Endocrine Abstracts

Background: In acromegaly, chronic GH hypersecretion with secondary IGF-1 excess sustains proliferative signalling and stimulates widespread growth-factor activity. Although tissue overgrowth is typical, salivary-gland involvement is rarely reported.

Case reports: The first, a 69-year-old woman, was assessed in 2019 with acromegalic features and elevated IGF-1 (3.7 × ULN). MRI showed a pituitary macroadenoma and an incidental right parotid tumour (4.3 × 2.8 × 2.8 cm) with well-defined margins, not clinically apparent, possibly masked by cervical enlargement from underlying multinodular goitre. Transsphenoidal adenomectomy confirmed a somatotroph adenoma (Ki-67 = 3%). GH hypersecretion persisted despite combination therapy with lanreotide and cabergoline; biochemical control was achieved with pegvisomant. The parotid tumour was surgically removed in 2022, and histopathology confirmed pleomorphic adenoma. The second, a 60-year-old woman, presented at the end of 2018 with acromegalic features and elevated IGF-1 (2.4 × ULN). Clinical examination identified a left parotid mass. Cranial CT demonstrated a 2 × 2.5 × 1.4 cm, well-circumscribed parotid tumour, along with a concomitant pituitary microadenoma. Following the diagnosis, cabergoline was initiated. Parotid tumour excision in 2019 confirmed pleomorphic adenoma, followed later that year by transsphenoidal pituitary surgery. Histopathological examination confirmed a GH-secreting adenoma with focal PRL co-expression (Ki-67 = 2%). Lanreotide therapy achieved and maintained biochemical control, with sustained remission after discontinuation in 2022.

Discussion: Pleomorphic adenoma, the most frequent benign tumour of the salivary glands, predominantly affects the parotid. Although IGF-1 excess in acromegaly is associated with increased tumour prevalence, evidence for salivary involvement is limited. PLAG1-driven IGF2 upregulation in pleomorphic adenoma suggests a plausible local mechanism that may act synergistically with systemic IGF-1 signalling to promote tumour growth.

Conclusion: These cases suggest a possible interaction between systemic GH/IGF-1 excess and local PLAG1-driven pathways in benign salivary-gland tumour formation, supporting consideration of parotid assessment during acromegaly follow-up.