ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 EP101 | DOI: 10.1530/endoabs.63.EP101

Pituitary apoplexy and transient hypopituitarism

Teresa Rego1, Luis Cerqueira2 & Ana Agapito1


1Endocrinology Department - Centro Hospitalar Universitário de Lisboa Central, Lisboa, Portugal; 2Neuroradiology Department - Centro Hospitalar Universitário de Lisboa Central, Lisboa, Portugal.


Introdution: Pituitary apoplexy (PA) is a rare clinical syndrome caused by sudden hemorrhage or infarction of the pituitary gland. PA may be the form of presentation of a pituitary tumor or occur during follow-up of a previously diagnosed macroadenoma. A high suspicion índex is required to establish a timely diagnosis.

Case report: A 54-year-old man was referred to Endocrinology department (04/2015) due to a pituitary macroadenoma. He reported sexual disfunction for 2 years and no headache or visual changes. On physical examination he presented normal BP, facial/scalp vitiligo, no stigmata of hypercortisolism or acromegaly and absent visual field defects upon confrontation. Laboratory work-up showed normal pituitary function except slightly hiperprolactinemia - 43.9 ng/ml (3.4–19.4) and magnetic resonance imaging (MRI) (03/2015) revealed a macroadenoma with suprasellar extension (18×11×10 mm) that contacted optic chiasm and signs of small circumscribed intratumoral hemorrhage. Hook phenomenon and macroprolactinemia were excluded and Neurophthalmology observation was normal. Two months later the patient returned complaining of fatigue, adynamia, anorexia and weight loss of 10 kg. He denied headache or visual disturbance. At this time laboratory work-up showed: serum cortisol 1.1 ug/dl (3.7–19.4); ACTH 19.8 pg/ml (< 46); TSH 0.51 uUI/ml (3.4–19); FT4 0.46 ng/dl (0.7–1.48); total testosterone 0.35 ng/ml (1.4–9.2); LH 0.7 mUI/ml (0.57–12.07); FSH 1.71 mUI/ml (0.95–11.95); PRL 95 ng/ml (3.4–19.4), IGF-1 32.4 ng/ml (87–238). MRI revealed a large sellar lesion compressing optic chiasm and remodeling sellar floor with bilateral extension to cavernous sinus. In medial and right antero-lateral position a hypertense component was found in T1/T2 weights. PA and hypopituitarism were admitted and hormonal replacement therapy was started with prednisolone 7.5 mg/day, levothyroxine 75 mcg/day, testosterone 250 ml/1 ml 4/4 weeks and bromocriptine 5 mg/day. In the following 6 months, a complete recovery of the pituitary function was observed and replacement therapy was gradually withdrawn. Imaging study demonstrated collapse of the cystic/hemorrhagic macroadenoma measuring 14×10 mm with partial reabsorption of the hematic content. Surveillance was continued and at the last visit(10/2018) the patient was asymptomatic without therapy and imaging reevaluation showed expansion of the cystic/necrotic cavity of the pituitary macroadenoma, currently measuring 15×20 mm, with predominantly suprasellar development. Neurophthalmology reevaluation was normal.

Comments: In this patient, subclinical apoplexy of a non-functioning pituitary adenoma with transient hypopituitarism were observed. In the cases described about 80% of patients develop hypopituitarism, being ACTH deficiency the most relevant. In our patient we observed multiple pituitary deficiencies followed by full recovery. It should also be of note the reexpansion of necrotic/cystic cavity and consequent increase of the residual macroadenoma, that precludes a close surveillance.

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