Endocrine Abstracts

Introduction: Thyroid hormones play an important role in bone metabolism. The potential action of prolonged levothyroxine therapy on bone mass reduction is still a matter of debate.

Objective: The aim of the present study was to assess the effects of levothyroxine treatment on bone mineral density (BMD) and biochemical bone turnover markers.

Methods: We determined thyroid function – TSH and free T₄ (FT₄), regional BMD parameters (lumbar spine, femoral neck, trochanter and Ward’s triangle) and biochemical bone turnover markers (serum calcium, parathyroid hormone, alkaline phosphatase and osteocalcin and urinary deoxypyridinoline) in 58 women with benign nodular goiter. Forty one were submitted to suppressive levothyroxine therapy (group A) and seventeen remained without therapy for an identical period (group B). We performed initial and final biochemical and densitometric evaluations and compared variations between groups, for all parameters.

Results: The population studied was characterized by a mean age of 51±13 years and TSH 1.77±1.3 μUI/ml. None of the patients had initial osteopenia/osteoporosis or alterations in biochemical evaluation. The mean daily dose of levothyroxine was 97.5±32.8 μg and the mean duration of treatment was 10.3±6.8 months (mean cumulative dose of 30.8±24.3 mg). Considering all patients, there was a significant reduction in TSH (P=0.000) and an increase in FT₄ (P=0.001), alkaline phosphatase (P=0.004) and deoxypyridinoline (P=0.029) at the end of the study. Those variations were significantly more pronounced in group A (P=0.000, P=0.002, P=0.003 and P=0.02, respectively). There was no significant difference in BMD parameters between groups.

Conclusions: Our data suggest that levothyroxine suppressive therapy raises bone turnover. However, medium-term therapy does not seem to induce an increase in bone demineralization. It would be necessary to amplify the evaluation period to fully exclude a deleterious effect of levothyroxine therapy on BMD.