Successful Avoidance of Cicatricial Tracheobronchial Stenosis in a Patient With Endobronchial Tuberculosis by Early Administration of Systemic High-Dose Corticosteroids: A Case Report.

A 63-year-old Japanese woman was referred to our hospital due to dry cough, fever, hoarseness, stridor, and difficulty breathing. Chest computed tomography showed circumferential wall thickening in the trachea, carina, right main bronchus, and right upper lobe bronchus, and granular and nodular shadows in right S2. Flexible laryngofiberscopy showed yellowish dry respiratory secretions adhering to the subglottis. Bronchoscopic findings showed that the tracheobronchial mucosa was swollen, hyperemic, and covered with yellowish-white, cheese-like materials, and ulcerative lesions with white coatings were observed from the subglottis to the trachea, carina, right main bronchus, and right upper lobe bronchus. A diagnosis of endobronchial tuberculosis (EBTB) was confirmed by polymerase chain reaction testing, and cultures were positive for Mycobacterium tuberculosis. In addition to anti-tuberculosis chemotherapy, intravenous high-dose methylprednisolone reduced her severe respiratory symptoms and prevented cicatricial tracheobronchial stenosis. Early administration of systemic high-dose corticosteroids may be effective for EBTB patients with severely active tracheobronchial mucosal and submucosal lesions.

Atezolizumab-Induced Lambert-Eaton Myasthenic Syndrome in a Patient With Small-Cell Lung Cancer.

The case of a 70-year-old man who developed Lambert-Eaton myasthenic syndrome (LEMS) while receiving atezolizumab treatment for extensive-stage small-cell lung cancer (SCLC) is presented. He started receiving maintenance immunotherapy with atezolizumab following four cycles of combination therapy with atezolizumab, carboplatin, and etoposide. After five cycles of maintenance atezolizumab therapy, he complained of muscle weakness in the lower limbs and fatigue. Electromyographic findings and positive results for anti-P/Q-type voltage-gated calcium channel antibody made a diagnosis of LEMS. Based on the onset time of LEMS and the state of his underlying cancer at the time of the appearance of neurological symptoms, he was diagnosed with LEMS as an immune-related adverse event (irAE) induced by atezolizumab. After discontinuing atezolizumab treatment and initiating combination therapy with steroid pulse plus intravenous immunoglobulin, his neurological symptoms improved. Although 18 months have passed since the discontinuation of atezolizumab treatment, there has been neither recurrence of neurological symptoms nor a progression of his cancer without salvage chemotherapy. This is a rare case of LEMS as a neurological irAE induced by atezolizumab. Clinicians must be aware of the potential for LEMS to develop in SCLC patients taking atezolizumab treatment.