Endocrine Abstracts

We present a case of 71-year-old gentleman who presented with bitemporal hemianopia in 2008 with pituitary apoplexy compressing the optic chiasm. Prolactin was 55287MU/l, with deficiency of all other anterior pituitary hormones. He underwent transphenoidal adenectomy (TSA). Prolactin was 35633MU/l post-operatively and cabergoline was commenced. Histology was consistent with a lactotroph adenoma with MiB-1 index of 3–5%. Visual fields recovered and prolactin was normal until 2013. He re-presented with new visual field defect and the prolactin of 32558MU/l in 2014, with no response to escalation of cabergoline. He underwent debulking surgery in February 2015 and September 2015 due to progression; histology showed elevated MiB-1 (20–30%). The post operative MRI scan in December 2015 confirmed rapid regrowth of the tumour and further TSA and radiotherapy were performed. His prolactin was stable until September 2017. Slow rise in prolactin was seen initially with no change in pituitary MRI findings. Between March and May 2018 the rate of rise of the Prolactin was accelerated and reached 65807MU/l. MRI in May 2018 demonstrated two large extra-axial intra-dural enhancing masses at the level of C1-C2 junction with risk of neuronal compression. The patient underwent resection of the right intradural extramedullary lesion. Histology demonstrated a metastatic deposit with raised MiB-1 (10–20%), confirming lactotroph carcinoma. Post operatively the prolactin level to 50460MU/l. MRI spine and PET CT scan is planned to investigate for distant metastasis and possible resection of the left intradural extramedullary lesion will be performed if no other metastases are identified and possible temozolomide therapy. This case highlights the changing course of an aggressive lactotroph lesion with resistance to dopamine agonist therapy and subsequent development of metastatic disease. Lactotroph lesions with high MIB-1 and unusual course harbour malignant potential and warrant close follow up.