xRead - Nasal Obstruction (September 2024) Full Articles

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International consensus statement on rhinosinusitis

X.C.19 Contributing Factors for CRSwNP: Occupational and Environmental Factors Because of limited data, CRSsNP and CRSwNP are com bined in Section IX.C.17 . X.D Chronic Rhinosinusitis with Nasal Polyps: Management X.D.1 Management of CRSwNP: Saline (Spray and Irrigation) ICAR-RS-2016 found that nasal saline irrigation as an adjunct to other therapies improved symptoms and CRS specific QoL outcomes. High volume ( > 200 mL) was supe rior to low volume irrigation. Hypertonic and isotonic saline brought similar effects. An updated search identified 3 RCTs and 2 meta analyses. 442,1048,1049,1051,1058 Of the 3 RCTs, 2 were excluded due to mixed ARS/CRS (16% CRSwNP) 442 and mixed CRSsNP/CRSwNP (21% CRSwNP). 1058 One systematic review by Harvey et al. was excluded because data were from participants with mixed ARS/CRS (16% CRSwNP). 1051 As such, data from 1 randomized trial 1049 and 1 Cochrane review 1048 were assessed for this review. No pub lished studies compared the effects of saline treatment to non-saline treatment or placebo. We searched for non randomized controlled trials and observational studies but did not find any additional study. In an RCT, Cassandro et al. 1049 aimed to assess the effects of hyaluronan administered as a nebulizer in CRSwNP patients. They performed an open-label study and randomly assigned 80 patients with CRSwNP who had not undergone sinus surgery to 4 groups: nebulized saline solution (5 mL) bid, nebulized sodium hyaluronate, mometasone furoate nasal sprays 200 μ g bid, and both neb ulized sodium hyaluronate and mometasone furoate nasal sprays. The nebulized saline solution did not improve nasal symptom scores, endoscopic appearance scores, radiologic scores, rhinomanometry, or saccharine clearance tests at 1 month, 3 months, and 3 months after treatment compared with other treatment groups. It was concluded that neb ulized saline was inferior to intranasal steroid spray. This study by Cassandro et al. 1049 was 1 of the 2 included studies in a Cochrane review in 2016 by Chong et al. 1048 Theother study assessed a mixed patient population with the major ity experiencing ARS. Thus, we did not obtain any addi tional data from the systematic review by Chong et al. 1048 for further assessment. As such, this updated review included only 1 new ran domized controlled trial which used saline as a control

with AERD have the highest levels of tissue eosinophilia when compared to sinus tissue from patients with CRSsNP, inhalant allergies and/or aspirin-tolerant patients with CRSwNP. 1526 Genetic polymorphisms, or functional epigenetic dys function, may potentially play a causative role in the patho genesis of AERD. 1527,1528 These polymorphisms are thought to alter enzyme kinetics and receptor sensitivity. As a result, the activity of LT-synthase is increased, leading to an overproduction of cysLTs. Sensitivity of LT receptors is upregulated, as is the expression of cysLT receptor 1. Fur thermore, the production of prostaglandin E 2 is reduced, in addition to the downregulation of COX-2 and E-prostanoid receptor subtype-2. 1518,1525 All of these effects could add to an aggravation of the eicosanoid imbalance. The complexity in the interaction of inflammatory medi ators in AERD is underlined by the dysregulation of the prostaglandin E 2 -dependent control of LT production in peripheral granulocytes. When compared to those from patients with aspirin-tolerant asthma or healthy controls, granulocytes from patients with AERD generate more LTB 4 and cysLTs, and are more resistant to the PGE 2 mediated suppression of LT generation. 1529 This can be explained in part by an impaired protein kinase A func tion in AERD, which can lead to the deregulated control of 5-lipoxygenase activity by PGE 2 . Beyond the characteristic type 2 inflammatory signature of AERD, there is has been an increasing emphasis on the role of innate immune responses as a contributing factor to AERD. Type 2 innate lymphoid cells and the associ ated increased expression of IL-33 and thymic stromal lym phopoietin (TSLP), have been shown to further activate lymphoid and myeloid effector cells, in particular, mast cells. 1518,1519 Both IL-33 and TSLP are strongly expressed in nasal polyp tissue and exhibit a critical role in inflamma tory signaling in non-human models. 1524

Aspirin Intolerance as a Contributing Factor forCRSwNP Aggregate Grade of Evidence: C (Level 2: 1 study; level 3: 2 studies; level 5: 10 studies; Table X-16).

X.C.18 Contributing Factors for CRSwNP: Viruses Because of limited data, CRSsNP and CRSwNP are com bined in Section IX.C.16 .