Púrpura trombopénica inmune: múltiples tratamientos para una enfermedad

En el present treball es descriuen les principals característiques clíniques de la purpura trombopènica immune, com ara, la distribució per sexes, edat, la presència d'hemorràgies en el moment del diagnòstic i la seva gravetat, la xifra de plaquetes i la presència d'anticossos antiplaquetars. Posteriorment es valora el tractament de primera línia escollit enfront de la malaltia i la resposta aconseguida pel que fa a la xifra de plaquetes i hemostàtica, així com si s'han produït efectes secundaris, observant si succeeixen recidives posteriors i quins tractaments s'han aplicat davant elles i la resposta a aquests.

Factores asociados a la mortalidad en los pacientes con exacerbación de enfermedad pulmonar obstructiva crónica hospitalizados en servicios de medicina interna

Avaluació dels factors de risc que es relacionen amb la mortalitat en pacients amb exacerbació de la MPOC hospitalitzats en serveis de Medicina Interna en un estudi multicèntric transversal, valorant la possible associació de la mort hospitalitzats amb diferents variables: sociodemogràfiques, tractament abans i durant la hospitalització, característiques clíniques de la MPOC, comorbiditats prèvies, dades clíniques, resultats de laboratori i troballes electrocardiogràfics. Amb 398 pacients, 88,7% eren homes i amb una mitjana de 75 anys, va morir un 5,3%. Trobant associació entre el risc de morir durant l'hospitalització i el diagnòstic previ de pneumònia, malaltia coronària i ACV.

Antibioticoterapia Intravenosa domiciliaria mediante bomba de perfusión continua de la sobreinfección respiratoria por Pseudomonas aeruginosa en el paciente con enfermedad pulmonar obstructiva crónica.

La malaltia pulmonar obstructiva crónica (MPOC) té una prevalença elevada al nostra medi i un gran impacte econòmic. La sobreinfecció respiratoria en els pacients MPOC avançats, es bàsicament, per Pseudomonas. L´antibioticoteràpia domiciliaria endovenosa en aquest tipus de sobreinfecció es de gran importància. La forma d´administració de l´antibiòtic es mitjançant bombes d´infusió continues i bombes d´infusió intermitents. Es tracta d´un estudi comparatiu dels dos tipus de bombes d´infusió per l´erradicació de Pseudomonas aeruginosa en el pacient MPOC.

Pathological Reorganization of NMDA Receptors Subunits and Postsynaptic Protein PSD-95 Distribution in Alzheimer's Disease.

In Alzheimer's disease (AD), synaptic alterations play a major role and are often correlated with cognitive changes. In order to better understand synaptic modifications, we compared alterations in NMDA receptors and postsynaptic protein PSD-95 expression in the entorhinal cortex (EC) and frontal cortex (FC; area 9) of AD and control brains. We combined immunohistochemical and image analysis methods to quantify on consecutive sections the distribution of PSD-95 and NMDA receptors GluN1, GluN2A and GluN2B in EC and FC from 25 AD and control cases. The density of stained receptors was analyzed using multivariate statistical methods to assess the effect of neurodegeneration. In both regions, the number of neuronal profiles immunostained for GluN1 receptors subunit and PSD-95 protein was significantly increased in AD compared to controls (3-6 fold), while the number of neuronal profiles stained for GluN2A and GluN2B receptors subunits was on the contrary decreased (3-4 fold). The increase in marked neuronal profiles was more prominent in a cortical band corresponding to layers 3 to 5 with large pyramidal cells. Neurons positive for GluN1 or PSD-95 staining were often found in the same localization on consecutive sections and they were also reactive for the anti-tau antibody AD2, indicating a neurodegenerative process. Differences in the density of immunoreactive puncta representing neuropile were not statistically significant. Altogether these data indicate that GluN1 and PSD-95 accumulate in the neuronal perikarya, but this is not the case for GluN2A and GluN2B, while the neuropile compartment is less subject to modifications. Thus, important variations in the pattern of distribution of the NMDA receptors subunits and PSD-95 represent a marker in AD and by impairing the neuronal network, contribute to functional deterioration.

Utilidad de la ecografía abdominal con contraste en la valoración de la recurrencia quirúrgica en la enfermedad de Crohn.

