DISCUSSION
Subglottic stenosis is diagnosed after careful clinical and laboratory examination. The respiratory symptoms are nonspecific and present late in disease progression, necessitating a high clinical suspicion level [5]. In a retrospective study by Dion et al., out of 32 patients, 3 had autoimmune subglottic stenosis due to RA as the etiology. Other autoimmune etiologies were systemic lupus erythematosus and granulomatosis with polyangiitis, to name a few [6]. Consistent with our findings, subglottic stenosis appears to be associated with an underlying autoimmune etiology.
Treatment modalities have evolved from open surgical procedures to endoscopic dilation, laser surgery, and adjuvant intralesional steroid injections [7,8]. Interval dilation is the mainstay of treatment for idiopathic subglottic stenosis. In a study conducted by Menapace et al., they concluded that open surgery should only be reserved for refractory cases of subglottic stenosis, which had postoperative adverse effects such as a change in voice quality [9]. Recurrence was common in their study, highlighting the need for continued long-term follow-up in such patients, and our patient was scheduled for semi-annual follow-up. Generally, treatments are tailored to the severity and recurrence of a patient’s breathing and, possibly, voice dysfunction. Patients with autoimmune subglottic stenosis and severe intraluminal narrowing may require tracheostomy as a treatment modality [10]. In our patient, neither open surgery nor tracheostomy was needed, and was managed with a combination of endoscopic and medical therapy. There are controversial opinions on the use of immunotherapy for managing subglottic stenosis, and methotrexate has shown a prolonged interval before the requirement of another interval dilation session in patients [11]. Leflunomides can also be used for this purpose [11].
According to some reports, IBD may also be related to subglottic stenosis, which is also linked to lupus erythematosus, amyloidosis, Wegener granulomatosis, and tuberculosis [11]. Considering the suspected peripheral spondyloarthropathy and inflammatory bowel disease in the patient, there were questionable underlying autoimmune processes. The ESSG and Amor criteria, which were created for the complete SpA group, including peripheral SpA, were compared with ASAS criteria, which were devised for individuals with SpA with prominent peripheral signs after the development of the ASAS criteria for axial SpA [12].
The patient was initially diagnosed as having idiopathic subglottic stenosis. However, later assessments revealed peripheral joint involvement of the shoulders, knees, and first metatarsophalangeal joint, and a PET scan demonstrated diffuse uptake (including dens). These findings supported the diagnosis of spondyloarthropathy, and the patient was diagnosed with a subglottic stenosis accompanied by an underlying systemic disorder. For this variant, TNF-α inhibitors were efficacious, and the patient was prescribed and responded well.
Our case highlights the occurrence, effective management, and natural progression of subglottic stenosis in a patient with spondyloarthropathy. Given her son’s history of inflammatory bowel disease (IBD) and peripheral spondyloarthropathy, screening for IBD using colonoscopy to rule out occult illnesses is crucial.
Owing to the risk of sudden airway compromise possible with subglottic stenosis, our case highlights the importance of physicians being aware of this rare complication for quick diagnosis and effective management. However, a dual management strategy, involving medical therapy and endoscopic intervention, is generally sufficient. Long-term follow-up should be scheduled with the patient to reassess their status periodically.