Endocrine Abstracts

Introduction: The prevalence of pituitary thyrotropin secreting tumors (TSH-omas) is 1-2 cases per million inhabitants, most of them being macroadenomas. The differential diagnosis may be challenging, especially for microadenomas.

Case Report: A 50-year-old male was observed at the endocrinology department with multinodular goiter. He noticed progressive neck enlargement over the previous months but denied other complaints. There was no family history of thyroid pathology. He presented hot sudorific hands and a large nodular goiter. Laboratory evaluation revealed a predominantly high T3 with non-suppressed TSH (TSH 1.73 μU/ml (Reference range – RR: 0.55–4.78), T3-2.08 ng/ml (RR: 0.60–1.81), T4-11.7 μg/dl (RR:4.5-10.9), FT3-7.74 pg/ml (RR: 2.3–4.2), FT4-1.93 ng/dl (RR: 0.8–1.76)). The sonography showed an enlarged thyroid gland with bilateral nodules of 37, 50 and 70 mm. Additional evaluation revealed negative anti-thyroid antibodies, high total testosterone and SHBG, chromogranin A, alpha-subunit of glycoproteic hormones (αGS) and αGS/TSH ratio, but otherwise normal pituitary function and no evidence of other endocrine neoplasia. There was no TSH or αGS response to TRH administration and the MRI revealed a 6 mm pituitary lesion. Thyroid nodules cytology was benign. A TSH-oma was admitted and long-acting octreotide administered, with normalization of thyroid function and subsequent trans-sphenoidal tumor resection. Pathological analysis revealed an adenoma with positive TSH immunohistochemistry. Over the next months, there was TSH suppression and secondary hypothyroidism, during which levothyroxine was administered, and subsequent recovery of normal thyroid function. Slight reduction of the goiter was observed.

Discussion: Distinguishing pituitary TSH-omas from thyroid hormone resistances may be challenging, but it is important for correct therapeutic options and avoid endocrine and neurological complications. Baseline thyroid function and sonography do not adequately distinguish both entities, but the absent family history, high SHBG, αGS and αGS/TSH ratio, blunt TSH and αGS response to TRH, and FT3/FT4 normalization with long-acting octreotide, together with a small but existent pituitary adenoma, prompted a microthyrotropinoma diagnosis.