SFEBES2013 Poster Presentations Pituitary (71 abstracts)
University Hospitals Bristol NHS Trust, Bristol, Avon, UK.
A 35-year-old woman was referred with biochemical hyperthyroidism (T4 30 pmol/l; T3 7 pmol/l) without TSH suppression (5.4 mIU/l). She was 7 weeks pregnant following natural conception, and reported no symptoms of hyperthyroidism. Migraines had been a feature in very early pregnancy, but her medical history was otherwise unremarkable and there was no significant family history. Examination findings were entirely normal.
Investigations confirmed negative thyroid heterophile antibodies. Interpretation of usual investigations for a TSH-secreting pituitary adenoma was complicated by pregnancy (elevated α-subunit >24 μg/l, prolactin 722 mIU/l and SHBG 209 nmol/l; LH and FSH fully suppressed). Pituitary MRI showed asymmetrical enlargement (16×11 mm) considered to be disproportionate to the gestational period. Mutational analysis of the thyroid hormone receptor gene was negative (although 15% of cases have no detectable mutations).
As thyroid hormones were only mildly elevated, surveillance was commenced with regular thyroid function tests and trimesteral visual field assessment. There were no fetal or maternal complications encountered and she had a normal delivery at term. Post-partum investigations show persistent α-subunit elevation (4 μg/l), but the rest of her hormone profile including prolactin has normalised. We are currently planning future management.
There are only three reports of management of TSH-secreting pituitary adenoma in pregnancy, all identified before conception. Issues raised here are i) the difficulty distinguishing thyroid resistance syndrome from pituitary driven disease in pregnancy given the potential for false negative results and changes in hormone profiles; ii) the challenges identifying the appropriate time to commence treatment given the elevated risk of miscarriage and fetal morbidity in association with maternal hyperthyroidism; iii) concerns for potential complications of accelerated hyperthyroidism (due to the βHCG surge) or visual disturbance (due to pituitary enlargement); and iv) identifying the appropriate treatment to commence should it be required.