Contributed by Chih-Ying Wu, John Wang, Chii-Shuenn Yang, Fang-Yi Lee, Yee-Jee Jan
Department of Pathology and Laboratory Medicine, Taichung Veterans General Hospital
A 55-year-old male patient had a medical history of nephrotic syndrome and was followed up at a local hospital for many years. He had felt general fatigue for 2 years which became exacerbated 2 months ago. He visited our hospital where a series of laboratory tests showed hyponatremia and hypokalemia accompanied with low cortisol level. Other endocrinologic tests were within normal limits. After transsphenoidal adenomectomy, the patient developed panhypopituitarism, which has been managed by hormone substitution. No adjuvant therapy was administered. The patient made an uneventful recovery and has been receiving regular follow-up at our neurosurgery department without clinical or radiological evidence of a recurrent tumor for 7 years.
A 1.5 cm solid tumor over the sellar area was found by cranial magnetic resonance imaging (MRI) (Figure 1, Figure 2).
Light microscopy showed a solid tumor composed of spindle cells arranged in interlacing fascicles with increased cellularity. The tumor cells showed moderate to abundant eosinophilic and coarse granular cytoplasm. Mild nuclear atypia and pleomorphism were noted without increased mitotic count. Neither microvascular proliferation nor necrosis was noted (Figure 3). Immunohistochemically, most tumor cells expressed S-100 protein (Figure 4), vimentin, galectin 3 (Figure 5) and thyroid transcription factor 1 (TTF-1) antigen (Figure 6). Epithelial membrane antigen (EMA) was also focally and weakly expressed in tumor cells. There was no staining of tumor cells with pancytokeratin (AE1/AE3), neuroendocrine markers, glial fibrillary acidic protein (GFAP), CD68 and BCL-2. For definite diagnosis, ultrastructural examination (TEM, JEOL Jem1230) was performed which revealed numerous swelling mitochondria in the cytoplasm (Figure 7). No interdigitating cell process was clearly identified.