A 59-year-old male patient presented with fatigue, general weakness, erectile dysfunction, and loss of body hair, including pubic hair. The visual acuity showed 0.2 in the right eye and 0.8 in the left eye, and the visual field examination revealed bitemporal hemianopsia. There was no other neurological deficit except visual disturbance. The lab findings showed changes compatible with panhypopituiarism with low levels of thyroxine, cortisol, and testosterone. Complete blood count was hemoglobin 13.4 g/dL (13.0–17.0), white blood cells 7.28×10³/µL (4.0–10.0), and platelet 278×10³/µL (130–400). Serum electrolyte was sodium 140 mmol/L (135–145), potassium 3.0 mmol/L (3.5–5.5), chloride 106 mmol/L (98–110). Serum free T4 was 0.39 ng/dL (0.89–1.79), serum thyroid-stimulating hormone 3.90 µIU/mL (0.17–4.05), serum cortisol less than 1.0 µg/dL (4.3–22.4), plasma adrenocorticotropic hormone 18.3 pg/mL (6–60), and serum testosterone less than 0.01 ng/mL (1.81–7.58). The thyroid glands showed diffuse volume loss without focal lesion, suggesting hypothyroidism on thyroid ultrasonography.

Initial sellar MRI revealed a 3.3×3.5×2.3-cm sellar and suprasellar snowman-shaped enhancing mass (Fig. 1). Preoperative radiologic diagnosis was a pituitary macroadenoma. The lesion was homogeneous, solid, and hypo-enhanced compared with normal pituitary gland. It compressed the overlying optic chiasm, and there was no definite evidence of cavernous sinus invasion. According to the reading of MRI and a basal pituitary hormone study, it was compatible with non-functioning pituitary adenoma.

The tumor was partially resected via the trans-sphenoidal approach. There was no discernible surgical findings suspecting ependymoma. At first, we couldn't assume that the tumor was ependymoma. However, the mass was firm and bloody, unlike usual pituitary adenoma. There were no postoperative complications.

Microscopically, the tumor was highly cellular and composed of compactly arranged small round to oval cells. In area, the tumor showed glandular or papillary structures. These features were very similar to those of pituitary adenoma at a glance. In higher magnification, tumor cells showed somewhat elongated nuclei, and arranged in the fibrillary background, forming perivascular pseudorosettes (Fig. 2A and B), papillary configurations (Fig. 2C), or true ependymal rosettes (Fig. 2D). Immunohistochemical stains showed strong positive reactions to vimentin and S-100 protein (Fig. 2A). The tumor was also positive for S100 protein and glial fibrillary acidic protein (Fig. 3A and B) and CD99 (Fig. 3C). In epithelial membrane antigen staining, characteristic paranuclear dot-like positivity was also noted (Fig. 3D). The histologic and immunohistochemical findings were compatible with ependymoma. Mitoses were not found and there was no necrosis. Immunohistochemical stain for Ki-67 showed the labeling index was less than 1%.

Immediate postoperative MRI showed a 3.0×2.3-cm residual tumor in the suprasellar and sellar space (Fig. 4). It showed reduction of mass effect upon the optic chiasm. The patient was histopathologically diagnosed with an intrasellar ependymoma. After 2 months, he received adjuvant radiation therapy of 54 Gy over 30 fractions to intrasellar lesion for 6 weeks. A followed-up MRI was taken 3 months after radiation therapy, and it showed markedly decreased size of mass (Fig. 5A and B). It decreased to 1.7×2.1-cm sized mass, and its compressive effect on optic chiasm was much relieved.

Thyroid and steroid hormones were replaced. Symptoms of fatigue, general weakness, and visual field defect improved. There was no newly developed neurological deficit. Follow-up MRIs were performed every 3 months initially, then every 6 months. At the 10-year follow up, MRI revealed no evidence of tumor progression (Fig. 5C and D).