This study was approved by the review boards of Jishuitan Hospital and Fourth Medical College of Peking University. Patient consent to this study was not required because the retrospective nature of the study. A 56-year-old woman was admitted to our hospital on July 1, 2015 because of intermittent fever and nonproductive cough for 2 weeks and exertional dyspnea and chest pain for 1 week. She described no chills, rigors, and night sweats. The patient developed abdominal pain and had mucus stools on April 20, 2015. Laboratory tests at a local clinic on May 20, 2015 showed leukocytes at 6.9x109/L with 67.9% neutrophils and 0.12% eosinophils. Her hemoglobin level was 129 g/L and platelet count was 276x109/L. The occult stool test was weakly positive. She started mesalazine 0.5 g three times a day for 6 weeks without a prescription. The patient began coughing on June 17, 2015 and also had fatigue and fever (as high as 39.4 C). Laboratory examinations revealed leukocytes at 12.75x109/L with 76.2% neutrophils and 6.9% eosinophils. Her hemoglobin level stood at 124 g/L and platelet count was 485x109/L. A chest radiograph and computed tomography (CT) scan showed minor peripheral patchy opacity in bilateral upper and mid lungs with a narrowed right costophrenic angle (Figure 1A and B). A 10-day course of intravenous levofloxacin and ceftazidine was administered, and the patient continued mesalazine. Nevertheless, the patient was still febrile. On June 24, 2015, the patient developed right chest pain and aggravating exertional dyspnea. She denied symptoms of palpitations and paroxysmal nocturnal dyspnea. She denied the use of tobacco products and had no occupational exposure to chemical fumes, including biomass fuel. The patient was allergic to penicillin and metronidazole. She had hypertension for 5 years, which was controlled by taking sustained release nifedipine. There was no family history of asthma.
Physical examination at admission showed a blood pressure of 117/70 mmHg, a pulse rate of 101 beats/min, a respiratory rate of 20 breaths/min, and a temperature of 37.4 C. No crackles were noted in both lungs. Clubbing, cyanosis, or peripheral edema was absent. Cardiovascular and abdominal examinations were unremarkable. Review of the systems was unremarkable for skin rashes, joint pain, and weight loss.
Laboratory investigations revealed leukocytes at 25.54x109/L with 67.4% neutrophils and 21.8% eosinophils. Her hemoglobin was 111 g/L and platelet count 593x109/L. Renal and liver function were normal, and no splenomegaly was noted. Chest radiograph showed progressing opacity predominantly in bilateral upper lungs (Figure 1C). Chest CT scan revealed bilateral patchy consolidations with interlobular septal thickening (Figure 1D and 1E). The single-breath diffusing capacity of the lung for carbon monoxide (DLco) was 46% of the predicted values. Transbronchial biopsy revealed chronic inflammation and exudation of fibrin (Figure 2A), and bronchoalveolar lavage fluid (BALF) showed 1x106 cells/mL with 18% macrophages, 22% neutrophils, 33% eosinophils, and 27% lymphocytes (Figure 2B). Bone marrow aspirate showed infiltration by mature eosinophils (Figure 2C), but the ratio of promyelocytes to their precursors was normal, and the percentage of eosinophils was 18, with normal morphology. Arterial blood gas analysis revealed a pH of 7.523, a partial pressure of carbon dioxide (pCO2) of 29.7 mmHg, a partial pressure of oxygen (pO2) of 59.5 mmHg, and a bicarbonate level of 23.2 mmol/L on room air. Tests for adenovirus, respiratory syncytial virus, seasonal influenza A and B, parainfluenza virus, Mycoplasma pneumoniae, Chlamydia, and Legionella pneumophila were negative. Tuberculin skin test and sputum and BALF tests for acid-fast bacilli excluded tuberculosis. Rheumatoid factor, antinuclear antibodies, anti-double-strand DNA antibody, antiextractable nuclear antigen antibodies, and antineutrophil cytoplasmic antibody were negative. C-reactive protein was at 191 mg/dL, erythrocyte sedimentation rate was at 65 mm/h, and immunoglobulin E was at >100 IU/mL. Colonoscopy at 2 weeks after admission demonstrated focal erythema, erosions, and edematous swollen mucosa in the rectum.
Mesalazine-induced eosinophilic pneumonia was diagnosed, and mesalazine was discontinued. Currently, there is no consensus for the use of corticosteroid therapy for mesalazine-induced eosinophilic pneumonia, and our patient was not given corticosteroids. Besides, four out of nine reported cases also recovered without corticosteroid therapy. The patient improved in symptoms, and 4 weeks after cessation of mesalazine, she was discharged. CT scan showed bilateral ground glass opacity (Figure 1E). At 5 weeks of follow-up after discharge, the patient was asymptomatic with a normalized eosinophil count (Figure 3). Spirometry continued to show a restrictive defect and a reduced DLco (44%) (Table 1), but the patient felt no apparent exertional dyspnea after discharge.
Radiologic features of eosinophilic pneumonia in a 56-year-old woman who took mesalazine for suspected ulcerative colitis. bilateral patchy consolidations with interlobular septal thickening in both lungs on CT scan (July 15, 2015).