Macroprolactinoma with progressive resistance to high-dose cabergoline

  1. Lookup NU author(s)
  2. Dr Chankramath Arun
  3. Dr Stephen Ball
  4. Jonathan Hill
  5. Janet Lewis
  6. Dr Richard Quinton
Author(s)Arun CS, Mitra D, Ball SG, Hill J, Lewis J, Quinton R
Publication type Conference Proceedings (inc. Abstract)
Conference NameEndocrine Abstracts: 197th Meeting of the Society for Endocrinology
Conference LocationLondon, UK
Year of Conference2006
Source Publication Date6–7 November 2006
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Introduction True resistance to cabergoline in patients with hyperprolactinaemia has only rarely been reported. We describe a patient with macroprolactinoma who initially responded to cabergoline, but then developed a progressive increase in PRL levels. Clinical case A 78-year-old male presenting with headache and left temporal hemianopia was found to have a macroprolactinoma with suprasellar/cavernous sinus extension and panhypopituitarism. The biochemistry dataset revealed central hypothyroidism dating back >5 years. On cabergoline 3.5 mg/wk, PRL fell progressively from 51,299 to 4,833 mU/L over a 7-month period with some tumour shrinkage. However, 14 months after initiation of medical therapy, PRL had risen again to 13,597 with evidence of tumour regrowth, despite a stepwise increase in cabergoline dose to 7 mg/wk. There was little response to octreotide challenge (12,998→8,466) and PRL rose further to 22,227 over the next month. Transsphenoidal surgery (TSS) was limited by severe vascular disease (circle of Willis fed by a single hypertrophic vertebral artery). Histology confirmed lactotroph adenoma with unusually high mitotic index. Post-op PRL was 13,597 and adjuvant fractionated multiportal EBRT was administered, resulting in a nadir PRL 17-months later of 1,665. However, despite cabergoline 10 mg/wk, there has since been tumour regrowth and further rise in PRL, peaking 3-years post TSS/EBRT at 19,606. Discussion It is unusual to develop resistance to cabergoline in patients who are initially sensitive. Due to physical frailty and tumour anatomy, he is not a candidate for further TSS or stereotaxic radiosurgery. Tablet non-adherence is a theoretical possibility, but following periods of supervised twice-weekly administration, we are confident this is not the case. Tachyphylaxis (documented in one previous case) is also a possibility and this could potentially be established by withholding cabergoline for 1–3 months and then rechallenging. Finally, tumour growth might be E2-driven, in which case a trial of aromatase inhibitor±stopping androgen replacement might be beneficial.
PublisherBioScientifica Ltd.
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