Pituitary-Thyroid Hormone Interactions in States of Hyper- and Hypothyroidism

Abstract

Circulating thyroxine (T4) and triiodothyronine (T3) are regulated by a negative feedback system involving hypothalamic TRH, pituitary TSH, and the thyroid hormones, T4 and T3. In states of severe primary hypothyroidism, pituitary enlargement may occur as a result of thyrotroph hyperplasia and cause mass effects similar to pituitary adenomas. Conversely, thyrotoxicosis may be caused by pituitary TSH-secreting adenomas. States of thyroid hormone deficiency and excess play important roles in the regulation of all other protein hormones released by the pituitary. In hypothyroidism, alterations in growth hormone, gonadotropins, and prolactin, respectively, can be attended by impaired somatic growth, menstrual irregularities, and galactorrhea. In states of hyperthyroidism, most of these manifestations are reversed, as exemplified by the accelerated growth in children with thyrotoxicosis, delayed menarche, and oligomenorrhea in young thyrotoxic women, with contrasts with the syndrome of precocious puberty in children with 1° hypothyroidism. Hyperthyroidism can be attended by enhanced clearance of cortisol evoking rises in ACTH, and thyrotoxic patients on glucocorticoid replacement therapy may require additional steroid therapy. Finally, hyponatremia from impaired free water excretion can be seen in hypothyroidism. This can lead to lethargy and frank coma. This abnormality in water metabolism is corrected completely by thyroid hormone administration. Awareness of these thyroid hormone-dependent pituitary endocrinopathies should lead to improved diagnosis and management of these important problems. The Endocrinologist 2000; 10: 118-123 Learning Objectives: In what ways do hypothalamic and pituitary hormone release interact with thyroid hormone deficiency or excess to alter body growth, puberty, and reproductive function? Review interactions between hypo- and hyperthyroidism on the one hand, and changes in hypothalamic-pituitary-adrenal axis function and water/electrolyte homeostasis on the other. In patients with pituitary enlargement and abnormal thyroid function, when does the primary fault reside in the pituitary and when in the thyroid?