29 research outputs found

    Impact de l’infection à Helicobacter pylori sur la maladie d’Alzheimer

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    Helicobacter pylori infection seems to play a critical role in extra-­‐gastric diseases including Alzheimer’s dementia (AD). Chronic H. pylori infection could worsen AD lesions via atherosclerosis and inflammation.In a cohort study with 603 non-­‐institutionalized individuals aged 65 and older followed from 1989 to 2008, dementia was more prevalent in the H. pylori-­‐positive group at baseline compared to non-­‐infected group. After 20 years of follow-­‐up, H. pylori infection was determined to be a risk factor for developing dementia after controlling for AD risk factors. In a second study, including 53 AD patients, H. pylori infection was associated with a more pronounced cognitive impairment. Homocysteine levels were positively correlated to cerebrovascular lesions and to H. pylori immunoglobulin levels. To bypass possible confounding biases concerning socio-­‐economic conditions for instance, we evaluated the impact of H. pylori infection on the brain of non-­‐AD predisposed C57BL/6J mice. After an 18-­‐month infection, H. pylori SS1 and H. felis induced a significant gastric inflammation but no brain Aβ deposit was observed in their brain and the infection did not lead to neuroinflammation. To go further, we studied the impact of Helicobacter species infection on cerebral lesions and behaviour of AD transgenic (APPswe/PS1dE9) mice and their wild type littermates. H. pylori infection was associated with an increased number of brain amyloid plaques, but not with an increased neuroinflammation nor a worsening behaviour at 6 and 10 months of age.Although epidemiological studies provided new elements for an association between AD and H. pylori infection, animal model studies did not display a worsening behaviour or an increased neuroinflammation despite an increased number of amyloid plaques. More studies are needed to firmly conclude that there is an association between H. pylori infection and AD.L’infection à Helicobacter pylori est responsable d’une inflammation gastrique chronique qui pourrait contribuer à l’apparition ou l’aggravation de pathologies extradigestives comme la maladie d’Alzheimer (MA). A partir des données de la cohorte PAQUID explorant les facteurs de risque de démence dans une population de patients de plus de 65 ans, nous avons montré que la prévalence de la démence augmentait chez les sujets infectés. Après 20 ans de suivi, l’infection à H. pylori était associée à une augmentation de l’incidence de démence après ajustement aux facteurs de risque connus de MA. Dans une deuxième étude incluant 53 patients atteints de MA, l’infection à H. pylori était associée à des performances cognitives plus sévères et le taux d’homocystéine était positivement corrélé aux lésions cérébrovasculaires et au taux d’anticorps anti-­‐H. pylori. Pour s’affranchir de possibles biais confondant comme le niveau socio-­‐économique, nous avons ensuite évalué l’impact de l’infection à H pylori sur le cerveau de souris sauvages (C57BL/6J) non prédisposées à la MA. Après 18 mois d’infection, alors que l’infection était associée à une inflammation gastrique importante, il n’a pas été retrouvé de plaque amyloïde ou de majoration de la neuroinflammation. Pour aller plus loin, nous avons étudié l’impact de l’infection à H. pylori sur le comportement et les lésions cérébrales de souris transgéniques prédisposées à la MA (APPswe/PS1dE9). Après 6 mois d’infection, les souris transgéniques présentaient plus de plaques amyloïdes sans majoration de la neuroinflammation ni des troubles du comportement.Bien que les études épidémiologiques apportent de nouveaux éléments en faveur d’une association entre la MA et l’infection à H. pylori, les études sur modèle animal ne mettent pas en évidence de majoration des troubles cognitifs ni de la neuroinflammation des souris infectées malgré une majoration du nombre de plaques amyloïdes. D’autres études sont nécessaires pour conclure à une association

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    Mortalité et facteurs de risque associés des bactériémies aà Escherichia coli dans une population de patients jeunes, âgés et très âgés