En aquest estudi, s'ha intentat determinar si l'aplicació de contrast intravenós augmenta la rendibilitat de l'ecografia abdominal en l'estudi de la recurrència postquirúrgica de la malaltia de Crohn (EC). Per a això vam estudiar 40 pacients que complien uns determinats criteris d'inclusió, als quals se'ls va realitzar una colonoscopia (gold standar) i una ecografia abdominal (EA) amb contrast intravenós. Després d'analitzar els resultats, podem concloure, que l'ocupació de contrast durant la realització de l'ecografia abdominal permet augmentar la capacitat diagnòstica de la recurrència endoscópica en pacients amb EC i resecció intestinal, no obstant això la seva utilitat és menor per a valorar la gravetat de la recurrència

Análisis de 150 pacientes trasplantados pulmonares por Enfermedad Pulmonar Intersticial Difusa ( EPID )

Les malalties pulmonars intersticials difuses ( MPID) representen la segona indicación de trasplantamente pulmonar (TP) després del enfisema. El treball és un estudi retrospectiu de 150 malalts sotmesos a un TP per MPID entre agost-1990 i gener de 2010. Es tracta de 86 (57%) homes amb una edad mitja de 49 (r: 20-67) anys. Es van fer 104 (69%) trasplantaments unipulmonares ( TUP) i 46 bipulmonars ( TBP). El diagnòstic més freqüent va ser en 94 ( 63%) malalts la Neumonía intersticial Usual. L’objectiu ha estat establir els resultats significatius en quant a supervivència i ganància funcional del grup. La supervivència del TP en malalts amb MPID és comparable als registres internacionals. Un de cada 6 malalts torna a treballar i la realització d’un TUP o un TBP no suposa més ganància funcional.

Enfermedad neumocócica invasiva en adultos: Cambios en la presentación clinica y evolución tras la introducción del la vacuna neumococica conjugada heptavalente en niños

La introducción de la vacuna neumocócica conjugada ha modificado los serotipos causantes de enfermedad neumocócica invasiva (ENI). El objetivo de este estudio fue analizar las diferencias en la presentación clínica entre la época pre y postvacunal. Realizamos un estudio observacional de todos los adultos hospitalizados con ENI, entre 1997 y 2001 (periodo prevacunal), y de 2006 a 2009 (periodo postvacunal). Comparamos la incidencia, la distribución de serotipos y la presentación clínica entre ambos periodos. Nuestros hallazgos sugieren que la aparición de nuevos serotipos puede asociarse con un aumento de la incidencia de ENI, especialmente en adultos jóvenes, y una mayor severidad en la presentación.

Mutation screening of patients with Alzheimer disease identifies APP locus duplication in a Swedish patient.

BACKGROUND: Missense mutations in three different genes encoding amyloid-β precursor protein, presenilin 1 and presenilin 2 are recognized to cause familial early-onset Alzheimer disease. Also duplications of the amyloid precursor protein gene have been shown to cause the disease. At the Dept. of Geriatric Medicine, Karolinska University Hospital, Sweden, patients are referred for mutation screening for the identification of nucleotide variations and for determining copy-number of the APP locus. METHODS: We combined the method of microsatellite marker genotyping with a quantitative real-time PCR analysis to detect duplications in patients with Alzheimer disease. RESULTS: In 22 DNA samples from individuals diagnosed with clinical Alzheimer disease, we identified one patient carrying a duplication on chromosome 21 which included the APP locus. Further mapping of the chromosomal region by array-comparative genome hybridization showed that the duplication spanned a maximal region of 1.09 Mb. CONCLUSIONS: This is the first report of an APP duplication in a Swedish Alzheimer patient and describes the use of quantitative real-time PCR as a tool for determining copy-number of the APP locus.

Meta-analysis based SVM classification enables accurate detection of Alzheimer's disease across different clinical centers using FDG-PET and MRI.

The application of support vector machine classification (SVM) to combined information from magnetic resonance imaging (MRI) and [F18]fluorodeoxyglucose positron emission tomography (FDG-PET) has been shown to improve detection and differentiation of Alzheimer's disease dementia (AD) and frontotemporal lobar degeneration. To validate this approach for the most frequent dementia syndrome AD, and to test its applicability to multicenter data, we randomly extracted FDG-PET and MRI data of 28 AD patients and 28 healthy control subjects from the database provided by the Alzheimer's Disease Neuroimaging Initiative (ADNI) and compared them to data of 21 patients with AD and 13 control subjects from our own Leipzig cohort. SVM classification using combined volume-of-interest information from FDG-PET and MRI based on comprehensive quantitative meta-analyses investigating dementia syndromes revealed a higher discrimination accuracy in comparison to single modality classification. For the ADNI dataset accuracy rates of up to 88% and for the Leipzig cohort of up to 100% were obtained. Classifiers trained on the ADNI data discriminated the Leipzig cohorts with an accuracy of 91%. In conclusion, our results suggest SVM classification based on quantitative meta-analyses of multicenter data as a valid method for individual AD diagnosis. Furthermore, combining imaging information from MRI and FDG-PET might substantially improve the accuracy of AD diagnosis.

