In Response to <i>Impact of Obesity on the Structured Histopathology of Chronic Rhinosinusitis Patients</i>

We thank Dr. An and Dr. Li for their attention to our work and thank the editors for the opportunity to respond. The first concern discussed demographic collection timing. Demographics, including BMI, were collected concurrently with structured histopathology data from the electronic medical record. Thus, demographics reflect patient's status at the time of or shortly after surgery. Although CRS is associated with increased BMI, there is no evidence CRS is associated with increased BMI fluctuation versus the general population as suggested. The average BMI fluctuation over the letter's suggested 3-month window is 0.025–0.05 kg/m2 [1], thus significant fluctuation is unlikely. Given our study's large sample size, the largest to date on this topic, it is unlikely outliers significantly impact our results. The second concern discusses sampling sites of sinonasal tissue specimens. Given the wide range of anatomic subsites of CRS within our cohort, we analyzed tissues from all sinuses. This is a study limitation and future work could analyze histopathology based on anatomic location. The Busaba et al. [2] study cited by letter writers supports a strong correlation between inflammatory grade in the ethmoid and ipsilateral middle turbinate and demonstrates strong correlation between total and specific inflammatory cells across the two sites. Although lymphocyte and eosinophil counts differ, overall inflammatory predominance is unchanged. Thus, the core inflammatory pathways driving disease are likely unchanged, the focal point of our manuscript. Additionally, apart from three non-significant histopathologic markers, histopathology was analyzed binomially as present or absent. This means variability in lymphocyte or eosinophil counts or sinus specific histopathological marker quantity should not affect analysis. The third concern discusses corticosteroid use. We state FESS was pursued after failure of maximal medical therapy. Per American Academy of Otolaryngology guidelines, medical therapy for CRSwNP includes oral corticosteroids, while CRSsNP does not [3]. Because polyp status predicts oral steroid use, we can extrapolate from analysis comparing polyp status and obesity class. No relationship was found, suggesting obese patients did not receive more oral corticosteroids that non obese patients. Lack of detailed pre-op steroid use is a study limitation. Other comments mention the use of corticosteroids for comorbid asthma. As stated in our manuscript, we used multinomial regression analysis to correct for asthma status, given its association with obesity. Results remained significant. Additionally, we discuss multiple studies demonstrating asthma in obese patients is mediated by a neutrophil dominant non-type 2 inflammatory pathway, despite oral corticosteroid use. The authors have nothing to report. The authors have nothing to report. The authors declare no conflicts of interest.