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

Endocrine Abstracts (2017) 50 EP083 | DOI: 10.1530/endoabs.50.EP083

Secondary adrenocortical insufficiency and renal impairment in a patient presenting with Hyperprolactinaemia

Muhammad Waseem Aslam & Jonathan Rippin

Northampton General Hospital, Northampton, UK.

We report a rare case of 19 year old lady who was referred to us with galactorrhoea associated with hyperprolactinemia (PRL-1049 mU/L). MRI, arranged by GP, had revealed an enlarged pituitary with a 14×8 mm macroadenoma slightly distorting the optic chiasma. Visual fields were normal on confrontation but showed restricted fields in both eyes on Goldman perimetry. She was commenced on cabergoline to which her galactorrhoea responded quickly. Full pituitary profile was not completed at the first visit, but she acknowledged some fatigue and slight cold sensitivity on direct questioning at a subsequent visit.

Her profile revealed severe primary hypothyroidism (TSH- 742 mU/L and fT4<3.4). Cortisol was 283 nmol/L; gonadotrophins were normal, as was her IGF-1. Her creatinine was raised to 141 umol/L, despite her slender built. Creatine Kinase was moderately elevated (297 iU/L). She was commenced on Levothyroxine 50 ug OD along with hydrocortisone (15 mg Am and 10 mg mid-afternoon). A short synacthen test, carried out less than 2 weeks after starting hydrocortisone, showed an abnormal response with cortisol rising from 108 to 289 at 30 minutes and 390 at 60 minutes. Her subsequent ACTH (after omitting hydrocortisone the previous evening and delaying the morning does till after the test) was 17.1 ng/L; cortisol was 30 nmol/L at the time. Adrenal antibodies were negative. In due course her visual fields improved on perimetry with slight regression in size of pituitary gland.

Her primary Hypothyroidism appears to have caused compensatory pituitary hyperplasia with associated hyperprolactinaemia due to high TRH +/− pituitary stalk compression and her pituitary hyperplasia also caused secondary adrenal insufficiency. Her hypothyroidism was sufficiently profound to cause renal impairment.

Learning points: The various aetiologies need to be borne in mind when assessing patients with hyperprolactinaemia. Primary Hypothyroidism should be considered as a potential cause. Modest prolactin rises should not be attributed to macroadenoma without other causes having been ruled out.

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