Introduction
Proximal oesophageal strictures are less common than distal oesophageal strictures, but can share an aetiology such as eosinophilic or peptic. However, often proximal oesophageal strictures have an unclear aetiology. This results in symptomatic treatment with dilatation, without treatment of the underlying causative factor to prevent further stricture formation. We hypothesised that most proximal oesophageal strictures without a clear aetiology may be secondary to Candida oesophagitis.
Aims & Methods
The aim was to determine the cause of proximal oesophageal strictures of unclear aetiology, and examine the outcomes of medical and endoscopic treatment. Retrospective analysis was performed to identify all cases of proximal oesophageal stricture (≤30cm from incisors) without clear aetiology at Guy’s and St. Thomas’ Trust from 2007 to 2024. Procedures were extracted from the electronic endoscopy database using the keyword ‘dilat’. Patients with Barrett’s oesophagus, Schatzki ring, eosinophilic oesophagitis, anastomotic stricture, radiofrequency ablation, peptic stricture, oesophagectomy, chemo/radiotherapy, Crohn’s disease, achalasia or caustic ingestion were excluded. Oesophageal histopathology taken at any point was assessed for candidiasis. Data collected included demographics, clinical presentation, endoscopic findings, histopathology results, medical and endoscopic treatment and outcomes.
Results
Between 2007 and 2024, 19 patients were identified with a proximal oesophageal stricture without an alternative aetiology. All patients had Candida oesophagitis at either at presentation with the stricture or predating it. The mean age at presentation was 57 years (range 40-80, 95% CI ±5.7) and 78.9% of patients were male. Eight patients (42.1%) were immunocompetent and not prescribed immunosuppressant drugs e.g. corticosteroids.
All strictures were between 15 and 30cm from the incisors (median 24cm). Only two strictures were passable with a standard endoscope, and thus were not dilated. Histopathology of the strictures confirmed no eosinophilia. The most common finding on histopathology was lymphocytic inflammation. On average, each patient had 2 balloon dilatations performed (range 0-12). Following treatment with antifungals and dilatation, 53.3% of patients had resolution of the stricture, 31.3% had ongoing Candida plus a stricture, 13.3% had a stricture without Candida present. Patients with failure of anti-fungal therapy to treat Candida had an increased number of dilatations required.
| Age (average) | 58.7 |
| Male | 78.9% (n=15) |
Immunosuppressive Conditions
- Asthma/COPD
- Diabetes
- Chronic Mucocutaneous Candidiasis
|
15.7% (n=3)
26.3% (n=5)
10.5% (n=2) |
Histopathology findings
- Lymphocytosis
- Microabscesses
|
63.2% (n=12)
10.5% (n=2) |
| Received anti-fungal therapy | 94.7% (n=18) |
| Dilatation performed | 84.2% (n=16) |
| Median number of dilatations required | 2 |
Table 1. Patient demographics and results
Conclusion
In conclusion, this case series of 19 patients shows that proximal oesophageal strictures due to Candida are more common than previously thought. At our centre, all patients with a proximal stricture of unknown cause had oesophageal candidiasis. Where a clear alternative cause has not been identified, Candida should be considered, even in patients who are immunocompetent. Anti-fungal therapy is essential to remove the underlying causative factor, and approximately half of patients will have resolution of their stricture following dilatation once Candida has been treated. Patients who did not have resolution of Candida with antifungals were more likely to require a higher number of dilatations.
