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Dopamine agonist-responsive Cushing’s disease
  1. Gurpreet Anand1,
  2. Andrea Bink2,
  3. Felix Beuschlein1 and
  4. Christoph Schmid1
  1. 1 Department of Endocrinology, University Hospital Zürich, Zürich, Switzerland
  2. 2 Department of Radiology, University Hospital Zürich, Zürich, Switzerland
  1. Correspondence to Dr Gurpreet Anand, gurpreet.anand{at}


A 47-year-old Caucasian man was referred to our clinic with a severe clinical and biochemical phenotype of endogenous hypercortisolism for further evaluation and treatment. In addition to confirming adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome, we found left temporal hemianopsia, massively increased prolactin, increased growth hormone/insulin-like growth factor 1 values, hypogonadotropic hypogonadism and central hypothyroidism. As the cause of these abnormalities we revealed an invasive macroadenoma of the pituitary secreting ACTH, prolactin and growth hormone, resulting not only in a clinically predominant picture of Cushing’s syndrome but also causing hypogonadotropic hypogonadism and central hypothyroidism. The patient responded surprisingly well to dopamine agonist treatment leading not only to normalisation of prolactin levels but also to clinical and biochemical remission of Cushing’s syndrome. Tumour size decreased successively in follow-up MRI scans. Despite lacking immunohistochemical analysis of tumour tissue, we assume plurihormonal secretion of ACTH, prolactin and growth hormone from pituitary macroadenoma, which fortunately responded well to dopamine agonist treatment.

  • pituitary disorders
  • endocrine system

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  • Patient consent for publication Obtained.

  • Contributors GA: wrote the case report and had also treated the patient. AB: provided expert advice as neuroradiologist and delivered appropriate MRI sections for the case report. FB: also offered input in modifying some aspects of the manuscript. CS: offered his expert advice and some important insights into modifying the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.