Case Report Endoscopic Management of Severe Subglottic Stenosis in Wegener’s Granulomatosis I. Stappaerts 1 , C. Van Laer 2 , K. Deschepper 3 , P. Van de Heyning 2 and P. Vermeire 1 1 Department of Respiratory Medicine, 2 Department of Oto-Rhino-Laryngology, University Hospital Antwerp, Edegem; 3 Department of Respiratory Medicine, Maria Middelares Hospital, St-Niklaas, Belgium Abstract: The optimal treatment for severe subglottic stenosis secondary to Wegener’s granulomatosis remains controversial. We report the case of a symptomatic middle-aged woman who was successfully treated with intratracheal dilation and intralesional injection of corticosteroids. The literature related to this issue is being reviewed. Keywords: Intratracheal dilation-injection therapy; Subglottic stenosis; Wegener’s granulomatosis Introduction Subglottic stenosis (SGS) arises in approximately 16% of patients suffering from active Wegener’s granuloma- tosis (WG). Although it represents a life-threatening complication, the gold standard for treatment remains controversial. The therapeutic arsenal consists of urgent tracheostomy, resection of the stenotic segment followed by reconstruction, increasing immunosuppression and endoscopic dilation. The case of a patient successfully managed by endoscopic dilation and glucocorticoid injection is here described. Case Report A 58-year-old white woman was referred to the Department of Respiratory Medicine of our hospital for further investigation and management of progressive exertional dyspnoea and stridor. Four years earlier she had suffered from a broad QRS tachycardia. At that time the diagnosis of idiopathic myocarditis was made and a pacemaker had to be implanted. Two years before referral, a dermatologist treated the patient with antibiotics and corticosteroids for a biopsy-proven vasculitis of the lower limbs. No further diagnostic work-up was performed. Six months prior to referral she consulted a pulmonologist because of progressive dyspnoea and abnormal fatigue. Bilateral pulmonary nodules, some of them cavitating, were seen on chest X- ray. CT scan demonstrated discrete mucosal thickening in the frontal, left maxillary and left sphenoidal sinuses. Ear–nose–throat examination and pulmonary function tests (PFTs) were normal. Her medical history and the radiological abnormalities caused a strong suspicion for WG. Antineutrophil cytoplasmic antibodies (c-ANCA) proved to be positive with indirect immunofluorescent antibody testing (IIF) in a titre of 1/320. Enzyme-linked immunosorbent assay identified the antibodies as antiproteinase 3. Urine analysis was normal. No further attempts were made to obtain a histological diagnosis and a treatment with 64 mg methylprednisolone was started. Over the following months her clinical condition improved, the pulmonary nodules disappeared and the ANCAs became negative. Six months after the diagnosis of WG was made, the patient again started to complain of dyspnoea and, for the first time, of stridorous breath sounds. Laboratory analysis, including c-ANCAs, remained negative. No relapse of the pulmonary lesions could be detected. However, PFTs now clearly demonstrated an obstructive ventilatory pattern with a 1-second forced expiratory volume (FEV 1 ) of 1.61 (66% pred.) and a vital capacity Clin Rheumatol (2000) 19:315–317 ß 2000 Clinical Rheumatology Clinical Rheumatology Correspondence and offprint requests to: Dr Inge Stappaerts, Respiratory Medicine, Kerkelei 32, 2610 Antwerp, Belgium. Tel: 0032-3-8213537; Fax: 0032-3-8214447; e-mail: inge.stappaerts @uza.uia.ac.be