A 19-year old female was admitted to our hospital because of a sudden onset fever and cough. She had developed the cough, fever and progression of dyspnea two days before admission. Antibiotic treatment prior to hospitalization was not effective for the clinical symptoms. She had started to smoke 20 cigarettes per day two weeks before the admission. She had a history of pollinosis, but no previous history of bronchial asthma. On admission, her temperature was 39.4  C. Auscultation revealed wheeze in the bilateral lung fields.
An arterial blood gas analysis on room air revealed a pH of 7.434, PaO2 of 58.1 torr and PaCO2 of 34.2 torr, indicating hypoxemia. A chest radiograph revealed diffuse bilateral infiltrates and pleural effusion in the right lung, as shown in Fig. 1. The patient's peripheral white blood cell (WBC) count was 18,600 cells/mm3, with 84.4% neutrophils, 11.8% lymphocytes and 1.0% eosinophils. The serum C-reactive protein was 11.5 mg/dl. Her serum immunoglobulins (Ig) were: IgG, 1048 mg/dl; IgA, 166.0 mg/dl; IgM, 199.0; IgE, 196.8 U/ml. Bronchoalveolar lavage fluid (BALF) was obtained from right B5 area on the third hospital day. The total cell count in the BALF was 98.0 x 104/ml, which contained 5.6% neutrophils, 12.0% lymphocytes and 66.6% eosinophils. The CD4/CD8 lymphocytes ratio in the BALF was 1.26. Cultures of the BALF proved negative for bacteria and fungi. A specimen obtained from transbronchial lung biopsy (TBLB) demonstrated eosinophilic infiltration with fibrin exudates into the air space and edematous alveolar walls, indicating eosinophilic pneumonia.
On the fourth hospital day, her chest radiograph and symptoms had remarkably improved without corticosteroid treatment. Her hypoxemia had been gradually improving, and her SpO2 was 97% under room air on the forth hospital day. The peripheral eosinophil count, which had been 186 cells/mm3 on admission, increased gradually to 1400 cells/mm3 on the seventh hospital day. Although the eosinophilia was prolonged over 1 month, the peripheral eosinophil count decreased to 504 cells/mm3 2 months after the development of AEP. The peripheral lymphocyte count also increased from 2195 cells/mm3 on admission to 3367 cells/mm3 on the seventh hospital day, and decreased to 2720 cells/mm3 2 months after the development of AEP. Therefore, the peripheral eosinophil count appeared to fluctuate in parallel with the peripheral lymphocyte count (Fig. 2).
The patient was discharged on the 13th hospital day. She quit smoking and has not resumed. Three months later, she continued to be asymptomatic. She reported having smoked two kinds of cigarettes. The lymphocyte stimulation tests (LSTs) for the both kinds of cigarette smoke extract were negative.
A cytokine analysis of the serum was performed on admission and on the 13th hospital day, and a cytokine analysis of the BALF was performed on the third hospital day (Fig. 3). The levels of IL-6, IL-5, IL-4, regulated on activation, normal T cell expressed and secreted (RANTES) and eotaxin in the serum on admission were 28.7 pg/ml, 2590 pg/ml, 98.5 pg/ml, 20000 pg/ml and 171 pg/ml, respectively. The cytokine analysis of the serum performed on the 13th hospital day revealed that the levels of IL-6, IL-5, IL-4 and eotaxin had decreased to 1.0 pg/ml, <5.0 pg/ml, 71.9 pg/ml and 104 pg/ml respectively, but that RANTES had increased to 78900 pg/ml. The levels of IL-6, IL-5, IL-4, RANTES and eotaxin in the BALF were 19.4 pg/ml, 883 pg/ml, 6.0 pg/ml, 42.1 pg/ml and 59.3 pg/ml, respectively. The levels of all cytokines in the BALF were lower than those in the serum obtained on admission. In particular, the level of RANTES in the BALF was much lower than that in the serum.
Chest X-rays and CT scans. B. A chest CT on admission showed diffuse ground-glass opacification in the right lung, patchy opacification in the left lung, and a small amount of pleural effusion in the right lung, consist with the opacification on chest X-ray.