Placental transmogrification of the lung is a histologic pattern frequenctly associated with pulmonary fibrochondromatous hamartoma

Archives of Pathology & Laboratory Medicine,  May 2002  by Xu, Ruliang,  Murray, Melissa,  Jagirdar, Jaishree,  Delgado, Yara,  Melamed, Jonathan

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* Context.-Placental transmogrification of the lung is a term introduced to describe a peculiar histologic pattern characterized by formation of placental villuslike structures in the lung parenchyma. It has been reported to occur in association with bullous emphysema and lipomatosis.

Objectives.-To study the relationship between placental transmogrification and pulmonary hamartomas.

Design and Methods.-Reports of 38 cases of pulmonary hamartomas during 18 years (1982-1999) were reviewed. All histologic slides of these cases were examined for the presence of villuslike papillary projections and placentalike structures. Hamartomas with prominent papillary projections or placenta-like structures were further investigated to assess the histogenesis and proliferation of epithelial and stromal cells. Immunohistochemical analysis was performed on paraffin-embedded tissue using monoclonal antibodies against Ki-67 and thyroid transcription factor 1 (TTF-1) and polyclonal antibodies against c-Kit antigen (a stem cell factor receptor/mast cell growth factor receptor) in conjunction with Leder stain for naphthol-ASD-chloroacetate esterase.

Results.-Placental transmogrification was identified in 6 of 38 cases of pulmonary fibrochondromatous hamartomas. The histologic change consisted of an abundant myxoid or edematous fibroadipose stroma with a respiratory epithelial lining, resulting in papillary projections that resembled immature placental villi. Epithelium lining the papillary projections was positive for TTF-1 (70%-90%) and Ki-67 (3%-5%). In contrast, stromal cells were negative for TTF-1 with only rare cells immunoreactive for Ki67. A number of stromal spindle cells and occasional cells in epithelium were c-Kit immunoreactive; however, concurrent Leder stain demonstrated that these c-Kit-positive cells were mast cells and not stem cells.

Conclusions.-Placental transmogrification is frequently associated with pulmonary fibrochondromatous hamartomas and may be induced by or associated with a proliferation of lining epithelial components in the hamartomas. The significance of numerous mast cells within stroma of placental transmogrification is unclear and their possible role in inducing stromal proliferation needs to be further evaluated.

(Arch Pathol Lab Med. 2002;126:562-566)

Pulmonary placental transmogrification (PT), also called placentoid bullous lesion, is an unusual condition first described in 1979.1-9 It is so named because morphologically it resembles immature placental structures, although it does not bear any biological and biochemical properties of a placenta.2,3 The presentation of PT ranges from asymptomatic to clinically overt and is associated with other pulmonary diseases, such as chronic obstructive airway disease, repeated pneumothoraces, bronchopneumonia, and even respiratory distress.2-8 The lesions are occasionally incidental masses seen by radiography.1,9 The PT lesion usually does not cause diagnostic difficulty; however, some rare cystic tumors, such as alveolar adenoma, sclerosing hemangioma, and congenital lesions (eg, adenomatoid cystic malformation), should be differentiated from it.4 In one unusual case, a papillary adenocarcinoma has been reported to arise in this lesion,5 but in general, PT is regarded as a benign lesion curable by resection.'1-4,6-9 The origin and pathogenesis of PT are unknown. Hypotheses of pathogenesis include a lymphatic or vascular proliferation in emphysematous lung parenchyma,3,4,6 a component of a congenital malformation,4 or an unrecognized hamartoma,1 but none of these hypotheses are based on sound morphologic or biological evidence.

Pulmonary hamartomas are common benign tumors considered to originate from primitive mesenchymal tissue.10 Most pulmonary hamartomas are fibrochondromatous type consisting of fibroadipose tissue and cartilage with varying degrees of epithelial invagination.10 Our hypothesis is that the epithelial invagination, if prominent, may account for the resemblance to immature placental villi, as seen in PT. In this report, we identified 6 cases of pulmonary hamartomas associated with characteristic PT. We further investigated the roles of proliferation of epithelium and a possible stromal stem cell in induction of pulmonary PT by immunostaining for proliferating index (Ki-67) and thyroid transcription factor 1 (TTF-1)11 and cKit antigen (a stem cell factor receptor/mast cell growth factor receptor).12,13

MATERIALS AND METHODS

Patients

A total of 38 cases of pulmonary hamartomas diagnosed at the Department of Pathology, New York University Medical Center, from 1982 to 1999 were retrieved. The patients' age and sex, the site and number of hamartomas, and concurrence with other lesions were recorded.

Pathologic Examination

Hematoxylin-eosin-stained slides of all 38 cases of pulmonary hamartoma were reviewed for the presence of villus papillary projections or placenta-like structures. The hamartomas with prominent papillary projections or placenta-like structure (as defined in previous publications1-9) were further characterized morphologically and immunohistochemically (Table 1).