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-yr-old man had a 5-yr history of cough and dyspnea on 28th March 2007. Initial FEV1 was 2.51 L (62.6%), FVC was 3.65 L (77.8%), and FEV1/FVC was 68.8%. BD response was negative. The results of a MBPT were positive (PC20 4.36 mg/mL). A CXR showed miliary nodules in both lungs, but he didn't have sinusitis. A chest CT showed bronchiolectasis and centrilobular nodules on both lungs (). Induced sputum showed severe eosinophilia (42%). The AFB studies were negative. He took inhaled fluticasone combined with salmeterol, montelukast, and theophylline, and he intermittently used 30 mg of prednisolone (PL) for asthma attacks. After the patient took clarithromycin 250 mg twice a day for 9 months, his FEV1 improved from 62.6% to 88.4%, and he could reduce the amount of PL. Before the patient had started taking clarithromycin, he had taken 720 mg of PL per year. After he treated with clarithromycin, he was able to reduce use of oral steroids by about 80%, such that he took 150 mg per year.