Long-Term Effect of Prolonged TSH Suppression on the Skeletal System / 대한갑상선학회지

ABSTRACT

Thyroid hormone (TH) has a pivotal role in skeletal development, linear growth and maintenance of adult bone mass. Additionally, there are several studies which supported the direct effect of thyroid-stimulating hormone (TSH) on bone metabolism. As thyroid disease is one of the most common endocrine problems, the clinical impact of thyroid dysfunction on bone metabolism has been elucidated in various studies. Hyperthyroidism is associated with excessive loss of bone mass and an increased life-time risk for fractures. Adverse effects of hyperthyroidism in bone metabolism are distinct in postmenopausal women. Subclinical hyperthyroidism may also affect bone mineral density, however, its effect on fracture rate remains to be established. The effect of exogenous TH on bone tissue is somewhat controversial. Patients with hypothyroidism or differentiated thyroid carcinoma showing suppressed TSH caused by excessive TH replacement, especially postmenopausal women, appear to have lower bone mineral density and higher incidence of fractures than euthyroid subjects without exogenous TH. On the contrary, patients who are on exogenous TH with a normal range of TSH seem to have similar bone mineral density and fracture rates as euthyroid subjects. As most patients with differentiated thyroid carcinoma are taking exogenous thyroid hormone to suppress TSH, individual risks of both fracture and recurrence of carcinoma should be evaluated during the follow-up period of those patients. In general, in the management of thyroid disease, it should be taken into account that most thyroid dysfunction may result in reduced bone density and an increased fracture rate.