Placental Transmogrification of the Lung: A Exceptionally Rare and Intriguing Condition

Abstract Introduction: Placental transmogrification of the lung (PTL) is an extremely rare, benign lung malformation of unknown etiology. Chest imaging typically reveals bullous emphysema, thin-walled cystic lesions, nodules, or a combination of these findings. Histopathology shows papillary structures resembling placental villi, although these tissues do not have placental function. Patients with PTL often develop respiratory symptoms, such as dyspnea and cough, due to unilateral large emphysematous bullae. The primary treatment is surgical resection, which generally results in a favorable long-term prognosis. We present a case of PTL, highlighting the clinical presentation, diagnostic workup, and surgical management. Case Presentation: A 36-year-old male presented to the emergency department with acute shortness of breath for one day. His medical history included asthma and recurrent respiratory infections during childhood. He denied the use of tobacco, marijuana, or other drugs. He was born in Romania and previously worked as a delivery driver. There was no family history of lung disease. On physical examination, wheezing was noted in the upper lung fields, with decreased breath sounds in the right lower lung field. His vitals were stable, except for SpO₂ at 88% on room air. A chest X-ray revealed a giant emphysematous bulla in the right lung, and a CT scan of the chest confirmed unilateral emphysematous bullae (Fig. 1A and 1B). A ventilation-perfusion scan demonstrated near-absence of perfusion and ventilation in the right lung. Given these findings, the decision was made to proceed with a right pneumonectomy. Final pathology demonstrated villous structures resembling placental chorionic villi, along with bullous emphysema, thin-walled cystic lesions, and small nodules—consistent with placental transmogrification of the lung (Fig. 1C). Discussion: PTL was first described in 1979 due to the lung tissue's resemblance to placental tissue, both grossly and microscopically. Although the exact etiology remains unknown, it is hypothesized that PTL may result from the proliferation of interstitial clear cells following the destruction of elastic fibers in the alveolar walls, leading to alveolar degeneration and the formation of bullae. It remains unclear whether PTL is congenital or acquired. Approximately 40 cases have been reported; however, despite its rarity, PTL has an excellent long-term prognosis, with only one documented recurrence after definitive surgical intervention. There have been no reported cases of malignant transformation or bilateral PTL. This case underscores the importance of considering PTL in the differential diagnosis of unilateral bullous lung disease and highlights the favorable prognosis following surgical resection.