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Summary: A poorer functional status at the time of fracture is a predictor of non-adherence to oral bisphosphonates initiated after a hip fracture, and suggests further opportunities for optimization of secondary fracture prevention in this high-risk population.Introduction: Low adherence to treatment is a problem in post-fracture secondary prevention. We aimed to analyze the prognostic factors (related and predictive) associated with non-adherence to oral bisphosphonate prescription for hip fracture due to bone fragility (HFBF) 12 months after discharge from an acute geriatric unit.Methods: Prospective study of bivariate data analyzing related and multivariate factors predicting non-adherence of oral bisphosphonates at 12 months after treatment for HFBF. The statistical study was performed with SPSS 19.0.0.Results: We attended 368 patients with HFBF. At discharge, oral bisphosphonates were prescribed to 226 (61.42%) patients. At 12 months, we followed up 160 (70.7%) patients, 104 (65%) of whom had non-adherence to oral bisphosphonates. Bivariate analysis (adherent vs. non-adherent): age (83.79 ± 5.82 vs. 85.78 ± 5.80, p = .029); Lawton and Brody Index (4.29 ± 3.40 vs. 2.67 ± 3.31, p = .004); baseline Barthel Index (BI) (85.89 ± 21.99 vs. 74.18 ± 26.70) (p = .004); BI at admission (18.84 ± 10.00 vs. 14.47 ± 11.71, p = .004); BI at discharge (34.20 ± 15.40 vs. 27.45 ± 16.71, p = .011); baseline Functional Ambulation Classification (5.66 ± 0.98 vs. 5.43 ± 0.99, p = .025). Multivariate analysis: BI 0.980 (0.965-0.995, p = .007). Discriminatory capacity of the AUC model (± 95% CI): 0.634 (0.545-0.722).Conclusions: At 12 months, there was low adherence to treatment with oral bisphosphonates in our model. A lower BI prior to treatment is a predictive factor for non-adherence treatment with oral bisphosphonate. [ABSTRACT FROM AUTHOR]

Objectives: Hip fracture is often associated with loss of physical function and institutionalization. The aim of this study is to describe the prognostic factors for discharge to home and residing there 12 months after a hip fracture., Methods: A prospective study that includes patients aged ≥ 69 years that live at home before the fracture, admitted from June 1st, 2010, to May 31st, 2013. We registered the demographic data, presurgical function and cognitive assessment, surgical waiting time, type of fracture and complications during hospitalization., Results: We included 273 patients (mean age 84.8 ± 6.1 years; 80% women), 130 (47.6%) were discharged directly to their own home. The predictors of discharge to home were a lower Geriatrics Dementia Scale score (OR 1.42; 95% CI 1.17-1.71; p < 0.001), a higher Barthel Index score at discharge (OR 1.07; 95% CI 1.05-1.10; p < 0.001) and a longer hospital stay (OR 1.14; 95% CI 1.02-1.27; p = 0.019). At 12 months, 169 (63.5%) were still residing at home. Predictors of residing at home 12 months after the hip fracture were age (OR 1.07; 95% CI 1.02-1.12; p = 0.010), the discharge Barthel Index score (OR 0.96; 95% CI 0.94-0.98; p < 0.001), the Geriatrics Dementia Scale score (OR 1.27; 95% CI 1.05-1.52; p = 0.013), the surgical waiting time (OR 3.42; 95% CI 1.077-10.89; p = 0.037) and Charlson comorbidity index (OR 1.27; 95% CI 1.05-1.55; p = 0.016)., Conclusion: Prognostic factors for discharging to home and remaining there 12 months after a hip fracture are those that reflect a better health condition prior to the fracture and better functionality at the hospital discharge for hip fracture.

Aim: Hip fracture as a result of bone fragility is characterized by poor health outcomes in the medium and long term. Our goal was to compare a new orthogeriatric model with the old trauma model and evaluate improvements in clinical management., Methods: We carried out a comparative unicentric study, a historical sample (trauma model) collected from 1 June 2007 to 31 May 2010, versus a prospective sample (orthogeriatric model) collected from 1 June 2010 until 31 May 2013. We included all patients aged >69 years with hip fracture as a result of bone fragility., Results: A total of 792 patients were evaluated (mean age 84.3 years). The surgical waiting period went from 2.70 days in the trauma model to 1.86 days in the orthogeriatric model (P < 0.001); the average stay was 15.76 days in the trauma model, and for the orthogeriatric model was reduced to 5.90 days (P < 0.001); mortality went from 4.5% to 1.3% (P ≤ 0.010); 1 month readmission for hip dislocation was reduced from 2.3% to 0.5% (P = 0.032). After a 6-month follow up, we had 302 trauma model patients and 287 orthogeriatric model patients. After 1 year, we had 288 patients in the trauma model and 264 patients in the orthogeriatric model. The main cause of abandonment was death, 108 patients (27.3%) in the trauma model and 100 patients (27.5%) in the orthogeriatric model (P = 0.951)., Conclusions: When we compared the two models, we found statistically significant better results in the preoperative waiting period, average stay, hospital mortality and 1 month readmission as a result of hip prosthesis luxation in favor of the orthogeriatric model. Geriatr Gerontol Int 2018; 18: 407-414., (© 2017 Japan Geriatrics Society.)

Introduction and Development: Angelman syndrome (AS) is characterised by severe mental retardation (MR), the absence of language, ataxia and/or tremors in the extremities and a characteristic behavioural phenotype with a happy behaviour and hyperactivity. Patients often show signs of microcephaly and convulsions. Prader-Willi syndrome (PWS) is characterised by acute hypotonia and feeding problems in the neonatal period, and triggers an uncontrollable appetite in the infant that leads to obesity. Most patients have some degree of MR, behavioural disorders and hypogonadism. Both pathologies are caused by a number of genetic mechanisms that affect the 15q11-q13 region regulated by genomic imprinting, which means that only one of the two copies of the genes in this region will be functional, depending on which parent they come from. The physical or functional absence of genes that are only expressed by the mother's chromosome 15 causes PWS and gentic anomalies which affects the UBE3A gen mother's copy causes AS., Conclusions: It is important to confirm the clinical diagnosis and to establish the genetic mechanism responsible for the two syndromes, both for their consequences as regards the prognosis and for genetic counselling; it is therefore important to draw up a diagnostic algorithm.