MON-368 - Pituitary Hyperplasia and Hyperprolactinemia in Uncontrolled, Episodic Primary Hyperthyroidism

Background:
Pituitary hyperplasia due to long standing, uncontrolled primary hypothyroidism is rare. Lack of negative feedback from very low circulating thyroid hormone levels results in excessive TRH secretion, which in turn leads to thyrotroph and lactotroph hyperplasia. Here, we present an interesting case of episodic severe hypothyroidism during periods of infection resulting in pituitary hyperplasia and hyperprolactinemia.
Clinical

Case:
A 23-year-old woman with a history of endometriosis and primary hypothyroidism presented to the endocrine clinic for initial evaluation of a pituitary lesion. She was diagnosed with hypothyroidism at the age of 18 and was noted to have positive anti-TPO and anti-thyroglobulin antibodies. Her thyroid function was well controlled with Synthroid 75-125 mcg daily from age 18 to 20 years. Following this, she was switched to Tirosint due to concern for malabsorption and her TSH levels were stable while on 125 mcg daily. In 2023, she was hospitalized with TSH levels between 100-400 µIU/mL (NR 0.4-5.0) and very low free T4 after she had a sinus infection/bronchitis treated with antibiotics. Symptoms of hypothyroidism at these times included fatigue, cold intolerance, constipation and swelling in face, hands, arms and legs. Repeat episodes of infections and antibiotic treatment were associated with several recurrences of significantly elevated TSH levels and low free T4 despite compliance with therapy. Patient underwent levothyroxine absorption testing, which showed adequate absorption. Ultimately, her Tirosint dose was increased to 1050 mcg weekly. In between these episodes of severe hypothyroidism, her thyroid function was well controlled. MRI showed heterogenous enhancing abnormality (2.0 x 0.8 x 1.2 cm) involving entirety of pituitary fossa extending into the suprasellar cistern, with mass effect on the optic chiasm and hypervascularity suggestive of pituitary hyperplasia. Biochemical workup showing elevated prolactin 117 ng/ml (NR 5-26), and low IGF-1 of 99 ng/dl (NR 101-347), both of which subsequently normalized without specific intervention. Further biochemical testing showed normal AM cortisol, ACTH, FSH, LH, and dexamethasone suppression test.

Conclusion:
Pituitary hyperplasia may mimic adenomas and can be difficult to distinguish on imaging. It is important to adequately differentiate between them, as pituitary hyperplasia due to severe hypothyroidism can be treated with levothyroxine replacement therapy whereas pituitary adenoma may require surgical or dedicated medical management. Close follow up with repeat imaging is vital, with many patients demonstrating a decrease in size of pituitary abnormality after thyroid levels start to improve.

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