xRead - Nasal Obstruction (September 2024) Full Articles

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International consensus statement on rhinosinusitis

asthma exacerbations prospectively in a nested cohort fol lowed up for 20 years. 1455 In a study investigating the immune profiles of recur rent vs non-recurrent polyp disease at the first surgery, SE IgE was with other factors (total IgE, ECP, IL-5) signifi cantly increased in recurrent polyps, whereas IFN- γ was increased in non-recurrent CRSwNPs. 1456 SA also is fre quently found in patients with AFRS (37) and could be demonstrated to coexist with Aspergillus sp . in the sinuses, and to modulate the typical IgE immune response in those patients. In summary, based on a wealth of in vitro , ex-vivo , and clinical data, S. aureus and its products including super antigens appear to have a significant role in the initiation, severity and persistence of CRSwNP as well as in asthma comorbidity and disease recurrence after surgery.

to be a post-obstructive phenomenon in the setting of CRSwNP. Jain et al. 338 found a significantly higher average number of anatomical anomalies (accessory ostia, conchae bullosae, infraorbital ethmoid cells, lateralized uncinated processes, and paradoxical middle turbinates) in patients with limited disease compared to a cohort with pansinusi tis or control group without disease. The authors found 96 anatomic variations in 22 patients in the limited sinus surgery group, while the control group had 68 variants in 27 patients, and the pansinusitis group had 72 variants in 28 patients ( p = 0.003). In a study by the same group the authors also found a lower rate of anatomic variation in CRSwNP patients undergoing extensive ESS compared with patients with CRSsNP undergoing ESS and patients undergoing limited ESS. 788 Both of these articles suggest that anatomical variants may be related to impairment of the OMC seen in patients with limited disease or undergo ing a limited ESS, whereas a primary mucosal abnormal ity contributes to more diffuse CRSwNP disease. 338 Incon trast, a study by Bilge et al. 1458 retrospectively compared CT scans of a cohort of 155 patients with CRSwNP to a con trol group of 100 patients without RS. The authors found a statistically higher rate of nasal septal deviation (NSD), concha bullosa, agger nasi cell, frontal sinus hypoplasia, and accessory os in the CRSwNP group and concluded that this may be a contributing factor to the disease process in CRSwNP. This finding contrasts with most other studies, which have found higher rates of anatomic abnormalities in patients with more limited disease. In conclusion, the relationship between anatomical vari ants and development of disease in patients with CRSwNP is unclear given the limited amount of literature on the subject. Most of the studies seem to suggest that CRSwNP is a diffuse disease process and, therefore, less influenced by anatomic variation.

Superantigens as a Contributing Factor for CRSwNP Aggregate Grade of Evidence: B (Level 1: 1 study, Level 3: 4 studies, Level 4: 3 studies; Table X-9).

X.C.9 Contributing Factors for CRSwNP: Microbiome Disturbance Because of limited data, CRSsNP and CRSwNP are com bined in Section IX.C.8 . X.C.10 Contributing Factors for CRSwNP: Anatomic Variation The degree to which anatomic variation in the paranasal sinuses might contribute to disease pathophysiology in CRSwNP (ie, concha bullosae, paradoxical positioning of the middle turbinate, infraorbital ethmoid (Haller) cells, and NSD, among others) is less clear. 338,783–785 CRSwNP patient populations have rarely been independently stud ied to determine the influence of anatomic variation on disease. The relationship of anatomic variation and disease burden is therefore not well understood in CRSwNP. Leung et al. 1457 investigated obstruction at the OMC in CRSwNP and CRSsNP and noted that OMC obstruc tion was associated with increasing Lund-Mackay scores in both forms of CRS. In CRSsNP OMC obstruction was associated with adjacent sinus inflammation, while in CRSwNP, this correlation was absent. The authors con cluded that paranasal sinus inflammation was not likely

Anatomic Variation as a Contributing Factor forCRSwNP Aggregate Grade of Evidence: Grade C (Level 4: 4 studies). Results of studies are conflicting (Table X-10).

X.C.11 Contributing Factors for CRSwNP: Septal Deviation Because of limited data, CRSsNP and CRSwNP are com bined in Section IX.C.10 .