Fragility fractures in older persons with altered thyroid function
Abstract
Thyroid hormones are pleiotropic peptides with complex action on the human economy. The skeleton is a
target tissue for thyroid hormone’s action, which is illustrated by the consequences of thyroid hormone excess
and deficiency during development and during aging. Thyroid disorders are more frequently observed in older
than in younger persons. Thyrotoxicosis is an established cause of secondary osteoporosis. Overt hyperthyroidism and iatrogenic hyperthyroidism due to over-replacement of thyroid hormone may result in fragility fractures. Endogenous or exogenous subclinical hyperthyroidism is associated with reduced bone density, especially in cortical bone in older women. Fragility fracture risk seems to be closely related to the degree of thyroid-stimulating hormone suppression and to other risk factors, including older age. Overt hyperthyroidism and endogenous subclinical hyperthyroidism in older persons should be treated to reduce the risk for fragility fractures, atrial fibrillation and related mortality risk. The risk for fragility fractures in older people, especially in postmenopausal women, taking suppressive doses of levothyroxine for thyroid cancer can be diminished by treatment with the minimal effective suppressive dose and in some cases, by adding an antiresorptive or bone forming therapy where indicated. Replacement therapy for overt hypothyroidism should be regularly adjusted to avoid TSH suppression and consequent increased risk of fragility fractures.
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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Copyright
© Società Italiana di Gerontologia e Geriatria (SIGG) , 2016
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