Osteoporotic hip fractures in non-elderly patients: relevance of associated co-morbidities

Pasoto, Sandra Gofinet; Yoshihara, Liz Andrea Kawabata; Maeda, Lucy C.; Bernik, Márcia Martins Silveira; Lotufo, Paulo A.; Bonfá, Eloísa; Pereira, Rosa Maria Rodrigues

doi:10.1007/s00296-011-2154-x

Cited by 15 publications

(12 citation statements)

References 22 publications

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“…Relatively few studies regarding the effects of estrogens on bone loss in men have been conducted 9 . Chronic alcohol abusers have a higher risk for osteoporotic fractures compared to non-drinkers 37,38 . Findings from this study may be used to better understand the biological effects of GEN and to provide additional information regarding use of isoflavone supplements to reduce the risks of osteoporosis in men.…”

Section: Discussionmentioning

confidence: 99%

Genistein supplementation increases bone turnover but does not prevent alcohol-induced bone loss in male mice

Yang

Mercer

Alund

et al. 2014

Exp Biol Med (Maywood)

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Chronic alcohol consumption results in bone loss through increased bone resorption and decreased bone formation. These effects can be reversed by estradiol (E2) supplementation. Soy diets are suggested to have protective effects on bone loss in men and women, as a result of the presence of soy protein-associated phytoestrogens such as genistein (GEN). In this study, male mice were pair-fed (PF) a control diet, an ethanol (EtOH) diet or EtOH diet supplemented with 250 mg/kg of GEN for 8 weeks to test if GEN protects against bone loss associated with chronic drinking. Interestingly, alcohol consumption reduced cortical area and thickness, and trabecular bone volume in both EtOH and EtOH/GEN groups when compared to the corresponding PF and PF/GEN controls, p<0.05. However, in the trabecular bone compartment, we observed a significant increase in overall trabecular bone density in the PF/GEN group compared to the PF controls. Bone loss in the EtOH-treated mice was associated with inhibition of osteoblastogenesis as indicated by decreased alkaline phosphatase staining in ex vivo bone marrow cultures, p<0.05. GEN supplementation improved osteoblastogenesis in the EtOH/GEN cultures compared to the EtOH group, p<0.05. Vertebral expression of bone formation markers, osteocalcin, and runt-related transcription factor 2 (Runx2), were also significantly up-regulated in the PF/GEN and EtOH/GEN groups compared to the PF and EtOH-treated groups. GEN supplementation also increased expression of receptor activator of nuclear factor κ-B ligand (RANKL) in the PF/GEN, an increase that persisted in the EtOH/GEN-treated animals (p<0.05) and increased basal hydrogen peroxide production and RANKL mRNA expression in primary bone marrow cultures in vitro, p<0.05. These findings suggest GEN supplementation increases overall bone remodeling, and in the context of chronic alcohol consumption, does not protect against the oxidative stress associated EtOH-mediated bone resorption.

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Section: Discussionmentioning

confidence: 99%

Genistein supplementation increases bone turnover but does not prevent alcohol-induced bone loss in male mice

Yang

Mercer

Alund

et al. 2014

Exp Biol Med (Maywood)

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“…Given the association between older age and substance abuse with reduced bone mineral density (BMD) and osteoporosis in the general population [31,32,33], the choice of antiretroviral regimen in patients with HIV infection with additional risk factors for osteoporosis needs to be carefully considered. Although the rarity of these events precluded multivariate analysis in the current report, on univariate analysis, fractures occurred significantly less frequently with EFV/FTC/TDF versus EVG/COBI/FTC/TDF (IRR 0.47; 95% CI: 0.27, 0.81 and IRD −3.85 per 1000 person-years; 95% CI: −5.02, −2.78).…”

Section: Discussionmentioning

confidence: 99%

Real-World Assessment of Renal and Bone Safety among Patients with HIV Infection Exposed to Tenofovir Disoproxil Fumarate-Containing Single-Tablet Regimens

