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These findings suggest that bone mineral density is decreased in patients with hyperthyroidism and that TSH receptor antibody, osteocalcin, and alkaline phosphatase are sensitive markers of bone metabolism alterations in hyperthyroidism.

Because of the previous controversial findings in studies of bone mineral density in patients with hyperthyroidism with older methodologies, we assessed bone mineral density in 15 Japanese patients with Graves' disease (8 males and 7 females) before and after treatment using dual energy X-ray absorptiometry (DEXA). Bone mineral density of the lumbar vertebrae and the femur, and thyroid function, and several metabolic parameters were measured before treatment and again after patients achieved a euthyroid state following treatment with methimazole for 4 to 20 months (mean 10.6 months). The bone mineral density of patients was calculated as the percentage of the mean value (%BMD) in an age- and sex-matched control group, and correlations between the changes in bone mineral density and metabolic parameters before and after treatment were investigated. The %BMD of vertebrae in patients with Graves' disease before treatment was 89.7% of that found in the normal population. When patients became euthyroid after treatment, %BMD increased significantly to 94.9%, although it still remained below the control level. TSH receptor antibody, osteocalcin, and alkaline phosphatase were elevated before treatment, but decreased significantly after treatment. The change between pre- and posttreatment TSH receptor antibody was negatively correlated with the change in bone mineral density. In conclusion, these findings suggest that bone mineral density is decreased in patients with Graves' disease and that successful treatment of hyperthyroidism results in a significant increase in bone mineral density within a short period of time. Furthermore, TSH receptor antibody is a useful marker of changes in bone metabolism in this group of patients.

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