Galactorrhea associated with a sellar mass results in a large differential diagnosis. We discuss the case of a female patient harboring an invasive macroadenoma upon MRI, clinically associated with galactorrhea and mild hyperprolactinemia. The discrepancy between the large tumor size and mild prolactinemia, as well as the rapid normalization of prolactinemia under cabergoline without associated tumor volume reduction were considered arguments pleading against the lactotroph tumor diagnosis. Despite the lack of hypercortisolism-related clinical symptoms, with normal free urinary cortisol levels and normal cortisol suppression under dexamethasone, a silent corticotroph adenoma was suspected preoperatively, owing to the mildly-elevated ACTH levels in contrast with normal cortisol levels.
What is already known about the topic?
Corticotroph tumors without clinical hypercortisolism-related signs have been recognized since 1975. Based on experience, these tumors appear to secrete less biologically active ACTH, whilst being less differentiated yet more aggressive
What does this article bring up for us?
This case illustrates the relevance of systematically dosing ACTH in clinically non-functioning tumors in order to be able to detect a silent corticotroph adenoma, while anticipating the risk of postoperative adrenal insufficiency. This case has enables us to discuss the mechanism underlying the associated hyperprolactinemia.
Key Words
Hyperprolactinemia, silent corticotroph adenoma, stalk compression, β-endorphins, subclinical Cushing’s disease