Endocrine Abstracts

Introduction: In primary hypothyroidism, the increase in TRH may cause hyperplasia in the pituitary gland. It has been reported that long-standing hypothyroidism might also cause irreversible pituitary damage, which may lead to a deficiency in one or more pituitary hormones. Herein, we report a case with primary autoimmune hypothyroidism causing pituitary enlargement mimicking pituitary macroadenoma and secondary adrenal insufficiency.

Case: A 17-year-old female patient was diagnosed with primary hypothyroidism when she was 12 years old and levothyroxine-sodium treatment was started. Three years ago, she applied to a tertiary medical center with headache. A solid mass lesion in pituitary gland measuring approximately 15 mm diameter was reported at magnetic resonance imaging (MRI). After hormonal evaluation the mass was considered as a non-functioning macroadenoma and follow-up was recommended. Secondary adrenal insufficiency was observed in follow-up and hydrocortisone treatment was added. She referred to neurosurgery for the operation. Repeated MRI of the sella reported that there was a 10 x 10 mm nodular lesion suspicious for macroadenoma, and pituitary hyperplasia and hypophysitis should be considered in the differential diagnosis. Serum TSH was found suppressed while ft4 and ft3 were in normal range. The patient referred to our center for a differential diagnosis. The patient had fatigue and hair loss complaints. She had regular menstrual cycle and no galactorrhea. The visual field examination was normal. She was using levothyroxine-sodium and hydrocortisone. Macroadenoma wasn’t considered when the serial MRI of sella was reevaluated. Pituitary hyperplasia or hypophysitis was suspected as a primary diagnosis. No signs of systemic disease were found clinically in terms of hypophysitis. Serum acute phase reactants and IGG4 levels were normal, and the anti-PIT 1 antibody was negative. Thyroid autoantibodies were positive. Serum TSH level was found increased (>100 uIU/ml) while serum fT4 was low. The hypothalamic-pituitary-adrenal axis couldn’t be evaluated due to long-term steroid usage. Other pituitary hormones were normal. We found out that she didn’t use levothyroxine-sodium regularly. Previous TSH measurements were occasionally >300 uIU/ml. Pituitary hyperplasia due to irregular replacement was considered. She was warned about regular usage. It was planned to taper and discontinue hydrocortisone during follow-up and reevaluate the pituitary-adrenal-axis.

Discussion: Despite the recent advances in MRI examinations, it might be still difficult to differentiate pituitary adenoma, hyperplasia and hypophysitis. Therefore, the patient’s medical history, clinic and laboratory results should be evaluated together carefully. Accurate identification of such patients is important for avoiding unnecessary surgery and costly MRI follow-up.