DECREASED SERUM IGF-I AND DEHYDROEPIANDROSTERONE-SULFATE MAY BE RISK-FACTORS FOR THE DEVELOPMENT OF REDUCED BONE MASS IN POSTMENOPAUSAL WOMEN WITH ENDOGENOUS SUBCLINICAL HYPERTHYROIDISM

Postmenopausal women with endogenous subclinical hyperthyroidism seem to have reduced bone mass, which does not correlate with serum thyroid hormone levels. Relative insufficiencies of IGF-I and dehydroepiandro sterone sulphate (DHEAS) might be additional risk factors for low bone density in these patients. We measured IGF-I, IGF-binding protein-3 ( IGFBP-3) and DHEAS levels together with bone mineral density (BMD) of the femoral neck and lumbar spine in women with an autonomously functi oning thyroid nodule, Sixty-three women were classified as subclinical hyperthyroid (31 pre- and 32 postmenopausal) and 39 as overt hyperthy roid (16 pre- and 23 postmenopausal) and results were compared with da ta obtained from 41 age-matched euthyroid healthy women. In premenopau sal women BMD was reduced only in the overt hyperthyroid group, and on ly in the spine, to 92% (P <0.05). Serum IGF-I as well as IGFBP-3 were increased in the manifest hyperthyroid group, to 157% (P <0.001) and 129% (P <0.05) respectively, whereas DHEAS levels did not change in ei ther premenopausal patient group, In postmenopausal women BMD was sign ificantly reduced both in the subclinical hyperthyroid group (spine to 90% and femoral neck to 88%; P <0.05), as well as in the hyperthyroid group (spine to 78% and femoral neck to 86%; P <0.01). In contrast to premenopausal women, serum IGF-I and IGFBP-3 did not change in the tw o groups who were postmenopausal and serum DHEAS levels were reduced t o 58% (P <0.001) in both postmenopausal groups with subclinical as wel l as overt hyperthyroidism. In the same two groups of patients, serum IGF-I and DHEAS levels correlated with BMD (femoral neck; both r=0.50, P <0.05). In conclusion, women with a solitary autonomous thyroid nod ule with subclinical hyperthyroidism have reduced BMD only if they are postmenopausal. This is probably due to the effect of subtle increase s in thyroid hormone production together with lack of oestrogen protec tion of the skeleton. But additional risk factors for the development of enhanced bone loss might be a state of relative IGF-I and DHEAS ins ufficiency in these patients as well as in postmenopausal women with o vert hyperthyroidism.