DIAGNOSIS OF ENDOCRINE DISEASE: Evaluation of bone fragility in endocrine disorders

Abstract

An underlying disease affecting bone health is present in up to 40 and 60% of osteoporotic postmenopausal women and men respectively. Among the disorders leading to a secondary form of osteoporosis, the endocrine diseases are highly represented. A frequent finding in patients affected with an endocrine-related forms of bone disease is that the skeletal fragility is partially independent of the bone density, since the fracture risk in these patients is related more to a reduction of bone quality than to a decrease of bone mass. As a consequence, bone mineral density evaluation by dual-X-ray absorptiometry may be inadequate for establishing the risk of fracture in the setting of the endocrine-related forms of osteoporosis. In the recent years, several attempts to non-invasively estimating bone quality have been done. Nowadays, some new tools are available in the clinical practice for optimising the fracture risk estimation in patients with endocrine disorders. The aim of this review is to summarise the evidence regarding the role of the different imaging tools for evaluating bone density and bone quality in the most frequent forms of endocrine-related osteoporosis, such as obesity, diabetes, acromegaly, thyrotoxicosis, primary hyperparathyroidism, hypercortisolism and hypogonadism. For each of these disorders, data regarding both the current available tools and the future possible new techniques for assessing bone fragility in patients with endocrine diseases are reported.

Bone Metabolism and Vitamin D Implication in Gastroenteropancreatic Neuroendocrine Tumors

“…This association with low BMD observed in GEP-NET patients could be explained by the fact that, besides bone metastasis [13], GEP-NETs are associated with several factors that could interfere with the normal bone homeostasis, including hypersecretion of substances biologically active on bone tissue, miRNA expression, nutritional status, which in turn could be affected by medical and surgical treatments, vitamin D deficiency, worsening quality of life and aspects correlated to MEN1 [21]. Among the hormones that could be secreted by functioning GEP-NET, 5-HT, cortisol and PTH-rp could play a major role in affecting bone metabolism [28,41,48,53]. Nutritional status in GEP-NET patients is deeply affected by the excessive production of gastrointestinal hormones, surgical resection changing the anatomy of the gastrointestinal tract, and treatment with SSA and chemotherapy.…”

“…Similarly, hypersecretion of parathyroid hormone (PTH)-related protein determines, with different mechanisms, an imbalance between bone resorption (normal or increased, especially in the early phase) and bone formation (impaired, particularly in the chronic phase), with a consequent increased risk of fractures [53]. In addition to this direct effect on bone, glucocorticoid excess may also have a negative impact on vitamin D levels [52].…”

Thyroid Hormone Diseases and Osteoporosis

“…Data of both techniques are reported in terms of T scores (i.e., standard deviations from the young adult values) or Z scores (i.e., standard deviation from the expected normal values). DXA scanners are also used for vertebral fracture assessment, which offer a high degree of accuracy in diagnosing fractures [34]. Other methods include quantitative computed tomography (QCT), which is likely more accurate than DXA.…”

Bone densitometry by radiofrequency echographic multi-spectrometry (REMS) in acromegaly patients

“…Acromegaly is a rare disease characterised by elevated levels of growth hormone (GH) and insulin-like growth factor I (IGF-I) mainly due to pituitary adenoma [1]. An excess amount of these hormones leads to a lot of systemic complications including secondary osteoporosis and vertebral fractures [2,3]. Growth hormone and IGF-I are anabolic hormones responsible for enhanced bone formation and achievement of peak bone mass.…”

“…The impact on cortical bone is complexthe excess of GH and IGF-I promotes development of cortical thickness, but at the same time it contributes to increased cortical porosity [9]. What is more, a negative impact on trabecular tissue was observed [2,10]. Impaired structure of trabecular bone was reported not only in active disease but also after achieving remission [11,12].…”