Your guide to Understanding Alzheimer's Disease and other dementias

��The purpose of this booklet is to give you general information about Alzheimer's Disease and other dementias, and to highlight their early signs and symptoms.It offers a number of tools that can be helpful in establishing whether you or someone you care for is experiencing memory problems, and there is a diary at the back of this book to help track and record various changes that you or the person you love maybe experiencing.This booklet also contains details of what steps to take next if you are concerned about someone, how a diagnosis is made, what to do if you or someone close is diagnosed with Alzheimer's Disease, and outlines the various treatments that are available.Understanding Alzheimer's Disease also focuses on the importance of the role of the carer, explains carer stress, and offers some useful suggestions for reducing the stress that can build up when caring for someone full-time.It is hoped this booklet will give you answers to the more frequently asked questions and therefore give you a better understanding of Alzheimer's Disease and dementia.��

Screening for memory disorders, dementia and Alzheimer's disease

Dementia and its most common cause, Alzheimer’s disease, affect memory and occur predominantly in the elderly. Dementia has become increasingly prevalent in the world as health has improved and life expectancy has increased. However, the fields of clinical care have not responded adequately to develop diagnostic tools and treatments for this rapidly increasing group of conditions. While scientists search for cures for the numerous causes of dementia, improvement of diagnostic measures are needed now and should begin with screening elderly populations for memory difficulties and other cognitive problems. This review examines the history of cognitive screening tests, the numerous excellent tests that are currently available and ready for use, and directions and methods that will lead to progressively better evaluations.

Demyelination in mild cognitive impairment suggests progression path to Alzheimer's disease.

The preclinical Alzheimer's disease (AD) - amnestic mild cognitive impairment (MCI) - is manifested by phenotypes classified into exclusively memory (single-domain) MCI (sMCI) and multiple-domain MCI (mMCI). We suggest that typical MCI-to-AD progression occurs through the sMCI-to-mMCI sequence as a result of the extension of initial pathological processes. To support this hypothesis, we assess myelin content with a Magnetization Transfer Ratio (MTR) in 21 sMCI and 21 mMCI patients and in 42 age-, sex-, and education-matched controls. A conjunction analysis revealed MTR reduction shared by sMCI and mMCI groups in the medial temporal lobe and posterior structures including white matter (WM: splenium, posterior corona radiata) and gray matter (GM: hippocampus; parahippocampal and lingual gyri). A disjunction analysis showed the spread of demyelination to prefrontal WM and insula GM in executive mMCI. Our findings suggest that demyelination starts in the structures affected by neurofibrillary pathology; its presence correlates with the clinical picture and indicates the method of MCI-to-AD progression. In vivo staging of preclinical AD can be developed in terms of WM/GM demyelination.

