Pituitary-thyroid hormone interactions in states of hyper- and hypothyroidism: Clinical implications in 2000

Circulating thyroxine (T4) and triiodothyronine (T3) are regulated by a neg ative feedback system involving hypothalamic TRH, pituitary TSH, and the th yroid hormones, T4 and T3. In states of severe primary hypothyroidism, pitu itary enlarge ment may occur as a result of thyrotroph hyperplasia and caus e mass effects similar to pituitary adenomas. Conversely, thyrotoxicosis ma y 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 hyp othyroidism, alterations in growth hormone, gonadotropins, and prolactin, r espectively, can be attended by impaired somatic growth, menstrual irregula rities, and galactorrhea. Tn states of hyperthyroidism, most of these manif estations are reversed, as exemplified by the accelerated growth in childre n with thyrotoxicosis, delayed menarche, and oligomenorrhea in young thyrot oxic women, with contrasts with the syndrome of precocious puberty in child ren with 1 degrees hypothyroidism. Hyperthyroidism can be attended by enhan ced 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 hy pothyroidism. 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 sho uld lead to improved diagnosis and management of these important problems.