MON-087 - Amyloid-Rich Macroprolactinoma with ICA Invasion: A Rare Variant with Distinct Endocrine Behavior

Background: Prolactinomas are characteristically sensitive to dopamine agonist therapy, with predictable biochemical and radiologic improvement in most patients. However, a subset behaves differently—showing limited shrinkage, increased firmness, or unexpected patterns of invasion. Amyloid deposition, while most often reported in sparsely granulated somatotroph adenomas, has also been described, though infrequently, in prolactin-secreting tumors. In lactotroph adenomas, amyloid may appear as spherical or calcified deposits near prolactin-staining cells, and its presence has been linked to reduced dopamine-agonist responsiveness, pronounced tumor firmness, and greater surgical difficulty. Together, these features raise the possibility that amyloid-rich prolactinomas represent a distinct biological subtype with multiple implications on both diagnosis and management.

Clinical

Case: A middle-aged man presented with hypogonadal symptoms, hyperprolactinemia, and central hypothyroidism. MRI revealed a 2.5-cm macroprolactinoma compressing the optic chiasm. He began cabergoline and underwent stereotactic Gamma Knife radiosurgery, achieving only partial biochemical improvement. Despite therapy, visual symptoms progressed. Follow-up MRI demonstrated a 23-mm mass with left cavernous sinus invasion and partial encasement of the cavernous internal carotid artery (ICA). Endoscopic endonasal resection was performed. Intraoperatively, the tumor was exceptionally firm and densely adherent to the ICA, limiting resection. Pathology demonstrated a lactotroph PitNET with 95% amyloid deposition, confirmed by Congo-red birefringence. PIT-1 staining and Ki-67 index were consistent with a typical adenoma. Postoperatively, prolactin improved but remained mildly elevated, and the patient required hormone replacement for central adrenal, thyroid, and gonadal insufficiency.

Conclusion: This prolactinoma with 95% amyloid deposition represents an exceptionally uncommon presentation that expands the recognized spectrum of lactotroph tumor behavior and offers insight into the potential influence of extensive amyloid on tumor characteristics. The constellation of a dense, rigid mass, limited response to standard therapy, and involvement of critical vascular structures highlights a functional and structural profile not typically seen in lactotroph tumors. Recognizing this variant is clinically important, as it may signal a distinct biological subtype with different therapeutic expectations. This case underscores the importance of further investigation into amyloid-related pathways and their potential role in defining a unique subgroup of prolactinomas.

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