Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 P448

ECE2007 Poster Presentations (1) (659 abstracts)

Hyperprolactinemia in post-acute phase after severe TBI or SAH is mostly iatrogenic or due to physical stress

Ingo Kilimann 1 , Günter Karl Stalla 2 & Friedrich von Rosen 1


1Neurological Hospital Bad Aibling, Bad Aibling, Germany; 2Max Planck Institute of Psychiatry, Munich, Germany.


Background: Recent studies demonstrated partial or complete hypopituitarism in 30–70% of survivors of traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH). Hyperprolactinemia may indicate damage of the pituitary stalk or the hypothalamus. Physical and psychological stress and a considerable list of medications can also lead to increased prolactin values.

Methods: Prolactin was measured in 103 male and 54 female patients aged 14 to 89 years after severe TBI or SAH in the post-acute or chronic state (mean 4 month after onset) as part of a hormone screening also including cortisol, fT4, testosterone, estradiol und IGF1. Cut-off levels for normal prolactin was 18.0 ng/ml in male and 25.0 ng/ml in female patients. Medication, body temperature, serum glucose and C-reactive protein were registered.

Results: 23% of the screened patients had increased levels of prolactin. Significantly more male were found to have hyperprolactinemia (25% of males vs. 8% of females).

All patients with hyperprolactinemia had common hyperprolactinemic factors such as infection (n=16), hypoglycemia (blood glucose below 70 mg/dl) (n=2) or medications known to increase prolactin levels such as dopamin antagonists (n=29), central catecholamine depletors (n=8), GABA agonists (n=6) or opiats (n=4).

Hyperprolactinemia was not correlated with deficiency of other hormones.

Conclusion: Hyperprolactinemia in patients after severe TBI or SAH is usually secondary to medication or physical stress and does not indicate damage to the hypothalamus or pituitary gland.