Recent findings suggest that thyroid stimulating hormone (TSH) is a negative regulator of skeletal remodeling by reducing both differentiation of osteoblasts and formation of osteoclasts. In addition, increased fracture risk in untreated hypothyroid patients has been reported to begin up to 8 years before diagnosis. The aim of the present study was to evaluate the effect of subclinical hypothyroidism on bone structure by using the heel QUS. Subjects were outpatients without any past or present history of thyroid disease. Among 210 postmenopausal women, 22 of 33 patients (Hypo), who had elevated serum TSH concentration (TSH≧4 μU/ml) with normal serum free thyroxine (FT 4) concentration, agreed to join to this study. We also randomly selected 24 control subjects (Cont) from 176 postmenopausal women with normal thyroid status. Calcaneus osteo sono assessment indices (OSI) of right feet were measured using the ultrasound bone densitometry AOS-100. Serum TSH concentrations in Hypo patients (5.31 ± 1.3 μU/ml) were higher than those in Cont patients (2.05 ± 1.1 μU/ml), and there was significant difference of FT4 concentrations (Cont 1.33 ± 0.15 ng/dl; Hypo 1.19 ± 0.17 ng/dl). OSI and its Z-score in Hypo subjects (OSI, 2.138 ± 0.152; Z-Score -0.322 ± 0.504 SD, Mean ± SD) were significantly lower than those in Cont subjects (OSI, 2.347 ± 0.243; Z-Score 0.322 ± 0.91 SD, Mean ± SD). Simple regression statistical analysis showed that OSI decreased according to the increase of serum TSH concentration (n = 47, P<0.037). In addition, multiple regression analysis showed that the elevation of serum TSH concentration was associated with the decrease of OSI. These results suggest that the elevation of serum TSH concentration in subclinical hypothyroidism affects not bone turnover but bone structure as assessed by QUS.
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