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Σάββατο 8 Ιουνίου 2019

The impact of race and insurance status on baseline histopathology profile in patients with chronic rhinosinusitis
Hannah N. Kuhar BA  Ashwin Ganti BA  Michael Eggerstedt MD  Mahboobeh Mahdavinia MD, PhD Paolo Gattuso MD  Ritu Ghai MD  Pete S. Batra MD, FACS  Bobby A. Tajudeen MD
First published: 12 February 2019 https://doi.org/10.1002/alr.22295
Funding sources for the study: Cohn scholarship program from Rush University (to M.M.); Medtronic (research grant to P.S.B.).
Potential conflicts of interest: P.S.B.: Optinose and Sanofi Regeneron (advisory board), and Springer (royalties).
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Abstract
Background
Chronic rhinosinusitis (CRS) is an inflammatory disease process characterized by different phenotypes and histopathology profiles. Race and access to care have been implicated in CRS disease severity. Structural histopathology reporting may aid in delineating the inflammatory burden responsible for this effect.

Methods
A structured histopathology report of 14 variables was utilized to assess sinus tissue removed during functional endoscopic sinus surgery (FESS). Histopathology variables and 22‐item Sino‐Nasal Outcome Test (SNOT‐22) scores were compared by race (Black, White, Latino, and Asian) and insurance status (Medicare, Medicaid, and private insurance).

Results
A total of 201 CRS patients (124 White, 38 Black, 28 Latino, and 9 Asian) undergoing FESS were included. Black patients demonstrated increased SNOT‐22 scores (50.74 ± 20.32 vs 41.47 ± 22.75, p < 0.022) and number of eosinophils per high‐power field (>5/HPF) (60.5% vs 44.8%, p < 0.05). White patients demonstrated decreased eosinophil aggregates (22.6% vs 35.1%, p < 0.039) and eosinophils/HPF (<5/HPF) (42.7% vs 55.8%, p < 0.048). Medicaid patients showed increased SNOT‐22 score (55.50 ± 24.46 vs 41.39 ± 21.74, p < 0.003), polypoid disease (61.5% vs 42.3%, p < 0.05), subepithelial edema (80.8% vs 53.1%, p < 0.006), hyperplastic/papillary changes (23.1% vs 8.0%, p < 0.028), fibrosis (61.5% vs 38.5%, p < 0.036), eosinophil aggregates (46.2% vs 24.6%, p < 0.022), and eosinophils/HPF (>5/HPF) (65.4% vs 45.1%, p < 0.043). When controlling for insurance status, Black race was no longer associated with increased SNOT‐22 (p < 0.104) or eosinophils/HPF (>5/HPF) (p < 0.183).

Conclusion
Black and Medicaid patients demonstrated more severe disease by histopathology and SNOT‐22 scores. These findings were no longer significant among Black patients after adjusting for insurance status, suggesting that the prevailing factor influencing worse disease may be access to care.

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