Bone mineral density in well‐differentiated thyroid cancer patients treated with suppressive thyroxine: A systematic overview of the literature

Quan, May Lynn; Pasieka, Janice L.; Rorstad, O.P.

doi:10.1002/jso.10043

Cited by 68 publications

(47 citation statements)

References 29 publications

(91 reference statements)

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“…Heemstra et al (2006) analysed four prospective and 12 cross-sectional studies of pre-menopausal women receiving suppressive doses of T 4 , and concluded that treatment with suppressive doses of T 4 did not affect BMD, although a full meta-analysis could not be performed due to heterogeneity. This conclusion was consistent with two preceding systematic literature reviews (Faber & Galloe 1994, Uzzan et al 1996, Quan et al 2002, Murphy & Williams 2004, Heemstra et al 2006 and two meta-analyses (Faber & Galloe 1994, Uzzan et al 1996. Currently, there are no prospective data on fracture risk in pre-menopausal women receiving suppressive doses of T 4 .…”

Section: Suppressive Doses Of T 4 In Differentiated Thyroid Cancersupporting

confidence: 87%

The skeletal consequences of thyrotoxicosis

Nicholls¹,

Brassill²,

Williams³

et al. 2012

Journal of Endocrinology

102

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Euthyroid status is essential for normal skeletal development and the maintenance of adult bone structure and strength. Established thyrotoxicosis has long been recognised as a cause of high bone turnover osteoporosis and fracture but more recent studies have suggested that subclinical hyperthyroidism and long-term suppressive doses of thyroxine (T 4 ) may also result in decreased bone mineral density (BMD) and an increased risk of fragility fracture, particularly in postmenopausal women. Furthermore, large population studies of euthyroid individuals have demonstrated that a hypothalamicpituitary-thyroid axis set point at the upper end of the normal reference range is associated with reduced BMD and increased fracture susceptibility. Despite these findings, the cellular and molecular mechanisms of thyroid hormone action in bone remain controversial and incompletely understood. In this review, we discuss the role of thyroid hormones in bone and the skeletal consequences of hyperthyroidism.

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Section: Suppressive Doses Of T 4 In Differentiated Thyroid Cancersupporting

confidence: 87%

The skeletal consequences of thyrotoxicosis

Nicholls¹,

Brassill²,

Williams³

et al. 2012

Journal of Endocrinology

102

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“…Consequently, thyrotoxicosis is an important cause of secondary osteoporotic fracture (Mosekilde et al 1990, Cummings et al 1995, Franklyn et al 1998, Vestergaard et al 2000, Vestergaard & Mosekilde 2002, Murphy & Williams 2004) and even subclinical hyperthyroidism has been associated with decreased bone mineral density and increased fracture risk in postmenopausal women (Bauer et al 2001, Quan et al 2002, Murphy & Williams 2004, Heemstra et al 2006, Kim et al 2006, Morris 2007.…”

Section: Thyroid Hormone Receptor Mutant Micementioning

confidence: 99%

The skeletal phenotypes of TRα and TRβ mutant mice

Bassett

Williams

2008

Journal of Molecular Endocrinology

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Analysis of mice harbouring deletions or mutations of T 3 receptor a (TRa) and b (TRb) have clarified the complex relationship between central and peripheral thyroid status and emphasised the essential but contrasting roles of T 3 in skeletal development and adult bone. These studies indicate that TRa1 is the predominant TR expressed in bone and that T 3 exerts anabolic actions during growth but catabolic actions in the adult skeleton. Examination of key skeletal regulatory pathways in TR mutant mice has identified GH, IGF-1 and fibroblast growth factor signalling and the Indian hedgehog/parathyroid hormone-related peptide feedback loop as major targets of T 3 action in chondrocytes and osteoblasts. Nevertheless, although increased osteoclastic resorption is a major feature of thyrotoxic bone loss and altered osteoclast activity is central to the skeletal phenotype of TR mutant mice, it remains unclear whether T 3 has direct actions in osteoclasts. Detailed future analysis of the molecular mechanisms of T 3 action in bone will enhance our understanding of this emerging field and has the potential to identify novel strategies for the prevention and treatment of osteoporosis.

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“…L-T4 therapy may also be accompanied by iatrogenic latent or even overt hyperthyroidism. Overt hyperthyroidism is associated with an increased risk of osteoporosis, while whether subclinical hyperthyroidism affects the skeleton is under debate [7,8]. Effects of the latter on bone mineral density (BMD) have been addressed in a number of studies with somewhat controversial results [9][10][11][12][13][14][15].…”

mentioning

confidence: 99%