Contributed by Thomas C. Wilson, MD, Patricia A. Kirby, MBBCh, MMed (Anat Path), FRCPath (Nu)
University of Iowa Hospitals and Clinics, Department of Pathology
CLINICAL HISTORY AND IMAGING
A 50-year-old man with a two-month history of severe back pain being treated for shingles complained of mild headaches and sudden-onset diplopia for two weeks. His medical history is significant only for heavy alcohol use. Neurologic examination revealed ptosis and complete plegia of his right eye. The remainder of the exam was within normal limits. MRI revealed a 3.0 x 2.9 x 1.5 cm circumscribed mass centered on the sella turcica extending into the superior aspect of the clivus and into the right cavernous sinus. It demonstrated mild, somewhat heterogeneous enhancement with intermediate signal intensity on T1 and was isointense on T2-weighted images (Figures 1 and 2). No normal pituitary gland was identified. Serum prolactin, follicle stimulating hormone and growth hormone levels were within normal limits.
Endoscopic transsphenoidal resection of the sellar mass was performed. It was noted that the bone adjacent to the lesion was eroded and the tumor appeared to involve the overlying dura with possible sinus mucosal involvement. Postoperative MRI showed residual tumor present posterior to the right internal carotid artery.
An intraoperative smear was performed which revealed cohesive nests of plump cells with abundant eosinophilic and often vacuolated cytoplasm and large nuclei, many with prominent nuclear pseudoinclusions and nucleoli (Figures 3 and 4). Permanent sections (Figures 5 and 6) showed tumor with an acinar to glandular growth pattern. The cells had eosinophilic to basophilic cytoplasm with abundant intracytoplasmic vacuoles which were negative for mucin on PASD and mucicarmine stains. However, there was abundant cytoplasmic glycogen on a PAS study. The nuclei were large with frequent nucleoli and mitoses were easily found. There were numerous clusters of foamy macrophages in between the tumor cells and thin walled vascular channels were uniformly dispersed throughout the tumor. Two tiny foci with pigment were identified on high power. Immunohistochemical stains revealed the cells were positive for pankeratin (Figure 7) and MOC31 and negative for synaptophysin (Figure 8). CD68 (Figure 9) highlighted the numerous foamy macrophages between the neoplastic cells and a stain for polyclonal CEA (Figure 10) showed a canalicular and luminal pattern of staining.