Chronic rhinosinusitis phenotypes

Steinke, John W.; Borish, Larry

doi:10.1016/j.anai.2016.06.006

Cited by 43 publications

(44 citation statements)

References 61 publications

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“…140 CRS represents >12 weeks of chronic inflammation in paranasal sinuses, and can be divided into two subtypes, CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP). 141 CRSsNP and CRSwNP show distinct inflammatory endotypes with CRSwNP being associated with increased levels of tissue IL-5, tissue eosinophilia, and concomitant asthma. 142 IL-33 was upregulated in nasal polyp tissues from patients with CRSwNP as compared with those of CRSsNP or healthy control subjects.…”

Section: Chronic Rhinosinusitismentioning

confidence: 97%

“…CRS is one of the most common chronic diseases in adults in the United States, and it produces significant morbidity and cost to the health care system . CRS represents >12 weeks of chronic inflammation in paranasal sinuses, and can be divided into two subtypes, CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP) . CRSsNP and CRSwNP show distinct inflammatory endotypes with CRSwNP being associated with increased levels of tissue IL‐5, tissue eosinophilia, and concomitant asthma .…”

Section: Il‐33 In Human Airway Diseasesmentioning

confidence: 99%

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IL‐33: biological properties, functions, and roles in airway disease

Drake

Kita

2017

Immunological Reviews

204

203

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Summary Interleukin (IL)-33 is a key cytokine involved in type 2 immunity and allergic airway diseases. Abundantly expressed in lung epithelial cells, IL-33 plays critical roles in both innate and adaptive immune responses in mucosal organs. In innate immunity, IL-33 and group 2 innate lymphoid cells (ILC2s) provide an essential axis for rapid immune responses and tissue homeostasis. In adaptive immunity, IL-33 interacts with dendritic cells, Th2 cells, follicular T cells, and regulatory T cells, where IL-33 influences the development of chronic airway inflammation and tissue remodeling. The clinical findings that both the IL-33 and ILC2 levels are elevated in patients with allergic airway diseases suggest that IL-33 plays an important role in the pathogenesis of these diseases. IL-33 and ILC2 may also serve as biomarkers for disease classification and to monitor the progression of diseases. In this article, we reviewed the current knowledge of the biology of IL-33 and discussed the roles of the IL-33 in regulating airway immune responses and allergic airway diseases.

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Section: Chronic Rhinosinusitismentioning

confidence: 97%

Section: Il‐33 In Human Airway Diseasesmentioning

confidence: 99%

IL‐33: biological properties, functions, and roles in airway disease

Drake

Kita

2017

Immunological Reviews

204

203

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“…In retrospect, the current result is reasonable because asthma itself can be an eosinophilic or noneosinophilic disease and AR can predispose to both eosinophilic and noneosinophilic presentations of NPs. 30 As with a history of AR, total IgE had no predictive value (Table II and Figure 3). Among the biomarkers we studied, only circulating eosinophilia was predictive of tissue eosinophil status (Table II).…”

Section: Discussionmentioning

confidence: 93%

Lack of Efficacy of Symptoms and Medical History in Distinguishing the Degree of Eosinophilia in Nasal Polyps

Steinke

Smith

Carpenter

et al. 2017

The Journal of Allergy and Clinical Immunology: In Practice

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BACKGROUND Distinguishing eosinophilic nasal polyps (NP) from noneosinophilic NP will impact prognosis and therapeutic responsiveness. OBJECTIVE To investigate the ability of clinical history and biomarkers to distinguish these conditions. METHODS A total of 74 consecutive patients undergoing surgery for NP were enrolled. Clinical presentations were evaluated using the 22-item sinonasal outcome test (SNOT-22). Biomarkers included absolute eosinophil count, IgE, and extent of tissue hyperplasia on sinus computed tomography scan. Tissue eosinophilia was quantified in 10 random hpf and data analyzed addressing both peak and average results. RESULTS No component of the SNOT-22 was predictive of tissue eosinophilia. Similarly, a medical history of allergic rhinitis, asthma, or aspirin-exacerbated respiratory disease was not predictive. An absolute eosinophil count of more than 300 was associated with NP tissue eosinophilia. In contrast, neither IgE nor extent of sinus computed tomography hyperplasia was predictive. CONCLUSIONS The ability to individualize therapies for NP is dependent on identifying clinical features or biomarkers of eosinophilia. However, with the exception of circulating eosinophilia, we could not identify a clinical feature or biomarker that robustly predicted the presence of tissue eosinophilia. Even more problematic, even the seeming “criterion standard” determination of tissue pathology was of limited value, as our cohort displayed a continuous spectrum of tissue eosinophil expression, making arbitrary any definitive cutoff distinguishing these conditions.

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“…There has been increasing recognition of the heterogeneity of CRS with a focus on multiple groups of endotypes . An important question is whether the clustering of symptoms we observed represents one or more endotypes with distinct underlying pathobiologic processes or anatomic relationships.…”

Section: Discussionmentioning

confidence: 95%

Longitudinal evaluation of clustering of chronic sinonasal and related symptoms using exploratory factor analysis

Cole

Bandeen‐Roche

Hirsch

et al. 2018

Allergy

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Background: Sinonasal symptoms are common and can have several underlying causes. When symptoms occur in specified patterns lasting three months or more they meet criteria for chronic rhinosinusitis (CRS). Approaches to CRS symptom measurement do not specify how to measure symptoms and treat six sinonasal symptoms as generally interchangeable, suggesting that such symptoms should cluster on one or two latent factors. Methods: We used questionnaire responses to 37 questions on presence, severity, bother, and frequency of cardinal sinonasal and related symptoms lasting three months, from 3535 subjects at three time points over 16 months. We completed five exploratory factor analyses (EFA) to identify symptom clustering, one for each time point and two for the differences between adjacent questionnaires. The baseline EFA was used to provide factor scores that were described longitudinally and examined by CRS status. Results: Five EFAs identified the same five factors (blockage and discharge, pain and pressure, asthma and cold/flu symptoms, smell loss, and ear and eye [mainly allergy] symptoms), with clustering determined by symptom frequency, severity, and degree of bother. Responses to individual questions showed changes over time but when combined into factor scores showed less longitudinal change. All symptom factor scores were progressively higher from never to past to current CRS status. Conclusions: Although the current approaches to symptom characterization in CRS imply a single underlying latent construct, our results suggest that there are at least three latent constructs relevant to CRS. Further studies are needed to evaluate if these clusters have identifiable underlying pathobiologies.

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Chronic rhinosinusitis phenotypes

Cited by 43 publications

References 61 publications

IL‐33: biological properties, functions, and roles in airway disease

IL‐33: biological properties, functions, and roles in airway disease

Lack of Efficacy of Symptoms and Medical History in Distinguishing the Degree of Eosinophilia in Nasal Polyps

Longitudinal evaluation of clustering of chronic sinonasal and related symptoms using exploratory factor analysis

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