Hyperthyroidism, thyroid hormone therapy, and bone.

Abstract

Clinically symptomatic osteoporosis and fractures from thyrotoxicosis have been rare since the availability of antithyroid drugs and radioiodine for the treatment of hyperthyroidism. However, the widespread use of bone density measurements and sensitive TSH assays in the past decade has demonstrated that women taking levothyroxine with subclinical hyperthyroidism have reduced bone density. Cortical bone is affected more than trabecular bone, and postmenopausal women are at a greater risk than premenopausal women. However, it is uncertain whether subclinical hyperthyroidism is associated with an increased risk of fracture. Hypothyroidism is associated with an increase in cortical bone width. The initiation of levothyroxine treatment in hypothyroid women results in a reduction in cortical bone width to levels seen in euthyroid controls after 6-12 months. There is no reduction in bone density when women with subclinical hypothyroidism are treated with levothyroxine for a year. A single study showing reduced bone density in patients receiving chronic levothyroxine replacement therapy requires confirmation and raises an important question: Does levothyroxine replacement therapy, which results in higher serum thyroxine concentrations than those seen in euthyroid controls, accurately mimic physiology?