PMC5088548_01
Thickening of the portal bile duct (arrows) and dilation of the intrahepatic bile duct (arrowheads) are observed on computed tomography (CT) (A). Chest CT shows air-space consolidations and ground-glass opacities primarily in the left lung. A honeycomb change is also evident in the left lower lobe (B).
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Abdominal CT revealed thickening of the portal bile duct and dilation of the intrahepatic bile duct (Fig. 1A). Pulmonary CT revealed a widespread air-space consolidations and ground-glass opacities (Fig. 1B).
A chest radiograph obtained on admission (A) and 3 months after admission (B). The rapid progression of bilateral infiltrative opacity is observed.
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Despite these intensive treatments, the lung infiltrates progressively expanded (Fig. 2).
Microscopic findings of the hepatic tumor. Adenocarcinoma is seen spreading along the bile duct wall (arrow) (A). The tumor shows stromal invasion forming irregular tubular structures with or without papillary projection (B, C). Exfoliation of carcinoma cell clusters (arrowhead) is observed in the ductal space (B). Carcinoma cells are diffusely positive for CK7 (D) and partially positive for CK20 (E).
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Microscopically, atypical cells grew along the surface of the intrahepatic bile duct (Fig. 3A) and showed stromal invasion forming irregular tubular structures with or without papillary projection (Fig. 3B and C). Exfoliation of tumor clusters was evident in the lumens (Fig. 3C). The tumor showed positivity for cytokeratin 7 (CK7; Fig. 3D) and cytokeratin 20 (CK20; Fig. 3E) on immunostaining.
Microscopic findings of the lung tumor. Carcinoma cells proliferate along the alveolar septum (arrow) (A, B). Exfoliation of carcinoma cell clusters (arrowhead) is observed in the alveolar cavity (B). The tumor shows stromal invasion forming irregular tubular structures with or without papillary projection (C, D). Carcinoma cells are diffusely positive for CK7 (E) and partially positive for CK20 (F). Neither TTF-1 (G) nor Napsin A (H) expression is detected.
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Atypical cells were observed along the alveolar wall in most pulmonary areas (Fig. 4A and B). In resemblance with a liver tumor, stromal invasion of the carcinoma forming irregular tubular structures with or without papillary projection (Fig. 4C and D) was also found in the lung specimen. Additionally, a large number of tumor clusters were found in the alveolar cavity, suggesting transbronchial spread of adenocarcinoma (Fig. 4B). Furthermore, in resemblance with the liver specimen, both CK7 and CK20 were positive on immunostaining (Fig. 4E and F). Immunostaining with thyroid transcription factor-1 (TTF-1; Fig. 4G) and Napsin-A (Fig. 4H) were additionally performed, both of which were negative in the pulmonary cancer lesion.
Mucin staining of the hepatic tumor (A-D) and the lung tumor (E-H). PAS staining shows mucin production by the hepatic tumor (A) and the lung tumor (E). Both the hepatic tumor and the lung tumor show negativity for MUC2 (B, F) and focal positivity for MUC5Ac (C, G) and MUC6 (D, H).
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Periodic acid-Schiff (PAS) staining showed that the tumors found in the liver and lung were rich in mucin production (Fig. 5A and E), and both tumors showed negativity for mucin2 (MUC2; Fig. 5B and F), focal positivity for mucin5Ac (MUC5Ac; Fig. 5C and G), and focal positivity for mucin6 (MUC6; Fig. 5D and H) upon immunostaining.