Objective As our understanding of autoimmune laryngeal stenosis evolves, distinguishing patients who may benefit from systemic immunosuppression versus those needing only local treatment is increasingly important. In this study, we identify a distinct subset of autoimmune laryngeal stenosis characterized by edema of the inferior true vocal folds that extends to the superior aspect of the cricoid cartilage, termed “subcordal stenosis.” The objective of this study is to characterize the clinical presentation and treatment outcomes of subcordal stenosis and compare it to typical autoimmune-related subglottic stenosis (AI-SGS).

Methods We conducted a retrospective review of patients with laryngeal stenosis evaluated by both rheumatology and otolaryngology at our institution to identify two groups: patients with subcordal stenosis and those with typical AI-SGS. Data on immunosuppressive treatments and airway dilation procedures were collected. Time to first dilation was compared between groups.

Results Among 49 patients with laryngeal stenosis, 11 had subcordal involvement. Five of these also had subglottic disease, while six had isolated subcordal stenosis. Kaplan-Meier analysis showed significantly longer time to first dilation in patients with subcordal involvement (median 792 vs. 44 days; p = 0.048). They also underwent fewer dilations within two years (median 0 vs. 1; p = 0.05).

Conclusion Among laryngeal stenosis patients referred to rheumatology, those with subcordal involvement experienced fewer dilations and longer intervals before first dilation compared to those with typical AI-SGS. These findings suggest that subcordal stenosis may represent a distinct, glucocorticoid-responsive phenotype within autoimmune laryngeal stenosis, with implications for treatment selection and multidisciplinary care.

The authors have declared no competing interest.

This work is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under award numbers 2T32AR048522-21, P30 AR070254 and K24 AR080217, and the National Institute on Deafness and Other Communication Disorders of the National Institutes of Health under award number 1R01DC018567. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. This work is also supported by the Jerome L. Greene Foundation and the Donald B. and Dorothy L. Stabler Endowed Fellowship.

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Ethics committee/IRB of Johns Hopkins Medical Institutions gave ethical approval for this work.

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Funding: This work is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under award numbers 2T32AR048522-21, P30 AR070254 and K24 AR080217, and the National Institute on Deafness and Other Communication Disorders of the National Institutes of Health under award number 1R01DC018567. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. This work is also supported by the Jerome L. Greene Foundation and the Donald B. and Dorothy L. Stabler Endowed Fellowship.

We have no conflicts of interest.

All data produced in the present study are available upon reasonable request to the authors