Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 13 P50

1Centre for Endocrine and Diabetes Sciences, University Hospital of Wales, Cardiff, United Kingdom; 2Department of Endocrine Surgery, University Hospital of Wales, Cardiff, United Kingdom; 3Department of Respiratory Medicine, Llandough Hospital, Cardiff, United Kingdom.


A 67 year old female presented with hypertension, oedema and cough. A CT scan of her abdomen showed an enlarged left adrenal gland. Urinary free cortisols were grossly elevated and low dose dexamethasone suppression testing confirmed Cushing’s Syndrome. 24 hour catecholamines were also elevated consistent with a diagnosis of phaeochromocytoma. ACTH levels were high (690 pg/ml) but pituitary MRI was normal. She was commenced on alpha and beta blockade in preparation for surgery; MIBG/octreotide scintigraphy confirmed uptake in the left adrenal gland only. Preoperatively she required ventilatory support for respiratory compromise, subsequently confirmed on bronchoscopy as aspergillosis (likely secondary to high cortisol levels). She underwent successful surgical removal of her phaeochromocytoma; histology demonstrated positive staining for ACTH and repeat biochemistry showed normalisation of hypercortisolism.

A 17 year old female presented with epistaxis and hypertension. She also gave a history of palpitations and syncopal episodes. She was noted to have acanthosis nigricans on examination. Urinary catecholamines were elevated as was IGF-1; subsequent glucose tolerance testing confirmed a diagnosis of acromegaly. A CT scan of the abdomen demonstrated a 5 cm left adrenal mass but pituitary MRI was normal. Following successful left adrenalectomy she developed hyponatraemia and marked hypoadrenalism requiring replacement hydrocortisone. Subsequently she became amenorrhoeic and dynamic testing confirmed severe panhypopituitarism; repeat pituitary MRI demonstrated pituitary infarction. Histological analysis confirmed an adrenal phaeochromocytoma but immunostaining for GH, GHRH and a constitutively active splice variant of the GHRH receptor was negative. We speculate that another GH secretagogue may have caused the GH excess. Our cases demonstrate that phaeochromocytomas can rarely secrete biologically active peptides, but the nature of these may not always be apparent. Hyponatraemia after surgery for phaeochromocytoma may serve as a clue to pituitary infarction.

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