently, 2 epidemiologic stud ies using radiologic confirmation of symptoms suggested a prevalence range of 1.7% to 8.8%. 18,19 The epidemiology of CRSwNP has been investigated uti lizing a variety of methods. In 2 survey studies 2.1% to 4.3% of European patients recalled being diagnosed with nasal polyps. 20,21 Using objective confirmation in a Swedish cohort, 2.7% were found to have nasal polyps. 22 This rate approximates the prevalence reported in the Korean National Health and Nutrition Examination Survey from 2008-2012 in which the prevalence of CRSwNP was 2.6% among 28,912 subjects undergoing nasal endoscopy. 23 While these numbers appear to converge around similar rates, interestingly between 26% and 42% of autopsy speci mens have been shown to contain NPs. 24,25 Acute exacerbations of chronic rhinosinusitis (AECRS) are described as a worsening of CRS intensity with a return to baseline symptoms frequently after intervention with corticosteroids and/or antibiotics. 1,26–30 Patients reporting greater than 3 episodes of oral corticosteroids or antibiotics use in the prior 12 months constituted 17.8% of CRS patients in a study by Yamasaki et al. 28 ARS is a common disorder within the pediatric popula tion, usually occurring in the context of an upper respira tory infection (URI). 31–33 When defining pediatric ARS as URI symptoms exceeding 2 standard deviations (range 16

22 days) above the mean (7.3 days), the prevalence has been reported between 4% and 7.3% 34,35 Epidemiologic data on pediatric CRS are more limited. Studies from the from the US Center for Disease Control National Center for Health Statistics 36 and a Swedish population-based cohort study 37 suggest a prevalence between 1.5-2.1% in patients under 20 years old. Furthermore, the prevalence in patients with underlying comorbidities may be higher than in healthy children. Several studies estimate the presence of CRS in children with CF, primary ciliary dyskinesia (PCD), and common variable immunodeficiency to be 11% to 38%, 38 40%, 39 and36%; 40 respectively. While the majority of epidemiologic, pathophysiologic, and therapeutic studies in CRS have utilized the presence of nasal polyps to distinguish CRS phenotypes, there has been greater recognition of substantial inflammatory het erogeneity and a continuum of pathophysiology between CRSwNP and CRSsNP patients. 41–45 Aided by advances in molecular and statistical techniques, several research groups have worked toward defining endotypes, or bio logical inflammatory subtypes of CRS, based on mucus and tissue biomarkers. 46–50 Overall, endotype research in CRS has drawn inspiration from a similar effort in the management of asthma, 51 which has led to improved understanding of the underlying pathophysiology and bet ter outcomes in treatment refractory patients. 52,53 While there remains a lack of consensus on the identity of ideal biomarkers for endotyping, it is evident that Th1, Th2, and Th17 markers (also referred to as type 1, 2, and 3 immune reactions) should be included. Further complicat ing this effort is the recognition of substantial global vari ations in the distribution of CRS endotypes, likely driven by undefined environmental factors which merit further study. 54 While specific biomarkers and biosignatures of each endotype will continue to be refined, there is already