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 71-yr-old woman referred for a 10-yr history of cough, dyspnea, sputum, post-nasal drip on 4th June 2010. Her breathing sound was clear. A chest x-ray (CXR) showed increased bronchovascular markings in the both lower lungs and consolidation in the left lower lung field (LLLF) (). Initial forced expiratory volume in 1 second (FEV1) was 1.21 L (64.9%) and forced vital capacity (FVC) was 1.70 L (75.5%) and FEV1/FVC was 71.1% without a bronchodilator (BD) response. The methacholine bronchial provocation test (MBPT) was positive as a result of provocative concentration (PC20) was 3.8 mg/mL. Induced sputum showed mild eosinophilia (3%). During one month of asthma treatment with inhaled budesonide combined with formoterol, theophylline, and montelukast, she complained of mild fever and yellowish sputum. Thus, we performed a chest CT and water's view x-ray. Bilateral maxillary sinusitis was observed (). CT showed bronchial wall thickening with centrilobular nodules, which was suggestive of DPB (). To differentiate from mycobacterial infection (), acid fast bacilli (AFB) studies were done and showed negative. The patient took clarithromycin 250 mg twice a day for 9 months, after which her FEV1 improved from 64.9% to 84.2%, FVC and FEV1/FVC also improved. A follow-up examination, LLLF consolidation and sputum eosinophilia disappeared. In addition, she was able to reduce the daily amount of inhaled steroid and discontinue theophylline.