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    Peu de données sont disponibles sur la mortalité et les facteurs de risque associés des bactériémies à E. coli chez le sujet âgé. Comparer, à partir d une cohorte prospective multicentrique française de 1051 adultes (COLIBAFI) présentant une bactériémie à E. coli, les caractéristiques démographiques, cliniques, microbiologiques et pronostiques des sujets jeunes (18 74 ans), âgés (75 84 ans) et très âgés (>= 85 ans). Les tests de Chi 2 et Student ont comparé les données qualitatives et quantitatives. Les facteurs de risque de mortalité ont été identifiés par une analyse multivariée pour chaque groupe d'âge. Quatre cent vingt cinq (40%) patients avaient plus de 75 ans (283 âgés et 142 très âgés). La moitié des sujets jeunes était immunodéprimée et un tiers des sujets très âgés présentait une insuffisance cardiaque. Le taux de mortalité était comparable entre les 3 groupes (12,1% vs 16,3% vs 9,9%, p=0,073). L âge, l hospitalisation, l immunodépression, la cirrhose, l alcoolisme et l origine cutanée de l infection pour les sujets jeunes, l immunodépression pour les sujets âgés et l insuffisance rénale et les souches multirésistantes pour les sujets très âgés étaient les facteurs de risque de mortalité. La porte d entrée urinaire était la plus fréquente et associée à une meilleure survie chez les sujets de moins de 85 ans ainsi que la présence des gènes de virulence ireA, traT et hra chez les sujets jeunes, âgés et très âgés respectivement. Le taux de mortalité des bactériémies à E. coli ne différait pas entre les groupes d âge, mais les facteurs de risque cliniques et microbiologiques de mortalité étaient spécifiques de chaque groupe d âge.PARIS6-Bibl.Pitié-Salpêtrie (751132101) / SudocSudocFranceF

    Alzheimer's disease and Helicobacter pylori infection: a possible link?

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    International audienceAlzheimer's disease (AD) is associated with Aß peptide and Tau protein deposits, but the initial process inducing the disease and ultimately neurodegeneration has not yet been elucidated. An infectious hypothesis is suggested by the alteration of the blood-brain barrier and the activation of neuroinflammation in the brain, which could play a role, especially in the decrease of Aß peptide clearance. Several viral or bacterial agents have been incriminated, including Helicobacter pylori. Infection by H. pylori is acquired during childhood and often lifetime persisting, inducing a chronic gastric inflammation, which remains asymptomatic in approximately 80% of cases. However H. pylori infection can induce systemic inflammation and increase homocysteine levels, contributing to worsen AD lesions. Association between H. pylori and AD is suggested by 1) epidemiologic studies, which show higher AD prevalence and more pronounced cognitive impairment in infected than in non-infected subjects; 2) experimental studies in murine models: a) in a first study we evaluated the impact of H. pylori infection on the brain of non-AD predisposed C57BL/6J mice. After an 18-month infection, H. pylori induced a significant gastric inflammation but no brain Aβ deposit nor increased neuroinflammation was observed in their brain; b) we currently study the impact of Helicobacter species infection on behavior and cerebral lesions of AD transgenic (APPswe/PS1dE9) mice and their wild type littermate. The results of these studies do not allow to conclude a significant association between AD and H. pylory infection but may contribute to a better understanding of the role of brain neuroinflammation in AD

    Alzheimer's disease: the infectious hypothesis

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    International audienceSeveral hypotheses are proposed for understanding the Alzheimer's disease (AD) pathological mechanisms, mainly the amyloid theory, but the process inducing Aß peptide deposit, tau protein degeneration, and ultimately neuronal loss, is still to be elucidated. Alteration of the blood-brain barrier and activation of neuroinflammation seem to play an important role in AD neurodegeneration, especially in the decrease of Aß peptide clearance, therefore suggesting a role of infectious agents. Epidemiological and experimental studies on cellular or murine models related to herpes simplex virus (HSV), spirochetes, Chlamydia pneumoniae or Borrelia, and systemic inflammation are reviewed. Aß peptide or tau protein could also behave like a prion protein. Infectious agents could thus have an impact on AD by direct interaction with neurotropism or systemic inflammation. Although the results of these studies are not conclusive, they may contribute to the understanding of AD pathology

    Highlights of the 14th International Congress of the European Geriatric Medicine Society

