ECE2013 Poster Presentations Clinical case reports - Thyroid / Others (62 abstracts)
UOC Endocrinology, Ospedale Fatebenefratelli, Isola Tiberina, Rome, Italy.
Introduction: Bone loss in thyroid dysfunction was first described by von Recklinghausen. Elevated bone turnover and decreased bone mass result when thyroid hormone levels are high and TSH levels suppressed. The changes in bone mass are impressive even in patients whit subclinical hypertiroidism, where thyroid hormones are within the normal range, but TSH is low or undetectable. Evidence show that endogenous and exogenous TSH suppression is associated with an increased fracture risk.
Methods: We studied 1487 postmenopausal women (average age 65.47±9.94). TSH (0.3 to 4.2 μUI/ml) were correlated with the prevalence of vertebral fractures, classified by morphometric study. Postmenopausal patients showed different thyroid functional status. They received DXA evaluation and fulfilled WHO criteria for Osteoporosis.
Results: Osteopenia was diagnosed in 587 patients (39.5%), osteoporosis in 875 (58.8%). In osteopenic group 148 women (10%) showed vertebral fractures, while 645 osteoporotic patients (42.7%) had fractures. In addition, major vertebral fractures (>25%) were present in 170 patients (11.4%) with subclinical hyperthyroidism (TSH <0.3 μUI/ml). This result was compared to group of 60 women (4%) that showed TSH>0.3 μUI/ml (total percentage significant (P<0.05)). There was a correlation between subclinical hyperthyroidism and BMD t-score values (correlation, Spearmans ρ=0.18 is P<0.001).
Conclusions: Our data suggest the relationship between TSH plasma levels and vertebral fractures in women with postmenopausal osteoporosis and osteopenia. Because of the strong correlation between low TSH levels and high fracture risk, which appears to be dissociable for long-term decrements in BMD, we suggest maintaing TSH levels during replacement therapy to above 1 mU/ml, unless there is a clinical rationale for TSH suppression as in thyroid cancer patients. In these patients, admittedly without clinical evidence of efficacy, we propose the empiric use of an oral biphosphonate to prevent the high turnover osteoporosis and associated fracture risk.