Endocrine Abstracts

Case history: A 51-year old female presented to emergency with occipital headache for 5 days on a background of recurrent headaches for over a year. She had been diagnosed with Hashimoto’s disease at the age of 30 and given levothyroxine, which she discontinued 5 years ago due to aversion to take medications. She had noticed cold intolerance and low energy. At presentation her body mass index was 25.26 kg/m² and the physical exam was unremarkable; specifically, there was no goiter, blood pressure was 99/71, heart rate was 70 bpm and her temperature was 36.5°C.

Investigations: A CT scan of the head was done for headaches that showed a 9 mm hypodense sellar lesion and the baseline pituitary hormone testing drawn at 10:30 AM in emergency showed: TSH=496.8 mIU/L, prolactin=44.4 ug/L (N=5.2–27 ug/L), IGF-1=(N=81–238 ug/L), and cortisol=131 nmol/L (N=120–500 nmol/L before 930AM). MRI of the sella showed a mildly expanded sella turcica with a homogeneously enhancing enlarged pituitary measuring 1.3 cm×1.7 cm×1.4 cm.

Results and treatment: Based on the investigations, a diagnosis of pituitary hyperplasia secondary to primary hypothyroidism was made and levothyroxine was initiated. She remained poorly compliant with levothyroxine and at 9-month follow-up her TSH had decreased to 13.9 mIU/L, MRI demonstrated a normal-sized homogeneous pituitary gland that measured 7.5 mm in maximal height. At 18 months TSH was 4.11 mIU/L, T4 13.5 pmol/L, prolactin 10.6 ug/L and pituitary MRI was stable.

Conclusions and points for discussion: A diffusely enhancing sellar mass may be due to pituitary hyperplasia or inflammatory/infiltrative disorders. In primary hypothyroidism, lack of feedback to the hypothalamus leads to increased TRH secretion and thyrotroph hypertrophy¹. Pituitary hyperplasia is reported in 25–81% of patients with untreated primary hypothyroidism and can develop within weeks of the onset of hypothyroidism^2,3. Clinical features may include signs of hypothyroidism, optic nerve compression, headaches, menstrual irregularity and galactorrhea; goiter is uncommon⁴. Hyperprolactinemia is thought to be due to the stimulatory effect of TRH on lactotrophs or inhibition of dopamine effect on prolactin release⁴. Thyrotroph hyperplasia can resemble an adenoma radiographically, which may result in inappropriate treatment with dopamine agonists or surgery^3,4. Thyroid hormone replacement rapidly shrinks hyperplasia^1,4,5; however, surgery is indicated in compressive symptoms or nonresponse to levothyroxine therapy^4,6,7.