Alzheimer's Disease Biomarkers, 2009

This report gives a comprehensive and up-to-date review of Alzheimer's disease biomarkers. Recent years have seen significant advances in this field. Whilst considerable effort has focused on A�_ and tau related markers, a substantial number of other molecules have been identified, that may offer new opportunities.This Report : Identifies 60 candidate Alzheimer's (AD) biomarkers and their associated studies. Of these, 49 are single species or single parameters, 7 are combinations or panels and 4 involve the measurement of two species or parameters or their ratios. These include proteins (n=34), genes (n=11), image-based parameters (n=7), small molecules (n=3), proteins + genes (n=2) and others (n=3). Of these, 30 (50%) relate to species identified in CSF and 19 (32%) were found in the blood. These candidate may be classified on the basis of their diagnostic utility, namely those which i) may allow AD to be detected when the disease has developed (48 of 75†= 64%), ii) may allow early detection of AD (18 of 75† = 24%) and iii) may allow AD to be predicted before the disease has begun to develop (9 of 75†= 12%). † Note: Of these, 11 were linked to two or more of these capabilities (e.g. allowed both early-stage detection as well as diagnosis after the disease has developed).Biomarkers: AD biomarkers identified in this report show significant diversity, however of the 60 described, 18 (30%) are associated with amyloid beta (A�_) and 9 (15%) relate to Tau. The remainder of the biomarkers (just over half) fall into a number of different groups. Of these, some are associated with other hypotheses on the pathogenesis of AD however the vast majority are individually unique and not obviously linked with other markers. Analysis and discussion presented in this report includes summaries of the studies and clinical trials that have lead to the identification of these markers. Where it has been calculated, diagnostic sensitivity, specificity and the capacity of these markers to differentiate patients with suspected AD from healthy controls and individuals believed to be suffering from other neurodegenerative conditions, have been indicated. These findings are discussed in relation to existing hypotheses on the pathogenesis of the AD and the current drug development pipeline. Many uncertainties remain in relation to the pathogenesis of AD, in diagnosing and treating the disease and many of the studies carried out to identify disease markers are at an early stage and will require confirmation through larger and longer investigations. Nevertheless, significant advances in the identification of AD biomarkers have now been made. Moreover, whilst much of the research on AD biomarkers has focused on amyloid and tau related species, it is evident that a substantial number of other species may provide important opportunities.Purpose of Report: To provide a comprehensive review of important and recently discovered candidate biomarkers of AD, in particular those with potential to reliably detect the disease or with utility in clinical development, drug repurposing, in studies of the pathogenesis and in monitoring drug response and the course of the disease. Other key goals were to identify markers that support current pipeline developments, indicate new potential drug targets or which advance understanding of the pathogenesis of this disease.Drug Repurposing: Studies of the pathogenesis of AD have identified aberrant changes in a number of other disease areas including inflammation, diabetes, oxidative stress, lipid metabolism and others. These findings have prompted studies to evaluate some existing approved drugs to treat AD. This report identifies studies of 9 established drug classes currently being investigated for potential repurposing.Alzheimer’s Disease: In 2005, the global prevalence of dementia was estimated at 25 million, with more than 4 million new cases occurring each year. It is also calculated that the number of people affected will double every 20 years, to 80 million by 2040, if a cure is not found. More than 50% of dementia cases are due to AD. Today, approximately 5 million individuals in the US suffer from AD, representing one in eight people over the age of 65. Direct and indirect costs of AD and other forms of dementia in the US are around $150 billion annually. Worldwide, costs for dementia care are estimated at $315 billion annually. Despite significant research into this debilitating and ultimately fatal disease, advances in the development of diagnostic tests for AD and moreover, effective treatments, remain elusive.Background: Alzheimer's disease is the most common cause of dementia, yet its clinical diagnosis remains uncertain until an eventual post-mortem histopathology examination is carried out. Currently, therapy for patients with Alzheimer disease only treats the symptoms; however, it is anticipated that new disease-modifying drugs will soon become available. The urgency for new and effective treatments for AD is matched by the need for new tests to detect and diagnose the condition. Uncertainties in the diagnosis of AD mean that the disease is often undiagnosed and under treated. Moreover, it is clear that clinical confirmation of AD, using cognitive tests, can only be made after substantial neuronal cell loss has occurred; a process that may have taken place over many years. Poor response to current therapies may therefore, in part, reflect the fact that such treatments are generally commenced only after neuronal damage has occurred. The absence of tests to detect or diagnose presymptomatic AD also means that there is no standard that can be applied to validate experimental findings (e.g. in drug discovery) without performing lengthy studies, and eventual confirmation by autopsy.These limitations are focusing considerable effort on the identification of biomarkers that advance understanding of the pathogenesis of AD and how the disease can be diagnosed in its early stages and treated. It is hoped that developments in these areas will help physicians to detect AD and guide therapy before the first signs of neuronal damage appears. The last 5-10 years have seen substantial research into the pathogenesis of AD and this has lead to the identification of a substantial number of AD biomarkers, which offer important insights into this disease. This report brings together the latest advances in the identification of AD biomarkers and analyses the opportunities they offer in drug R&D and diagnostics.��

World Alzheimer Report 2009

Download: World Alzheimer Report 2009 executive SummaryAlzheimer’s disease and other dementias have been reliably identified in all countries, cultures and races in which systematic research has been carried out. However, levels of awareness vary enormously. Alzheimer’s Disease International (ADI) has identified raising awareness of dementia among the general population and among health workers as a global priority.