Hormone replacement after thyroid and parathyroid surgery

Abstract

Background: Hypothyroidism and hypocalcemia are common after thyroid and parathyroid surgery. In this article, the authors provide clinically-oriented recommendations to help surgeons, general practitioners, internists, and endocrinologists give their affected patients adequate hormone replacement therapy.

Methods: Selective evaluation of original articles and reviews that were retrieved by a PubMed search over the years 1980 to 2010, as well as of the recommendations of medical societies including the Endocrine Society (USA), the German Society for Endocrinology (Deutsche Gesellschaft für Endokrinologie), and the American and European Thyroid Associations.

Results: Important issues in L-thyroxine replacement therapy include: the selection of the hormone preparation (T4 or T4/T3), combination with iodine (yes/no), the definition of therapeutic TSH ranges (particularly after surgery for thyroid cancer), the extent of remaining thyroid tissue after goiter surgery and its significance, underlying diseases, and drug interactions. The major issues in the treatment of postoperative hypoparathyroidism are: the selection of suitable calcium and vitamin D preparations, the definition of therapeutic goals, the treatment of hypercalciuria and hyperphosphatemia, and the option of recombinant parathormone therapy.

Conclusion: Effective treatment requires an appropriate choice of medication and an understanding of its pharmacokinetics as well as of the possible effects of the patient's underlying disease, comorbidities, and other medications on its absorption and metabolism.

Figure

The hierarchical functional organization of the thyrotropic axis. The hypothalamus secretes thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary lobe to secrete thyrotropin, also known as thyroid-stimulating hormone (TSH). TSH, in turn, regulates the synthesis and release of the thyroid hormones T4 (ca. 100 μg/day) and T3 (ca. 10 μg/day). This regulation occurs by way of negative feedback of the T4 and T3 concentrations on the secretion of TRH and TSH. Nearly all of the T4 and T3 in the bloodstream is bound to the binding proteins thyroxine-binding globulin (TBG), thyroxine-binding albumin (TBA), and thyroxine-binding prealbumin (TBPA). The free hormones fT4 and fT3 account for only 0.1% and 1% of circulating T4 and T3, respectively. Deiodinase enzymes in the peripheral tissues catalyze the conversion of fT4 to the biologically more active hormone fT3, while a small amount of inactive reverse T3 (rT3) is also produced. An important consideration for the design of an effective treatment regimen is the half-life of the two main thyroid hormones: ca. 190 hours for T4 and ca. 19 hours for T3