ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 S10.3 | DOI: 10.1530/endoabs.63.S10.3

TSH suppressive therapy and bone

Claudio Marcocci


Italy.


Thyroid hormones stimulates bone turnover. Increased blood levels of thyroid hormones are associated with a negative balance at individual bone remodeling unit and bone loss. It is well know that hyperthyroidism is a common cause of secondary osteoporosis and increased risk of fragility fractures. Mild hyperthyroidism (suppressed TSH and normal free thyroid hormones), as observed in autonomous thyroid nodules or following administration of TSH-suppressive doses of thyroid hormones (TSH-ST), may be associated with bone loss and fragility fractures, particularly in postmenopausal women. Low/undetectable TSH may also contribute to the deleterious effects of TSH-ST on bone, as suggested by animal studies showing that TSH inhibits osteoclastogenesis, promotes apoptosis of mature osteoblasts and stimulate osteoblast differentiation and the association of bone mineral density and TSH in postmenopausal women. The guidelines suggest measuring bone mineral density (BMD) in assessing skeletal health women under TSH-ST, but recent data suggest that BMD measured by DXA may not be a reliable marker of bone fragility in this context. In this regard an increased rate of vertebral fractures has been reported in postmenopausal women receiving TSH-ST independently of BMD (normal, osteopenia and osteoporosis), suggesting a potential role of structural abnormalities. As a matter of fact, recent studies in postmenopausal women under long-term TSH-ST have shown a deterioration of trabecular bone score (TBS) in the absence of a decline in vertebral BDM measured by DXA, but a significant association of TBS with volumetric BMD as assessed by central quantitative computed tomography.

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