Chronic rhinosinusitis in the setting of other chronic inflammatory diseases

Abstract

Objectives The objectives of the study were to determine the prevalence of chronic rhinosinusitis (CRS) overall and its 2 phenotypic variants, CRS with and without polyposis (NP), in patients with chronic inflammatory comorbidities including autoimmune disorders, inflammatory bowel disease, and atopic dermatitis. These findings were compared with data in patients with asthma. Patients with hypertension were also used as a reference group to estimate the incidence of CRS in a group with regular medical follow-up. Study design A retrospective, cross-sectional query of a large tertiary care electronic medical record database was performed. Results Electronic medical record database prevalence of CRS in patients with hypertension was 4.4%. The prevalence of CRS was 18% in asthma (P < .0001), 7% in atopic dermatitis, 3.5% in inflammatory bowel disease, and ranged from 1.4% to 5.9% in autoimmune disorders. The frequency of CRS patients exhibiting the NP phenotype was similarly low in patients with autoimmune disease and hypertension, but was significantly greater in patients with asthma (P < .0001), inflammatory bowel disease (P = .033), and atopic dermatitis (P = .049), Conclusions These findings suggest similar prevalence of overall CRS in patients with autoimmune disease and inflammatory bowel disease, and background rates as estimated by observations in hypertension patients. Inflammatory bowel disease and atopic dermatitis patients with CRS exhibit some skewing toward the NP phenotype, as do asthmatics, where this association is well known.

Impact of omalizumab therapy on medication requirements for chronic rhinosinusitis

“…Although this is less than other published series, 6 it is consistent with another report of 2063 asthmatics with CRS, where 22% had polyp-forming disease. 16 The present series, although small, is therefore reflective of typical patients with combined upper and lower airway inflammatory disease. It should also be noted that the retrospective nature of this study introduced some limitations related to strict determination of whether steroids were prescribed for exacerbations of CRS, asthma, or both.…”

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

“…490 Similar concepts have been proposed with regard to asthma pathogenesis 535 and although the association of asthma and CRS is well established, the prevalence of other chronic inflammatory disorders within the CRS population is close to background. 288,556 These observations suggest that host defects in CRS will be centered in the airway mucosa, giving rise to the "immune barrier hypothesis," which proposes that genetic and epigenetic variation in the coordinated mechanical barrier and/or the innate immune response of the sinonasal epithelium manifests as CRS. 530 Diminished innate host defense coupled with a porous barrier should theoretically lead to altered microbial colonization, accentuated barrier damage, and a compensatory adaptive immune response.…”

The Etiology and Pathogenesis of Chronic Rhinosinusitis: a Review of Current Hypotheses

“…It remains unclear whether any barrier defects are due to primary genetic variation in the host, epigenetic changes induced by environmental insults, or both. It should be kept in mind, however, that epidemiological studies indicate, for the most part, that CRS patients exhibit chronic inflammation in the nose, sinuses, and often the lower respiratory tract [108, 109]. This makes it more likely that the host genes mediating CRS pathogenesis will primarily be those that govern the immunobiology of the respiratory mucosa, as opposed to the systemic immune response.…”