chemical, and flow cytometric study of 35 cases. Am J Surg Pathol 1991; 15:529 –553 5 Iyoda A, Hiroshima K, Toyozaki T, et al. Clinical character- ization of pulmonary large cell neuroendocrine carcinoma and large cell carcinoma with neuroendocrine morphology. Cancer 2001; 91:1992–2000 6 Patel AM, Jett JR. Clinical presentation and staging of lung cancer. In: Aisner J, Arrigada R, Green MR, et al, eds. Comprehensive textbook of thoracic oncology. Baltimore, MD: Williams & Wilkins, 1996; 293 Pulmonary Eosinophilia Following Lung Transplantation for Sarcoidosis in Two Patients* Susan G. Gerhardt, MD; Rubin M. Tuder, MD; Reda E. Girgis, MB, BCh, FCCP; Stephen C. Yang, MD, FCCP; John V. Conte, MD, FCCP; and Jonathan B. Orens, MD, FCCP Pulmonary eosinophilia is an uncommon problem in lung transplant recipients. We report the unique occurrence of two cases of pulmonary eosinophilia in pulmonary allografts for sarcoidosis. Both patients rapidly acquired bronchiolitis obliterans syndrome (BOS) after resolution of pulmonary eosinophilia. It is known that peripheral eosinophilia is a marker for pulmonary allograft rejection, but its potential in the pathogenesis of BOS is unclear. (CHEST 2003; 123:629 – 632) Key words: eosinophilic pneumonia; lung transplantation; sar- coidosis Abbreviations: BOS  bronchiolitis obliterans syndrome; OB  obliterative bronchiolitis P ulmonary eosinophilia is an uncommon problem in lung transplant recipients, perhaps because of the use of long-term steroids and other immunosuppressive agents. It is known that peripheral eosinophilia is a marker for pulmonary allograft rejection, but its potential in the pathogenesis of bronchiolitis obliterans syndrome (BOS) is unclear. 1 In nontransplanted patients, pulmonary eosino- philia is a rare but clinically important pulmonary disease with diverse presentations including Loeffler syndrome, acute eosinophilic pneumonia, bronchopulmonary as- pergillosis, and hypereosinophilic syndrome. 2 Despite the variability in clinical presentations, his- topathologic changes in the lung are alike regardless of the cause of pulmonary eosinophilia. 3 The disease is largely the product of infiltration of lung parenchyma with eosin- ophils, and to a lesser degree, lymphocytes, neutrophils, and plasma cells. 3 Giant cells and “Charcot Leyden” (eosinophilic) granules may be seen. The inflammation leads to variable alveolar wall damage, fibrinous exudate, and reactive hyperplasia of type II pneumocytes. 2 In pulmonary transplant recipients, peripheral eosino- philia can be a marker for episodes of acute rejection; however, the role of the eosinophil in the pathogenesis of cellular rejection is unclear. 1 Data regarding the long-term outcome and complications for lung transplantation for sarcoidosis are limited. We report the unique occurrence of two cases of pulmonary eosinophilic infiltrates in the pulmonary allografts following transplantation for sarcoid- osis. In both cases, the pulmonary eosinophilia was fol- lowed by the development of BOS. Case Reports Case 1 A 51-year-old African-American woman presented with a 1-week history of increased dyspnea on exertion 27 months after single left lung transplantation for advanced fibrocystic sarcoid- osis. The dyspnea progressed to marked shortness of breath at rest 2 days prior to hospital admission. She denied fever, chills, night sweats, cough, hemoptysis, or chest pain. Her posttransplant course was complicated by the develop- ment of a native lung aspergilloma requiring right-upper lobec- tomy at 33 weeks posttransplant. Persistence of aspergillus growth in BAL fluid necessitated long-term oral itraconazole treatment at a dose of 200 mg bid. Surveillance bronchoscopies had revealed two episodes of A1B0 rejection that were untreated as well as one episode of A2B0 rejection, treated with an augmented oral prednisone dose. Bronchoscopy 2 months prior to presentation revealed no aspergillus or rejection. Her medi- cations included tacrolimus (3 mg bid), prednisone (5 mg qd), azathioprine (50 mg qd, dose limited by low WBC count), acyclovir, omeprazole, conjugated estrogen, pravastatin, meto- prolol, trimethoprim/sulfamethoxazole, magnesium oxide, iron sulfate, calcium, and vitamin D. Physical examination was remarkable for labored respirations with a rate of 22 breaths/min and inspiratory crackles at the left lung base. The heart was regular with an S 4 gallop and a grade 2/5 systolic murmur at the right lower sternal border. She was afebrile, and the remainder of the physical examination was normal. Laboratory studies revealed an elevated leukocyte count of 13,100/L with 655 eosinophils. Spirometry demonstrated a decrease in FEV 1 from 1.09 to 0.93 L (32.6% predicted) and a decrease in FVC from 1.88 to 1.74 L (49.2% predicted), as compared with 4 weeks prior. Peak posttransplant values had been as high as 2.31 L for FVC and 1.60 L for FEV 1 . A chest radiograph revealed patchy interstitial and alveolar opacifications of the left lung with bronchiectasis of the right middle lung and volume loss. Chest CT scan showed patchy ground-glass opaci- fications throughout the left lung as well as emphysematous changes and fibrosis of the native right lung (Fig 1). To further assess the abnormal findings of the allograft, the patient underwent bronchoscopy with transbronchial biopsies. All culture and stain results for infectious organisms from BAL and biopsies including bacterial, fungal, mycobacterial, and viral, *From the Department of Medicine, Division of Pulmonary and Critical Care Medicine (Drs. Gerhardt, Girgis, and Orens); the Department of Pathology, Division of Cardiopulmonary Pathol- ogy (Dr. Tuder); and the Department of Surgery, Divisions of Cardiac Surgery (Dr. Conte) and Thoracic Surgery (Dr. Yang), Johns Hopkins University School of Medicine, Baltimore, MD. Manuscript received January 15, 2002; revision accepted July 25, 2002. Correspondence to: Jonathan B. Orens, MD, FCCP, Associate Professor of Medicine, Johns Hopkins Hospital, Division of Pulmonary and Critical Care Medicine, 600 N. Wolfe St, Blalock 910, Baltimore, MD; e-mail: jorens@jhmi.edu www.chestjournal.org CHEST / 123 / 2 / FEBRUARY, 2003 629 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21989/ on 06/21/2017