A 63-year-old man presented to a local hospital with fever and hypoxia. The patient experienced respiratory distress and dizziness without cough for 1 day, prior to the first visit. He had a history of hypertension and subarachnoid hemorrhage, and was allergic to penicillin. He had been prescribed OJT 6.0 g/day (Kracie Holdings, Ltd) for the past 4 weeks. He was an ex-smoker and had no episodes of resumption of smoking. His bodyweight was 55 kg. His initial vital signs were as follows: Glasgow Coma Scale score, 15 (E4V5M6); blood pressure, 114/86 mmHg; heart rate, 100 b.p.m.; respiratory rate, 42 breaths/min; oxygen saturation, 65% while breathing ambient air; and body temperature, 38.7°C. He was transferred to our hospital on the same day, intubated, and placed on a ventilator. The initial arterial blood gas showed pH 7.40, PaCO2 52 mmHg, PaO2 63 mmHg, HCO3 − 32.2 mmol/L, and lactate 10 mg/dL at FIO2 0.75. Blood tests showed an elevated inflammatory response, with a white blood cell count of 9700/mm3, eosinophil count of 0.0/mm3, and serum C-reactive protein level of 18.5 mg/L. The following autoantibody screening was negative; antinuclear antibody, rheumatoid factor, myeloperoxidase-antineutrophil cytoplasmic antibody, and proteinase-3-antineutrophil cytoplasmic antibody tests were negative. Bacteriological and virological tests did not detect any infectious pathogens, including Legionella pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, cytomegalovirus, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Echocardiography revealed a normal ejection fraction of 60%. Chest radiography and computed tomography revealed bilateral ground-glass opacity with air bronchograms and pleural effusion. In view of the clinical presentation, mild hydrostatic pulmonary edema might be possible, however, the most plausible diagnoses were drug-induced interstitial lung disease and severe ARDS due to OJT. He was admitted to the intensive care unit and started on meropenem and azithromycin, intravenous methylprednisolone (80 mg/day), and prone positioning (16 h/day). He was deeply sedated to suppress breathing efforts without neuromuscular blockade. In the ventilator setting, the tidal volume was limited to ≤8 mL/kg, and positive end-expiratory pressure was maintained above 10 cmH2O. All oral medications were discontinued. On day 3, the patient's respiratory condition improved. The PaO2/FIO2 ratio was 238 at FIO2 0.40 and brain natriuretic peptide level was 35.2 pg/mL. Prone positioning and antimicrobial treatment were terminated, ventilator settings were weaned, and deep sedation was switched to light sedation. The patient was extubated on day 4. On day 7, his oxygen saturation was 97% on 1 L/min oxygen by nasal cannula, and the ground-glass opacity was reduced. Methylprednisolone was switched to oral prednisolone and the dose was reduced to 40 mg/day. The clinical course in the intensive care unit is described in Figure. On day 12, the Krebs von den Lungen-6 (KL-6) level was 798 U/mL. The patient was discharged on day 16. The dose of prednisolone was reduced based on clinical course indicators of interstitial lung disease such as KL-6 and chest radiographs: 40 mg on day 7, 20 mg on day 10, 15 mg on day 20, 10 mg on day 26, 7.5 mg on day 40, 5 mg on day 61, 2.5 mg on day 89, and discontinued on day 116.