Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP36 | DOI: 10.1530/endoabs.37.EP36

ECE2015 Eposter Presentations Adrenal cortex (94 abstracts)

Pituitary macroadenoma with adrenocortical hypersecretion as the initial presentation of compensated adrenocortical failure

Serafino Lio & Monica Albin


Endocrine Unit, Ospedale Civile Oderzo-ASL n.9, Oderzo-TV, Italy.


Long-standing primary failure of pituitary-dependent endocrine glands may induce pituitary hyperplasia and adenoma both related to duration and severity of peripheral gland insufficiency, although the formation of an adenoma is rare. We report the case of an elderly man with pituitary macroadenoma but compensated adrenocortical failure. A 70-year-old man referred our centre in 2013 for headache and horizontal diplopia. MRI revealed pituitary macroadenoma (1.9×1.1×2.2 cm) with suprasellar extension, invasion of cavernous sinus, very close to the optic chiasm, localised T1 weighted-hyperintensity area suggestive of bleeding. Hormonal evaluation showed central hypothyroidism, hypogonadotropic hypogonadism, normal PRL, and GH/IGF1 serum levels, ACTH hypersecretion (fourfold above normal upper limit) with cortisol basal serum level at 6.1 μg/dl and peak level after corticotropin stimulation test (1 μg i.v.) at 21.2 μg/dl; renin and aldosterone serum levels were in the normal range; antibodies to adrenal cortex were negative, while those 21OH-Ab and very-long chain fatty acid unfortunately could not sampled; ANA-AMA-ADNA-ASMA-APCA, antiphosholipid Ab and TgAb-TPOAb were negative. Adrenal glands appeared normal at CT scan. Medical history was negative for tubercolosis. Weigt loss, hypotension, dehydratation, hyperpygmentation, fever, abdominal pain, as well as hyponatremia, hypo- or hyperkaliemia, hypo- or hypercalcaemia were not present; type 2 diabetes mellitus was diagnosed. Transphenoidal endoscopic excision was performed; the specimen was identified as adenoma at microscopical examination and immunocytochemical analysis showed diffuse immunoreactivity for ACTH, absent immunoreactivity for FSH, PRL, TSH, and GH; Ki67 <3% with p53 not expressed. In conclusion, this case shows that the formation of a pituitary adenoma is also possible in the forms yet compensated adrenal insufficiency; likely duration of adrenal failure, rather than the severity, may led a major role in the formation of the pituitary adenoma.

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