INTRODUCTION: Steroid-unresponsive asthma has an interesting differential diagnosis. Correct diagnosis requires integration of history and physical exam with pulmonary physiology, selective testing, and imaging.
CASE PRESENTATION: A 41 year-old female presented to asthma clinic with worsening wheezing over the past six months. The patient had a history of mild intermittent asthma diagnosed twelve years prior, after the birth of her second child, managed with bronchodilators and montelukast. She had no prior asthma hospitalizations or intubations. Her worsening asthma symptoms coincided with a new job as a patient care representative. She noted no occupational exposures. She had daily symptoms at rest, with exertion, and during sleep. Triggers included cold air, humidity, emotion, and aerosols. Her peak flows at home were 150–200 L/min. She had tried salmeterol/fluticasone, esomeprazole, and short prednisone courses that only temporarily relieved symptoms. Two weeks prior she went to the emergency room, had a clear chest radiograph and was sent home on prednisone 50mg daily for five days and referred to asthma clinic.Her current regimen was montelukast, esomeprazole, salmeterol/fluticasone 50/250, and albuterol 4–5 times daily. She was born in the United States and was married with three children. She had a ten pack-year history of tobacco abuse, quit 8 months ago, but her husband still smoked. She had wood floors, and had not recently moved. She had hamsters, three parakeets, a dog, lizard, and fish. She had no aspirin sensitivity or nasal polyps. On physical examination she appeared well and was in no respiratory distress. Her vital signs were stable and she had a peak flow of 150 L/min. She had a clear oropharynx, normal nasal mucosa, and no sinus tenderness. She had a prolonged expiratory phase with quiet breathing and expiratory wheezing diffusely on forced exhalation. Her cardiac, abdominal and extremity exams were normal. She was treated with an increased fluticasone dosage, a two-week prednisone taper and discharged home with further outpatient testing and follow-up planned. Subsequent laboratory testing demonstrated a normal eosinophil count and IgE level, and reaction to dust mites, cat, dog, and cockroach on radioallergosorbent testing. Her pulmonary function testing suggested a variable intrathoracic airway obstruction. On return visit, she reported worsening dyspnea and was noted to have a barking cough. CT scan demonstrated a 7×12mm soft tissue opacity in the trachea. Flexible bronchoscopy identified a tracheal mass arising from the membranous wall. This was resected using a combination of rigid and flexible bronchoscopy along with argon plasma coagulation and electrocautery. Final pathology was a glomangioma.
DISCUSSIONS: The differential diagnosis of steroid-unresponsive asthma includes allergic bronchopulmonary aspergillosis, drug-induced asthma, hypersensitivity pneumonitis, heart failure, and airway obstruction –whether via intraluminal mass or extrinsic compression, benign or malignant. In this case, pulmonary function testing suggested an intrathoracic obstruction, which was then demonstrated on chest imaging. Glomus tumors were originally described in 1924 by Masson. They are believed to arise from stem cells differentiating into a cell resembling the smooth muscle of the glomus body –an arteriovenous anastomosis that regulates vascular flow via temperature sensation. They are differentiated based on electron microscopy and immunohistochemical staining. There are three subtypes: 75% of cases are the classic glomus tumors, 20% glomangioma, and 5% percent glomangiomyomas. They are most often benign, but malignant forms have been described.
CONCLUSION: Thorough evaluation and close follow-up are most important in patients with steroid-unresponsive asthma. Consideration of alternative diagnoses is warranted when patients fail to respond in a typical manner. Large airway obstruction may mimic steroid unresponsive asthma. Although uncommon, the glomus tumor must be considered in the differential diagnosis for airway obstruction.
DISCLOSURE: Eric Bonura, No Financial Disclosure Information; No Product/Research Disclosure Information