A 60-year-old man who never smoker was a professor of humanities and had no experiences of exposure to noxious materials. He has not traveled or moved anywhere in recent years. He had been diagnosed with acute hypersensitivity pneumonitis 18 months previously and was treated with a steroid therapy for 6 weeks. Cause of hypersensitivity pneumonitis had been confirmed as being fungus derived from old wallpapers at the time. After the cause removed, it had not recurred over 2 years. He had also been administered metformin 500 mg daily for 16 months for diabetes mellitus. For a transient ischemic attack secondary to vertebral artery stenosis, he was hospitalized and started on acetyl-L-carnitine, cilostazol, and rosuvastatin according to the following schedule: acetyl-L-carnitine, 500 mg, once daily for 48 days prior to this hospitalization; cilostazol, 100 mg, twice daily; and rosuvastatin, 5 mg, once daily for 27 days prior to this hospitalization. While continuing those medications, he developed a fever and cough 3 days prior to this hospital visit. Although he was prescribed an antibiotic (Augmentin) for 3 days at a local clinic, his dyspnea, cough, and fever gradually increased. He was referred to our hospital for proper evaluation and management. He had no known drug allergies.
Upon admission, the patient's vital signs were as follows: blood pressure, 116/77 mm Hg; pulse, 114 beats per minute; respiratory rate, 26 breaths per minute; and body temperature, 36.9℃. On physical examination, a coarse breath sound with fine crackles but without wheezing was heard upon auscultation of both lungs. The patient's laboratory test results were as follows: hemoglobin, 14.1 g/dL; white blood cell count, 8,770 cells/µL (neutrophils, 62.6%; lymphocytes, 26.0%; monocytes, 7.2%; eosinophils, 3.9%; and basophils, 0.3%); and platelet count, 391,000 cells/µL. The patient's serum biochemistry test results revealed the following: aspartate aminotransferase, 35 IU/L; alanine aminotransferase, 35 IU/L; total bilirubin, 0.4 mg/dL; alkaline phosphatase, 311 IU/L; total protein, 7.6 g/dL; albumin, 4.0 g/dL; blood urea nitrogen, 26.0 mg/dL; creatinine, 0.84 mg/dL; total cholesterol, 106 mg/dL; C-reactive protein, 1.06 mg/dL; and LDL cholesterol, 56 mg/dL. His coagulation profile was within normal limits. A urinalysis with microscopy was clear. An arterial blood gas analysis of the fraction of inspired oxygen (FiO
2) was conducted with the patient breathing room air and revealed the following: pH, 7.46; partial pressure of oxygen (PaO
2), 54.6 mm Hg; partial pressure of carbon dioxide (PaCO
2), 37.4 mm Hg; bicarbonate (HCO
3-), 26.0 mEq/L; and saturation level of oxygen (SaO
2), 85.9%. A chest radiograph showed a subtle, diffuse ground-glass opacity in both lower lung fields and subsegmental atelectasis in the left lower lobe. A chest computed tomography scan revealed diffuse ill-defined ground-glass opacities with septal line thickening bilaterally, combined with several subpleural ground-glass opacity nodules (
Figure 1). A pulmonary function test revealed the following: forced expiratory volume in 1 second (FEV
1)/forced vital capacity (FVC) ratio, 102; FEV
1, 2.8 L (94%); FVC, 3.47 L (92%); and diffuse capacity for carbon monoxide (DLCO), 57%. Based on his past medical history, clinical symptoms, and laboratory findings, a diagnosis of DILD was suspected. Consequently, bronchoscopy with bronchoalveolar lavage (BAL) was performed. There were no endobronchial lesions revealed with bronchoscopy. The BAL fluid results were as follows: white blood cell count, 480 cells/µL (neutrophils, 9%; lymphocytes, 30%; macrophages, 57%; eosinophils, 4%; and basophils, 0%); and red blood cell count, 30 cells/µL. Microbiological culture and polymerase chain reaction of the bronchoscopic wash specimens were negative for
Mycobacterium tuberculosis, pneumococcus and respiratory virus. The real-time polymerase chain reaction of bronchial washing specimens was performed as following:
Mycoplasma,
Chlamydia,
Legionella,
Bordetella,
Haemophilus pneumonia, adenovirus, rhinovirus, coronavirus, influenza virus A and B, parainfluenza virus, respiratory syncytial virus A and B, bocavirus, metapneumovirus. The results were all negative. Additionally, the urine antigen and immunologic study were performed to exclude others pathogen. The results revealed the following: streptococcal pneumonia and
Legionella urinary antigen, negative;
Mycoplasma pneumoniae IgG/IgM, negative; and
Chlamydia pneumoniae IgG (17.65, positive; normal range, <9 index), IgM (4.62, negative; normal range, <9 index). According to the cytology, the majority of the alveolar macrophages had a foamy appearance (
Figure 2). To make a differential diagnosis of connective disease or allergic disease, immunologic studies and multiple allergosorbent test system (MAST) were performed as follow: all allergens of MAST, class 0 (0.00-0.34 IU/mL); rheumatoid factor, negative; C3 complement, 135.00 mg/dL (normal range, 90-180 mg/dL); C4 complement, 42.20 mg/dL (normal range, 10-40 mg/dL); anti-nuclear antibodies and anti-neutrophil cytoplasmic antibodies, negative.