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    Purpose: To report the most important messages of the 2018 EuGMS Congress in Berlin. Methods: Review based on an on-site attendance in the sessions by the European Academy for Medicine of Aging graduates. Results: The 14th Congress of the European Geriatric Medicine Society which took place in Berlin, Germany, from 10 to 12 October 2018, addressed the issue of challenges and opportunities associated with a fast changing modern world. Covering among other topics social issues, new technologies and the much-awaited new European definition of sarcopenia, the meeting streamed with important information. Conclusions: Attended by more than 1800 participants from Europe and from across the world, it was one of the most successful geriatric events in 2018. In the following text, in preparation to the next, 15th Congress in Kraków, Poland, we briefly describe the highlights of the Berlin Congress

    Acute Clostridioides difficile Infection in Hospitalized Persons Aged 75 and Older: 30-Day Prognosis and Risk Factors for Mortality

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    International audienceObjectives: To assess the 30-day mortality predictive markers in the oldest patients with Clostridioides difficile infection (CDI) and to analyze the accuracy of the European severity risk markers in this population.Design: Observational prospective multicenter cohort study conducted by the French Infectious Diseases Society and Geriatrics Society networks. An electronic questionnaire was sent to members of both societies regarding their participation. Each investigator used an online survey to gather the data.Setting and participants: Patients aged ≥75 years hospitalized in French geriatric or infectious wards with confirmed diagnosis of CDI between March 1, 2016 and May 1, 2017.Methods: Clinical and laboratory parameters included medical history and comorbidities with the Cumulative Illness Rating Scale (CIRS). Criteria increasing the risk of severe disease were recorded as listed in the European guidelines. Therapeutic management, recurrence, and mortality rates were assessed at day 30 after diagnosis.Results: Included patients numbered 247; mean age was 87.2 years (SD 5.4). Most of the CDI incidences (66.4%) were health care-associated infections, with 81% diagnosed within 30 days of hospitalization; CIRS mean score was 16.6 (SD 6.6). Markers of severity ≥3 included 97 patients (39.3%). Metronidazole was the main initial treatment (51.0%). C difficile infection in the older adult was associated with a 30-day mortality of 12.6%. Multivariate analysis showed that baseline CIRS score [hazard ratio (HR) 1.06 per 1-point increase, 95% confidence interval (CI) 1.00-1.12] and evidence of cardiac, respiratory, or renal decompensation (HR 3.04, 95% CI 1.40-6.59) were significantly associated with mortality.Conclusions and implications: European severity markers are adequate in the oldest old. Organ failure and comorbidities appeared to be the main markers of prognosis, and these should raise the awareness of practitioners. Although antibiotic treatment was not predictive of mortality, our results point out the lack of adherence to current guidelines in this population

    Structured Pre-Consultation Interview at the First Call of Caregiver Regarding Memory Consultation: Effects on Caregiver Burden, Expectations, and Quality of Life

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    Introduction: Case managers can guide caregivers during their search for care for relatives with neurocognitive disorders. The present study aimed to evaluate the effects of this procedure on caregiver burden and quality of life. Methods: Family caregivers searching for care at a memory clinic before the first consultation were provided written information and they provided verbal consent to participate in this pre-post intervention study. Intervention was a structured pre-consultation phone call interview given by the case manager to inform and organize individualize pathway of care. The mini-Zarit Burden Interview and the EuroQol five-dimensional questionnaire quality of life scores were recorded by an independent assessor before the intervention and 1 month thereafter. An expectation questionnaire was also completed during the assessments. The pre and post scores were compared using the Wilcoxon signed-rank test. Results: In total, 45 participants were enrolled and 35 were assessed twice. There was no significant change in the total mini-Zarit Burden Interview score; however, the levels of stress due to caring and meeting familial responsibilities (p = 0.025), and the fear of what the future holds for the participants’ relative (p = 0.01) was lower at 1 month. The need for information about the pathways of care decreased, but no change in support satisfaction was observed. Quality of life was good and did not change. Conclusions: During the pre-consultation intervention, the case manager may fulfill several needs of caregivers, particularly to obtain personalized information, which should be implemented in memory clinics
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