Thyroid-Stimulating Hormone-Mediated Hyperthyroidism

Abstract

Thyroid-stimulating hormone (TSH)-mediated hyperthyroidism is a rare condition, and the initial finding of an elevated serum T4 level but detectable serum TSH level must be confirmed by measuring serum free T4 by an equilibrium dialysis method. Serum-binding abnormalities and other confounding disorders and laboratory artifacts must be ruled out. Once inappropriate TSH hypersecretion is confirmed, one must differentiate between a pituitary neoplasm and the syndrome of thyroid hormone resistance. Patients with pituitary adenomas usually have no similarly affected family members, have minimal or no rise of serum TSH after thyrotropin-releasing hormone (TRH), have an elevated molar ratio of serum alpha subunits/TSH, and have imaging of the sella that could be abnormal. In contrast, patients with thyroid hormone resistance usually have affected relatives, show a brisk response of serum TSH after TRH, have a normal molar ratio of serum alpha subunits/TSH, usually have normal imaging of the sella, and a molecular diagnosis involving the beta receptor of thyroid hormone can be made in most cases. Therapy for TSH-producing adenomas is primarily surgical, and specific preoperative and postoperative measures could be indicated. Radiation therapy could be adjunctive, and long-term use of a slow-release somatostatin analog could improve patients not otherwise cured. Patients with thyroid hormone resistance need to avoid unwarranted thyroid ablative therapy. Their TSH level could be suppressed by cautious therapy with thyroxine with addition of a beta-blocker drug if tachycardia is a problem, although persons with certain mutations could respond favorably to every-other-day therapy with triiodothyronine.