| Literature DB >> 31296254 |
Jessica W Grayson1, Marina Cavada2,3, Richard J Harvey2,3.
Abstract
Following publication of the original article [1], the authors reported an error in Table 1. In the second columns of the 'Radiology' row, 'Normal anterolateral sinus mucosa' should read 'Normal superolateral sinus mucosa'. A corrected version of Table 1 is included in this Correction.Entities:
Year: 2019 PMID: 31296254 PMCID: PMC6625072 DOI: 10.1186/s40463-019-0355-6
Source DB: PubMed Journal: J Otolaryngol Head Neck Surg ISSN: 1916-0208
Summary of Key Findings of CRS Phenotypes
| Phenotype | |||
|---|---|---|---|
| Characteristics | CCAD (IgE mediated) | eCRS (AERD) | Non-eCRS |
| Clinical Presentation | - Young onset (teens to 20s) - Rhinitis symptoms - Smell preserved - Other atopic disease: ° Childhood asthma ° conjunctival symptoms, dermatitis | - Mid-Life “adult” onset (30–50 yo) - Occasionally post respiratory virus - “Completely well” prior to onset or if allergic, then symptoms limited to childhood - Smell loss (corticosteroid responsive) - Antibiotic seeking - Food and alcohol induced flares - Adult onset asthma linked temporally to CRS onset. | - Older onset 50 yrs.+ - Female, obese - Cough - Poor corticosteroid response - “Asthma” present but often poor response to inhaled preventive therapy (corticosteroid based) |
| Endoscopy | - Middle turbinate edema - Polypoid changes from turbinates and septum - No thick mucin - Normal sinus mucosa on surgery | - Polyps (small, multiple, large) from the middle meatus - Thick eosinophilic mucin - Secondary purulence | - Polyps or polypoid edema - Purulent secretions - Lack of eosinophilic mucin |
| Radiology | - Central thickening of septum and turbinates, peripheral clearing (CCAD) - Mucus trapping only in sinsues - Normal superolateral sinus mucosa (“black halo”) | - Pan-sinusitis (Lund-Mackay 24) - Neo-osteogenesis | - Pan-sinusitis (undistinguishable from eCRS) |
| Histopathology | - Elevated tissue eosinophilia - Often without activation (no eosinophil aggregates and charcot-leyden crystals) - No serum eosinophils - Elevated total and specific IgE | - Elevated tissue eosinophilia (>10eos/hpf, but often >100eos/hpf) - Evidence of eosinophil activation (eosinophil aggregates and charcot-leyden crystals) - Serum eosinophilia | - Lack of tissue eosinophilia (< 10/HPF) |
| Allergy | - + allergy testing (dustmite/perennial allergens) - Often monoallergen-sensitized | - Either negative IgE sensitization or multi-allergen sensitized | - Negative skin prick, immunocap/RAST |
| Treatment | - Allergen directed immunotherapy - Endoscopic sinus surgery - Topical corticosteroid (spray or irrigation) | - Systemic corticosteroid treatment (up to 2–3 times per year) if limited burden of disease - Endoscopic sinus surgery (Draf 3) - Topical corticosteroid irrigations (not sprays) For AERD: - Zileuton, Montelukast, Zafirlukast - Can take selective COX-2 inhibitors (Meloxicam) | - Saline or corticosteroid irrigations - Endoscopic sinus surgery - Macrolide therapy (Clarithromycin 250 mg daily for 3 months) - Continue 3/week until 12 months if responder |
| Difficult to control disease | - Omaluzimab (anti-IgE) | - Mepoluzimab (anti-IL5) - Other immune-modulating therapy (Benraluzimab, Dupiliumab, Reslizumab, etc) For AERD: - ASA desensitization (1300 mg commencement and 350–700 mg daily maintenance) | - Consider re-biopsy of a patient post-surgery and post-corticosteroid based treatment if not responding and may be re-classified under this phenotype |