xRead - Nasal Obstruction (September 2024) Full Articles

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International consensus statement on rhinosinusitis

proliferate, and our characterization of CRS pivots toward endotypes, simple answers to this question elude us. IgE-mediated allergy has been among the multiple eti ologies suggested to cause CRSwNP. Allergy is strongly associated with Th2-mediated response. Multiple studies suggest a prominent role for Th2–mediated inflammation in the pathogenesis of CRSwNP 821,1374,1375 Bachert et al. iso lated elevated Th2 cytokines IL-5 and IL-13 in nasal polyp tissue. 1374 Similarly, eosinophilic inflammation is com monly identified in both atopy and CRSwNP. 1376,1377 Inter pretation of these data are complicated by demonstration that Thymic Stromal Lymphopoetin (TSLP) induces a Th2 inflammatory response in nasal polyp tissue using non-IgE induction methods. 1378 Direct evidence of a causal connec tion between atopy and CRSwNP presents an equally com plex picture. Inhalants. Some observational population data suggest an association between atopic disease and CRSwNP. 1379 Tan et al. found a higher number of inhalant sensitiv ities in CRSwNP patients as compared to CRSsNP and rhinitis patients, although the overall sensitivity rates were similar. 1380 Several studies have identified associations between systemic hypersensitivity to specific allergens and CRSwNP. These include dust mite, 1381,1382 dust mite and Olea europaea, 1383 and dust and cockroach. 1384 Another group found increased rates of Candida hypersentivity in CRSwNP patients compared to both allergic controls and CRSsNP patients. 1382 The association of MT polyposis and newly described “central compartment atopic disease” (CCAD) postuates a strong association between allergy and CRSwNP for this specific subtype of CRSwNP. The evi dence addressing this specific entity is included in section X.C.2.1. Other studies have found no significant association between CRSwNP and allergy. Study findings include simi lar rates of hypersensitivity between CRSwNP and CRSsNP groups; 1385 similar incidence of allergy and endotype pro files between CRSwNP and CRSsNP; 1386 no difference in symptoms among allergic and non-allergic CRSwNP patients during pollen season 1387 no differences in nasal polyp size, CT scores, symptoms, or recurrence of disease between atopic and non-atopic CRSwNP patients 1388 ordif ference in presenting symptoms or post-operative course of CRSwNP patients based on allergic status 1389,1390 In con trast, 1 study found increased rates of atopy in CRSwNP patients, though no significant difference in symptoms scores. 1391 Complicating this picture, rates of systemic atopy vary between eosinophilic and non-eosinophilic CRSwNP populations. 1392 Additionally, local production of specific IgE is seen in the absence of systemic atopy. 1393 Evidence also suggests that circulating IgE is largely mucosally produced. 1394

Taken together, these data suggest that inhalant allergy may be a disease-modifying factor in CRSwNP. Food. Collins and colleagues found that CRSwNP patients exhibited positive intradermal testing to wheat, tomato, and potato, but not to inhalants. 1395 Another prospective study demonstrated nearly 8 fold higher inci dence of food allergy among polyp patients when com pared with healthy controls. 1396 Lill et al. found a strong association between CRSwNP and milk allergy, 1397 though neither wheat nor overall incidence of food sensitiv ity differed between diseased and healthy populations. Other studies comparing systemic IgE for food sensitiv ity between CRSsNP and CRSwNP demonstrated no such relationship, 1398 with Al-Quodah finding, “no significant differences in the prevalence, type, number of positive food allergens and class level between the 2 groups.” 1399 These studies present conflicting evidence for the role of food allergy in the pathogenesis of CRSwNP disease (Table X-5). In conclusion, despite an overlap of immunologic path ways and of symptoms, conflicting data in the litera ture prevents definitive conclusion about the association between atopy and nasal polyposis. Therefore, allergy can be considered a disease-modifying factor in CRSwNP. As the understanding of CRS and atopy evolve, further study will shed additional light on this relationship.

Inhalant Allergy as a Contributing Factor for CRSwNP Aggregate Grade of Evidence: C (Level 3: 7 studies; level 4: 8 studies; level 5: 1 study; Table X-4).

X.C.2.1 Central Compartment Atopic Disease Central compartment atopic disease (CCAD) was not included in ICAR-RS-2016, as this entity had not yet been described. In 2014, White et al. published a case series of patients with middle turbinate (MT) polyps or poly poid edema. 1 In this series 16/16 patients who underwent allergy testing demonstrated sensitivity to at least 1 aller gen on testing; this was the first report of an association between allergy and MT polyps/edema. Evidence support ing the strength of this association followed in 2017 in a cross-sectional study by Hamizan et al., which graded the degree of MT edema (normal-focal-multifocal-diffuse polypoid edema) and compared these findings with allergy testing results in 187 patients determining positive pre dictive value (PPV). This study reported that multifocal