A 76-year-old man was admitted to our hospital because of one-month history of dyspnoea on exertion, cough, and viscous sputum. He has been diagnosed with asthma since he was 62 years, and has been partially controlled (score 20 in Asthma Control Test) with inhaled corticosteroids/long-acting β2 agonist (ICS/LABA). When he was 75 years old, he noticed lymphadenopathy, and was diagnosed with follicular lymphoma. He received six courses of rituximab combined with pirarubicin-cyclophosphamide, vincristine and prednisolone (R-THP-COP) therapy, and a complete remission was achieved. After the chemotherapy, he noticed shortness of breath, cough, and viscous sputum. As chest computed tomography (CT) revealed diffuse granular shadows in bilateral lungs, he was referred to our hospital. He had a surgical history of chronic sinusitis at 28 years of age, and had a 30-pack-year history of smoking until the age of 62. Physical examination revealed hypoxia, peripheral capillary oxygen saturation (SpO2) 92% with a low-grade fever. Auscultation of the lungs showed coarse crackles and wheezes in both lung fields. On laboratory findings, white blood cell counts increased to 8670/μL with neutrophilia (72.6%). C-reactive protein level was 7.82 mg/mL. Pseudomonas aeruginosa was detected in sputum culture. The level of total immunoglobulin E was 288 IU/mL, and a titre of cold agglutinin was >64. Fibre-optic bronchoscopy was performed to evaluate the shadows; the cellularity of bronchoalveolar lavage fluid (BALF) was increased to 1.91 × 105/mL with increased proportion of both neutrophils (86.4%) and eosinophils (8.2%). Transbronchial lung biopsy revealed mild infiltration of lymphocytes, plasma cells, and foamy macrophages around the respiratory bronchioles, which was compatible with DPB, and goblet cell hyperplasia with thickness of basement membrane, which was compatible with asthma (Fig. ). As he fulfilled the diagnostic criteria for DPB, we started low-dose macrolide therapy. After erythromycin (400 mg/day) was added to ICS/LABA, his symptoms reduced, along with the improvements in pulmonary function, diffuse granular shadows, and airway clearance determined by saccharin test (Table ). Conversely, the level of fractional exhaled nitric oxide (FeNO), a biomarker of eosinophilic airway inflammation, increased 2 weeks after the macrolide therapy. The level of FeNO then gradually decreased (Table ).
A 25-year old male with uncontrolled asthma. Initial FEV1 was 2.51 L (62.6%) and severe sputum eosinophilia. His CT scan shows diffuse bronchitis with tree bud sign and then treated with clarithromycin for 9 months. FEV1was improved from 62.6% to 88.4%. He reduced daily amount of inhaled corticosteroid.