Cortisol suppression or peripheral sensitivity and activation are associated with diabetes, hypertension and fragility fractures in postmenopausal eucortisolemic women

2019 ◽  
Author(s):  
Carmen Aresta ◽  
Iacopo Chiodini ◽  
Agostino Gaudio ◽  
Cristina Eller-Vainicher ◽  
Valentina Morelli ◽  
...  
Keyword(s):  
Fragility Fractures ◽  
Cortisol Suppression

Systematic approaches to fragility fracture prevention

2014 ◽  
Vol 23 (01) ◽  
pp. 39-44
Author(s):  
D. B. Lee ◽  
P. J. Mitchell
Keyword(s):  
Fragility Fracture ◽  
National Policy ◽  
Fragility Fractures ◽  
Fracture Prevention ◽  
The United States ◽  
Fracture Liaison Service ◽  
Reimbursement Mechanisms ◽  
Future Fracture ◽  
National Coalition ◽  
Fracture Liaison

SummaryIndividuals who have suffered fractures caused by osteoporosis – also known as fragility fractures – are the most readily identifiable group at high risk of suffering future fractures. Globally, the majority of these individuals do not receive the secondary preventive care that they need. The Fracture Liaison Service model (FLS) has been developed to ensure that fragility fracture patients are reliably identified, investigated for future fracture and falls risk, and initiated on treatment in accordance with national clinical guidelines. FLS have been successfully established in Asia, Europe, Latin America, North America and Oceania, and their widespread implementation is endorsed by leading national and international osteoporosis organisations. Multi-sector coalitions have expedited inclusion of FLS into national policy and reimbursement mechanisms. The largest national coalition, the National Bone Health Alliance (NBHA) in the United States, provides an exemplar of achieving participation and consensus across sectors. Initiatives developed by NBHA could serve to inform activities of new and emerging coalitions in other countries.

Diabetes and osteoporosis

2011 ◽  
Vol 152 (29) ◽  
pp. 1161-1166 ◽  
Author(s):  
Zsuzsanna Valkusz
Keyword(s):  
Vitamin D ◽  
Type 1 Diabetes ◽  
Bone Mass ◽  
Fragility Fractures ◽  
Vitamin D Supplementation ◽  
Bone Collagen ◽  
Skeletal Changes ◽  
Glucagon Like Peptide 1 ◽  
Bone Quantity

Over the last decades a considerable amount of data has accumulated to indicate that metabolic and endocrine alterations of diabetes affect bone quantity and quality. These skeletal changes may increase the risk of bone fracture. There is strong evidence that in type 1 diabetes the decreased bone mass, lack of insulin and insulin-like growth factor-1, dysregulation of adipokines, and increased levels of proinflammatory cytokines are in the background of fragility fractures. In type 2 diabetes hyperinsulinemia, insulin resistance and increased body weight may result in an increase of bone mass; however, accumulation of advanced glycation end products within the bone collagen driven by glucotoxicity may increase the cortical porosity. There is a higher incidence of falls resulting from diabetes-related co-morbidities such as diabetic retinopathy, peripheral neuropathy, hypoglycemic episodes and sometimes from the medications. Vitamin D deficiency has special impact on glucose metabolism and the prevalence of diabetes. Vitamin D supplementation in childhood can decrease incidence of type 1 diabetes by 80%. The effect of thiazolidinediones, glucagon-like peptide-1 agonists and metformin, agents for treatment of diabetes open a new connection between bone, carbohydrate and fat metabolism. Orv. Hetil., 2011, 152, 1161–1166.

scholarly journals Early-Onset Osteoporosis

2021 ◽  
Author(s):  
Outi Mäkitie ◽  
M. Carola Zillikens
Keyword(s):  
Young Adults ◽  
Early Onset ◽  
Type I Collagen ◽  
Young Patients ◽  
Fragility Fractures ◽  
Underlying Disease ◽  
Bone Fragility ◽  
Sphingolipid Metabolism ◽  
Type I ◽  
Loss Of Function

AbstractOsteoporosis is a skeletal disorder with enhanced bone fragility, usually affecting the elderly. It is very rare in children and young adults and the definition is not only based on a low BMD (a Z-score < − 2.0 in growing children and a Z-score ≤ − 2.0 or a T-score ≤ − 2.5 in young adults) but also on the occurrence of fragility fractures and/or the existence of underlying chronic diseases or secondary factors such as use of glucocorticoids. In the absence of a known chronic disease, fragility fractures and low BMD should prompt extensive screening for secondary causes, which can be found in up to 90% of cases. When fragility fractures occur in childhood or young adulthood without an evident secondary cause, investigations should explore the possibility of an underlying monogenetic bone disease, where bone fragility is caused by a single variant in a gene that has a major role in the skeleton. Several monogenic forms relate to type I collagen, but other forms also exist. Loss-of-function variants in LRP5 and WNT1 may lead to early-onset osteoporosis. The X-chromosomal osteoporosis caused by PLS3 gene mutations affects especially males. Another recently discovered form relates to disturbed sphingolipid metabolism due to SGMS2 mutations, underscoring the complexity of molecular pathology in monogenic early-onset osteoporosis. Management of young patients consists of treatment of secondary factors, optimizing lifestyle factors including calcium and vitamin D and physical exercise. Treatment with bone-active medication should be discussed on a personalized basis, considering the severity of osteoporosis and underlying disease versus the absence of evidence on anti-fracture efficacy and potential harmful effects in pregnancy.

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