Factores pronósticos de buena funcionalidad a los 12 meses, de una fractura de cadera. Estudio Maluc Anoia / Pronostic factors of good functionality at 12 months of a hip fracture. Maluc Anoia study

ANTECEDENTES: La fractura de cadera suele ocurrir en pacientes frágiles de edad avanzada y va asociada a una importante morbimortalidad al al primer año. El objetivo del estudio es describir los factores pronósticos que permitirían mantener la funcionalidad a los 12 meses. MÉTODO: Desde el 1 de junio de 2010 hasta el 31 de mayo de 2013 se han incluido a todos los pacientes mayores de 69 años con fractura de cadera por fragilidad ósea ingresados en la Unidad Geriátrica de Agudos de nuestro hospital. Definimos como mantenimiento funcional a aquellos pacientes que han perdido entre 0-15 puntos en el índice de Barthel respecto al previo a la fractura. Estudio prospectivo de análisis de datos bivariado para los factores pronósticos relacionados y multivariado para los factores pronósticos predictores. RESULTADOS: Se incluyen 271 pacientes, de ellos, 146 (54,8%), mantienen funcionalidad a los 12 meses y 122 (45,2%) no. Los pacientes que mantienen el estado funcional son más jóvenes: edad media 83,4 vs. 85,80 años (p = 0,002); con mejores puntaciones en los índices de: Lawton previo a la fractura 4,42 vs. 2,40 (p < 0,001) y Barthel al alta 34,2 vs. 27,1 (p = 0,002). También hay diferencias en la puntuación de la «Geriatric Dementia Scale» 2,59 vs. 3,13 (p = 0,009), en la puntuación de la «American Society Anesthesiologist»

BACKGROUND: Hip fracture usually occurs in frail elderly patients and is associated with an important morbi-mortality in the first year. The objective of the study is to describe the prognostic factors that would allow maintaining functionality at 12 months. METHOD: From June 1, 2010 to May 31, 2013, all patients older than 69 years with hip fracture due to bone fragility admitted to the Geriatric Acute Unit of our hospital were included. We define as functional maintenance those patients who have lost between 0-15 points in the Barthel Index with respect to the previous to the fracture. Prospective study of bivariate data analysis for related and multivariate prognostic factors for predictive predictors. RESULTS: 271 patients were included, of them, 146 (54.8%), maintained functionality at 12 months and 122 (45.2%) no. Patients who maintain functional status are younger: average age 83.4 vs 85.80 years (P=.002); with better scores in the indexes of: Lawton prior to fracture 4.42 vs 2.40 (P<.001) and Barthel at discharge 34.2 vs. 27.1 (P=.002). There are also differences in the score of the "Geriatric Dementia Scale" 2.59 vs. 3.13 (P=.009), in the score of the "American Society Anesthesiologist"

Pronostic factors of good functionality at 12 months of a hip fracture. Maluc Anoia study. / Factores pronósticos de buena funcionalidad a los 12 meses, de una fractura de cadera. Estudio Maluc Anoia.

BACKGROUND: Hip fracture usually occurs in frail elderly patients and is associated with an important morbi-mortality in the first year. The objective of the study is to describe the prognostic factors that would allow maintaining functionality at 12 months. METHOD: From June 1, 2010 to May 31, 2013, all patients older than 69 years with hip fracture due to bone fragility admitted to the Geriatric Acute Unit of our hospital were included. We define as functional maintenance those patients who have lost between 0-15 points in the Barthel Index with respect to the previous to the fracture. Prospective study of bivariate data analysis for related and multivariate prognostic factors for predictive predictors. RESULTS: 271 patients were included, of them, 146 (54.8%), maintained functionality at 12 months and 122 (45.2%) no. Patients who maintain functional status are younger: average age 83.4 vs 85.80 years (P=.002); with better scores in the indexes of: Lawton prior to fracture 4.42 vs 2.40 (P<.001) and Barthel at discharge 34.2 vs. 27.1 (P=.002). There are also differences in the score of the "Geriatric Dementia Scale" 2.59 vs. 3.13 (P=.009), in the score of the "American Society Anesthesiologist"

Oral bisphosphonate prescription and non-adherence at 12 months in patients with hip fractures treated in an acute geriatric unit.

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.

[From the clinical to the genetic diagnosis of Prader-Willi and Angelman syndromes]. / Del diagnóstico clínico al diagnóstico genético de los síndromes de Prader-Willi y Angelman.

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.

Del diagnóstico clínico al diagnóstico genético de los síndromes de Prader-Willi y Angelman / From the clinical to the genetic diagnosis of prader-willi and angelman syndromes

Introduction and development. Angelman syndrome (AS) is characterised by severe mental retardation (MR), theabsence of language, ataxia and/or tremors in the extremities and a characteristic behavioural phenotype with a happybehaviour and hyperactivity. Patients often show signs of microcephaly and convulsions. Prader-Willi syndrome (PWS) ischaracterised by acute hypotonia and feeding problems in the neonatal period, and triggers an uncontrollable appetite in theinfant that leads to obesity. Most patients have some degree of MR, behavioural disorders and hypogonadism. Bothpathologies 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 theycome from. The physical or functional absence of genes that are only expressed by the mother’s chromosome 15 causes PWSand gentic anomalies which affects the UBE3A gen mother’s copy causes AS. Conclusions. It is important to confirm theclinical diagnosis and to establish the genetic mechanism responsible for the two syndromes, both for their consequences asregards the prognosis and for genetic counselling; it is therefore important to draw up a diagnostic algorithm

Introducción y desarrollo. El síndrome de Angelman (SA)se caracteriza por retraso mental (RM) grave, ausencia del lenguaje,ataxia y/o temblores de las extremidades y un fenotipo conductualcaracterístico con conducta feliz e hiperactividad. Con frecuencialos pacientes presentan microcefalia y convulsiones. Elsíndrome de Prader-Willi (SPW) se caracteriza por una hipotoníaaguda y dificultades para la alimentación en el período neonatal, ypresenta en la infancia un apetito incontrolado que conduce a laobesidad. La mayoría de pacientes presentan algún grado de RM,problemas de comportamiento e hipogonadismo. Ambas patologíasestán causadas por varios mecanismos genéticos que afectan a laregión 15q11-q13 regulada por la impronta genómica, por lo quesólo una de las dos copias de los genes de esta región será funcionalsegún su origen parental. La ausencia física o funcional de genesque se expresan sólo del cromosoma 15 paterno causa el SPW yanomalías genéticas que afectan a la copia materna del gen UBE3Acausan el SA. Conclusión. Es importante confirmar el diagnósticoclínico y establecer el mecanismo genético responsable de ambossíndromes, por sus implicaciones pronósticas y para el consejo genético;por ello, es importante elaborar un algoritmo de diagnóstico

Presentación atípica de infección por Plesiomonas shigelloides / Atypical presentation of Plesiomonas shigelloides infection

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