Hyperthyroidism is the most common cause of thyrotoxicosis. It is characterized by excessive activity of the thyroid gland and can manifest with symptoms such as tachycardia, palpitations, unintentional weight loss, diaphoresis, anxiety, and exophthalmos, especially in the case of Graves’ disease. The majority of cases of thyrotoxicosis are due to autoimmune phenomena (particularly Graves’ disease) as well as inflammatory phenomena (such as postviral subacute thyroiditis). Rare cases of hyperthyroidism are due to pituitary thyrotrope adenomas (a phenomenon called central hyperthyroidism), with an approximate prevalence of one per million for these adenomas [
1]. Pituitary thyrotrope adenomas are almost entirely benign and secrete thyroid-stimulating hormone (TSH) to stimulate the thyroid gland; thus, characteristic laboratory findings of central hyperthyroidism are elevated TSH, T4, and T3 levels. TSH-related compounds (especially the alpha subunit of glycoprotein hormones) also tend to be elevated in central hyperthyroidism [
2]. The majority of thyrotrope pituitary adenomas are macroadenomas [
3]. Thyrotrope macroadenomas frequently secrete more than one type of hormone (including growth hormone and prolactin), with 10 out of 21 patients in one study having ten plurihormonal adenomas and another study finding 14 of 90 thyrotrope adenoma patients with acromegaly [
3,
4]. Typical central hyperthyroid symptoms are less severe than the common autoimmune hyperthyroid symptoms and are usually limited to goiter and palpitations with rarer instances of cardiac arrhythmias [
1,
3]. Hyperthyroidism affects approximately 0.1–0.4% of all pregnancies [
5]. During pregnancy, hCG (human chorionic gonadotropin) stimulates the TSH receptor and increased levels of thyroxine-binding globulin are present [
6]. Increased stimulation of the TSH receptor may exacerbate a hyperthyroid state [
7]. Hyperthyroidism can have deleterious effects on pregnancy, including maternal hypertension, low birth weight, preeclampsia, heart failure, and even spontaneous abortion [
8]. Diagnosis of central hyperthyroidism is typically accomplished by measuring elevated TSH in the context of high T4 and T3 when compared with the reference range, and thyrotrope macroadenomas are usually found to be hypoenhancing macroadenomas when imaged with magnetic resonance imaging (MRI) [
4,
9]. Thyrotropin-releasing hormone stimulation testing and T3 suppression testing are used to confirm the diagnosis of central hyperthyroidism [
1]. Although diagnosis of TSH-secreting pituitary macroadenoma appears straightforward, there has been considerable diagnostic delay in many cases, with one study finding a mean diagnostic delay of approximately 6 years [
10].
Surgical removal of the thyrotrope pituitary adenoma is the first-line treatment of thyrotrope pituitary macroadenomas [
1]. Antithyroid drugs such as methimazole or propylthiouracil are used to achieve euthyroidism before resection of the adenoma. Surgical success rates are higher if the diagnosis is made earlier, and the effectiveness of the surgery may be diminished if the adenoma extends into the extrasellar and parasellar regions [
1,
3]. If this treatment fails, somatostatin analog therapy is typically used. This treatment both decreases circulating TSH levels and shrinks goiters. For patients who did not achieve complete resolution of central hyperthyroidism after pituitary resection, postoperative radiation or somatostatin analog therapy typically yielded favorable outcomes. No exact criteria currently exist to characterize successful remission of a thyrotrope adenoma, so success rates are usually determined by resolution of hyperthyroid symptoms and normalization of TSH, T4, and T3 [
1,
4]. Follow-up is typically done through two to three visits during the first postoperative year and once-yearly visits thereafter, and recurrence of the TSH-secreting adenoma does not typically occur.