Bone mass, bone turnover, body composition, and calcium homeostasis in former hyperthyroid patients treated by combined medical therapy.

Abstract

It is still uncertain whether bone mass and bone turnover are completely normalized after treatment of hyperthyroidism. The aim of the present investigation was to determine bone mass, bone turnover, body composition, and calcium homeostasis in former hyperthyroid patients who had been euthyroid for at least 4 years following combined medical therapy. Thirty-nine former hyperthyroid patients and 67 normal sex- and age-matched controls participated. Height, body weight, and body composition were similar in the two groups. All patients were euthyroid. However, serum FT3I (free T3-index) was reduced by 9% (p < 0.01) in the patients compared to controls, serum FT4I was normal, while serum TSH was nonsignificantly reduced by 39%. No significant differences were observed between patients and controls with respect to total or regional bone mineral content (BMC) or density (BMD). The former hyperthyroid patients had slightly higher serum calcium (2.35 +/- 0.06 vs. 2.32 +/- 0.07 mmol/L, p < 0.05) and lower serum phosphate (1.15 +/- 0.15 vs. 1.24 +/- 0.15 mmol/L, p < 0.01) than their controls. Renal excretion of calcium and serum levels of magnesium, 1,25-vitamin D and intact PTH were unchanged. Renal excretion of pyridinoline was increased by 30% (p < 0.05) in the patients, whereas the remaining resorptive markers, renal excretion of hydroxyproline and deoxypyridinoline and serum cross-linked carboxy-terminal teleopeptide of type I collagen (ICTP) were unaltered. Among the formative bone markers the average serum carboxy-terminal propeptide of human type I procollagen (PICP) level was 12% lower (p < 0.05) than in the control group, whereas serum levels of osteocalcin and total and bone alkaline phosphatase were normal. In conclusion, former hyperthyroid patients treated by combined medical therapy have normal bone mineral content and density in spite of minor variations in thyroid hormones and skeletal homeostasis.