et al. 2016

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ObjectivesTenofovir disoproxil fumarate (TDF)-containing antiretroviral regimens have been associated with an increased incidence of renal and bone adverse outcomes. Here, we estimated the real-world incidence of renal and bone adverse outcomes among patients with HIV infection receiving different TDF-containing single-tablet regimens (STRs).MethodsThis cohort study used US health insurance data spanning the years 2008–2014. We identified HIV-infected patients aged ≥18 years (all HIV patients) and those with ≥6 months of continuous enrollment prior to initiating efavirenz/emtricitabine/TDF (EFV/FTC/TDF), rilpivirine/FTC/TDF (RPV/FTC/TDF) or elvitegravir/cobicistat/FTC/TDF (EVG/COBI/FTC/TDF). Renal adverse outcomes were identified using renal International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis codes. Bone adverse outcomes were identified using ICD-9-CM diagnosis codes for fracture. Incidence rates (IRs) and associated 95% confidence intervals (CIs) were estimated assuming a Poisson distribution, and outcomes between STRs were compared using IR ratios (IRRs) and IR differences (IRDs).ResultsWe identified 9876 and 10,383 eligible patients for the renal and fracture analyses, respectively. Observed IRs for renal adverse outcomes were 9.7, 10.5, 13.6, and 18.0 per 1000 person-years among those receiving EFV/FTC/TDF, RPV/FTC/TDF, or EVG/COBI/FTC/TDF, or all HIV patients, respectively. Corresponding values for IRs of fracture were 3.4, 3.6, 7.2, and 4.4 per 1000 person-years, respectively. Renal adverse outcomes with EFV/FTC/TDF were significantly less frequent than with EVG/COBI/FTC/TDF (IRD −3.96; 95% CI: −7.31, −1.06). No IRR differences were identified for the renal analysis. Fractures with EFV/FTC/TDF were significantly less frequent than with EVG/COBI/FTC/TDF (IRR 0.47; 95% CI: 0.27, 0.81 and IRD −3.85; 95% CI: −5.02, −2.78).ConclusionsIn this large real-world database, observed IRs for renal adverse outcomes with TDF-containing STRs were lower or similar to those for all HIV patients, with the lowest IRs observed among patients receiving EFV/FTC/TDF. Compared with all HIV patients, the observed IR for fracture was higher with EVG/COBI/FTC/TDF, comparable with RPV/FTC/TDF, and lower with EFV/FTC/TDF.

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“…2 In fact, recent data suggests that diabetes may be the strongest independent risk factor for osteoporotic hip fracture in non-elderly patients 3–4 . Chronic hyperglycemia, hypoinsulinemia or insulin resistance, hypercalciuria, osteoblast dysfunction, inflammation, disruption of the growth hormone (GH): IGF-I: IGFBP system and diabetes pharmacotherapy may all contribute to this skeletal fragility.…”

Section: Introductionmentioning

confidence: 99%

The Role of Vitamin D in the Metabolic Homeostasis of Diabetic Bone

Thrailkill

Fowlkes

2012

Clinic Rev Bone Miner Metab

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Most studies across a variety of geographic locations suggest that vitamin D insufficiency is more common in individuals with type 1 diabetes (T1D) compared to the general population. In type 2 diabetes (T2D), while obesity is commonplace and lower vitamin D levels are present in obese adolescents and adults, the association between vitamin D insufficiency and T2D is less clear. Studies suggest that the relationship between T2D and vitamin D may be concurrently influenced by ethnicity, geography, BMI and age. None-the-less, diabetic osteopathy is a significant co-morbidity of both forms of diabetes, and is characterized by micro-architectural changes that decrease bone quality leading to an increased risk for bone fracture in both disorders. The question remains, however, to what degree vitamin D homeostasis contributes to or exacerbates skeletal pathology in diabetes. Proposed mechanisms for vitamin D deficiency in diabetes include: 1) genetic predisposition (T1D); 2) increased BMI (T2D); 3) concurrent albuminuria (T1D or T2D); or 4) exaggerated renal excretion of vitamin D metabolites or vitamin D binding protein (T1D, T2D, animal models). The specific effects of vitamin D treatment on diabetic osteoporosis have been examined in rodents, and demonstrate skeletal improvements even in the face of untreated diabetes. However, human clinical trial data examining whether vitamin D status can be directly related to or is predictive of bone quality and fracture risk in those with diabetes is still needed. Herein, we provide a review of the literature linking vitamin D, diabetes and skeletal health.

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Osteoporotic hip fractures in non-elderly patients: relevance of associated co-morbidities

Cited by 15 publications

References 22 publications

Genistein supplementation increases bone turnover but does not prevent alcohol-induced bone loss in male mice

Genistein supplementation increases bone turnover but does not prevent alcohol-induced bone loss in male mice

Real-World Assessment of Renal and Bone Safety among Patients with HIV Infection Exposed to Tenofovir Disoproxil Fumarate-Containing Single-Tablet Regimens

The Role of Vitamin D in the Metabolic Homeostasis of Diabetic Bone

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