Effects of thyroxine excess on peripheral organs

Aim of this paper is to review the effects of T4 excess due to exogenous thyroid hormone administration on target organs, with particular regard to heart, bone, liver and pituitary. Therapy with TSH-suppressive doses of T4 has been shown in a cross sectional echocardiographic study to increase left ventricular contractility and to induce mild myocardial hypertrophy. Whether the latter represents a risk for the patients remains a matter of debate. Clinically it does not seem to be important. The long-term evaluation of T4-therapy has provided controversial results. Some have reported that T4-treated patients under the age of 65 have an increased risk of ischemic heart disease, whereas others were unable to find any change in morbidity, mortality and quality of life, including cardiovascular events. Thyroid hormones enhance both osteoblastic and osteoclastic activities in cortical and trabecular bone. Overt hyperthyroidism is well known to represent a risk factor for osteoporosis. Studies in the late eighties have suggested a reduced bone density in T4-treated patients, with a particular risk for cortical bone in postmenopausal women. More recent studies have failed to show any substantial T4-related change in bone mass. Taken together the evidence of the literature suggests that TSH-suppressive therapy with T4 is, if well controlled, probably not associated with significant loss of bone mass at least in premenopausal women. A mild elevation of the activity of hepatic enzymes (glutathione-S-transferase, gamma glutamyltransferase, alanine amino-transferase, angiotensin-converting enzyme) has been observed in patients under T4 treatment in TSH-suppressive doses.(ABSTRACT TRUNCATED AT 250 WORDS)