title: Adverse effects of thyroid hormones.
abstract: The adverse health effects of thyrotoxicosis have been carefully documented and most practitioners are familiar with the clinical consequences for the patient. Until recently, many patients experienced the adverse effects of excessive thyroxine dosages. Which can now be avoided by the application of highly sensitive immunometric assays for monitoring serum thyrotrophin (thyroid-stimulating hormone; TSH) levels. However, sensitive monitoring of serum thyrotrophin levels has led to the frequent recognition of biochemical subclinical hyperthyroidism (isolated suppression of thyrotrophin). Because of the increased recognition of this condition, the adverse effects of thyroxine therapy can be divided into those associated with subclinical hyperthyroidism and those associated with the euthyroid state. Investigation of the potential clinical consequences of thyrotrophin-suppressing dosages of thyroxine has dominated studies over the last decade, with less attention being given to euthyroid patients. It appears that the adverse effects of thyroxine are considerably more common when serum thyrotrophin has been suppressed. They are usually manifested in older patients as increased bone mineral loss in postmenopausal women and as cardiac effects in patients with intrinsic heart disease. These patients may have subtle behavioural alterations and other clinically silent organ effects that occur infrequently. Children who are euthyroid while taking thyroxine occasionally develop pseudotumour cerebri shortly after starting hormone replacement for hypothyroidism. Otherwise, thyroxine dosages that render patients euthyroid, as evidenced by thyrotrophin values that are within the normal range, rarely cause adverse effects. Thus, avoidance of dosages that cause thyrotrophin suppression, when not clinically indicated, is the primary approach to the management of these adverse effects.
authors.affiliation: Division of Endocrinology and Diabetes, Vanderbilt University Medical Center, Nashville, Tennessee, USA. john.williams@mcmail.vanderbilt.edu
authors.forename: J B
authors.initials: JB
authors.lastname: Williams
mesh_terms: D000375:Aging / Q000097:blood; D002318:Cardiovascular Diseases / Q000139:chemically induced; D002986:Clinical Trials as Topic; D005067:Euthyroid Sick Syndromes / Q000097:blood / Q000139:chemically induced*; D005260:Female; D006801:Humans; D015663:Osteoporosis, Postmenopausal / Q000139:chemically induced; D011559:Pseudotumor Cerebri / Q000139:chemically induced; D018382:Thyroid Hormone Resistance Syndrome / Q000097:blood / Q000139:chemically induced*; D013971:Thyrotoxicosis / Q000097:blood / Q000139:chemically induced*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000009:adverse effects*
chemical_list: D013972:Thyrotropin; D013974:Thyroxine