Southcoast Health East Greenwich, Rhode Island, United States
A 75-year-old male presented with progressive lethargy and fatigue. Evaluation revealed secondary adrenal insufficiency, prompting endocrinologic and radiographic workup. MRI of the sellar region showed a nonfunctioning pituitary macroadenoma measuring 2.0 × 1.9 × 2.9 cm, with suprasellar extension and mass effect on the optic chiasm.
The patient underwent transsphenoidal resection in October 2024. Histopathology confirmed a nonfunctioning PIT-1 lineage pituitary adenoma, with immunohistochemical positivity for TSH, though without biochemical evidence of hyperthyroidism. Postoperatively, secondary adrenal insufficiency appeared resolved, confirmed by a normal cosyntropin stimulation test. Three-month postoperative endocrine evaluation demonstrated no hormonal abnormalities aside from hypogonadism with low testosterone levels which was attributed to history of prostate cancer and prior lupron therapy.
Surveillance MRI performed in February 2025 revealed persistent residual tumor, though decreased in size, measuring 1.4 cm transverse × 1.6 cm anteroposterior × 2.1 cm craniocaudal. Persistent mass effect seen on optic chiasm, with a small component extending into the cavernous sinus. Neurosurgery did not recommend repeat surgical intervention.
Unfortunately, no interval visual field testing was done. MRI performed in December 2025 demonstrated tumor progression, with the mass now 3.5 cm craniocaudal × 3.4 cm anteroposterior × 1.9 cm transverse. Imaging showed suprasellar extension with displacement and flattening of the optic chiasm, deviation of the infundibulum, and continued invasion of the cavernous sinus. The tumor demonstrated aggressive regrowth despite prior surgical debulking, an unexpected course for a “nonfunctioning” adenoma. Given the PIT-1 lineage of the tumor, this raises concern for a more proliferative biological phenotype than initially anticipated.
Repeat endocrine testing revealed recurrent secondary adrenal insufficiency, while the tumor otherwise remained hormonally nonfunctioning. Neurosurgical consultation determined that repeat surgical intervention is now required, with plans for a pterional craniotomy due to the extent of suprasellar and parasellar involvement. Complete resection is unlikely given cavernous sinus invasion, and the patient will likely require adjuvant postoperative radiation therapy for residual disease control.
Conclusion: This case highlights the potential for aggressive growth behavior in PIT-1 lineage pituitary adenomas, even when classified as nonfunctioning at presentation. Rapid postoperative regrowth underscores the importance of close radiographic surveillance, timely visual field assessment, and early multidisciplinary management. It also raises consideration for earlier adjuvant therapy in select PIT-1 adenomas exhibiting invasive or proliferative characteristics.
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