Endocrine Abstracts

TSH-secreting pituitary adenomas are a rare cause of hyperthyroidism. The diagnosis should be considered in all hyperthyroid patients, especially those with a diffuse goiter and no extrathyroidal manifestations of Graves’ disease. Most TSH-secreting adenomas secrete only TSH. Most patients have the typical symptoms and signs ofhyperthyroidism (eg, palpitations, tremor, heat intolerance), but a few patients have mild or even no hyperthyroid symptoms. Other clinical features include a diffusegoiter, visual field deficits, headache, and, in women, menstrual disturbances and galactorrhea. Thyroid function tests shows normal or high serum TSHconcentrations and high serum total and free thyroxine (T4) and triiodothyronine (T3)concentrations. Approximately 50 to 85 percent of patients with TSH-secreting pituitaryadenomas (particularly macroadenomas) have a high serum concentration of the alphasubunit of glycoprotein hormones. The differential diagnosis should be done with assay interference and resistence to thyroid hormone. The initial treatment of a TSH-secreting pituitary adenoma is medical therapy (withsomatostatin analogs) to restore euthyroidism prior to surgery. Once euthyroid, transsphenoidal resection of the tumor is the most appropriate definitive therapy forpatients with TSH-secreting pituitary adenomas.

Here I present the case of a 43-year-old woman, referred by her Primary Care physician due to an incidental analytical finding of hyperprolactinemia. The patient was clinically asymptomatic, without symptoms derived from pituitary hyper or hypofunction, nor compression symptoms. The initial study revealed a 12 mm pituitary adenoma on MRI. The pituitary function study revealed slightly elevated T4 levels, with TSH in the normal range and an elevated alpha subunit.

There was doubt between a non-functioning or a TSH-producing adenoma. Therefore, a new determination of thyroid hormones was obtained in another laboratory, with the same result; thyroid autoimmunity, which was negative, and a genetic study was subsequently performed, which ruled out resistance to thyroid hormones. The patient did not tolerate the TRH test. After one year of treatment with somatostatin analogues, TSH and T4 levels have been normalized, as well as the tumor has shrunk. Clinically, the patient remains asymptomatic, visual campimetry is normal, and she has not noticed adverse effects derived from medical treatment. In this case we see the difficulty of diagnosis, given the infrequency of the entity and the absence of florid symptoms, as well as the efficacy of treatment with somatostatin analogues, both in terms of normalization of thyroid function and reduction of tumor size.