Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 15 P220

SFEBES2008 Poster Presentations Pituitary (62 abstracts)

A case of post-traumatic brain injury with idiopathic hyperprolactinaemia and growth hormone deficiency in a child

Lanitha Srikugan & Ian Scobie


Medway Maritime Hospital, Gillingham, UK.


A 16-years old boy was referred for endocrine assessment of growth retardation. He had normal growth to age 7 years (tallest in his class) following which he sustained frontal head injury and subsequently exhibited growth retardation. There was no other confounding history. At age 16, height=1.47 m (below 3rd centile; mid-parental height=1.77 m), BMI=21, he was pre-pubertal. Full blood count, biochemistry and chest X-ray were unremarkable. He was 3 years behind in bone age, had low total testosterone (0.6 nmol/l), low GH (<1 mU/l) and elevated PRL (1713 mU/l). Insulin stimulation test demonstrated adequate cortisol and TSH response, but markedly blunted GH response. Pituitary MRI was normal. He was initiated on bromocriptine and Genotropin, with which his nadir PRL was 11 mU/l and progressed through puberty (without testosterone replacement), attaining a height of 1.7 m 2 years later. After 3 years, bromocriptine and genotropin were stopped. PRL rose to 1482 mU/l and he developed erectile dysfunction. Repeat MRI pituitary was normal. Five further attempts to withdraw dopamine agonist resulted in rebound hyperprolactinaemia, up to 2795 mU/l (undetectable macroprolactin). LHRH test revealed good LH but flat FSH response. He suffered fertility problems but did achieved natural conception. He was never re-started on GH replacement as his general well being was good. We withheld dopamine agonist for the last two years. He continues to remain well with normal libido, PRL=1278 mU/l, testosterone=13.4 nmol/l, FSH=3.5 U/l, LH=4.6 U/l, TSH=2.41 mU/l, IGF-1=12.5 mU/l, normal pituitary MRI.

We have illustrated a case of idiopathic hyperprolactinaemia, GH deficiency, abnormal hypothalamic-gonadotrophin axis in the absence of any anatomical hypothalamic, pituitary or stalk lesion. We conjecture that traumatic brain injury led to probable pituitary stalk injury. We wish to highlight some management issues arising from this case:

• whether continued treatment with dopamine agonist is indicated,

• what further biochemical monitoring is necessary bearing in mind the continuing good health of the patient.

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