Letteratura scientifica selezionata sul tema "Stéatose hépatique non alcoolique – complications"
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Articoli di riviste sul tema "Stéatose hépatique non alcoolique – complications":
Bebawi, Emmanuel, Mark Takla e Jennifer Leonard. "Stéatose hépatique non alcoolique". Canadian Medical Association Journal 195, n. 40 (15 ottobre 2023): E1388—E1389. http://dx.doi.org/10.1503/cmaj.221650-f.
Dalmat, Yann-Mickael. "Quid de la stéatose hépatique non alcoolique ?" Option/Bio 32, n. 635-636 (giugno 2021): 12. http://dx.doi.org/10.1016/s0992-5945(21)00132-x.
A., F. "Diagnostic de la stéatose hépatique non alcoolique". Médecine des Maladies Métaboliques 10, n. 4 (giugno 2016): 354. http://dx.doi.org/10.1016/s1957-2557(16)30127-4.
Rubbia-Brandt, Laura, e Antoine Hadengue. "Stéatose hépatique non alcoolique : faut-il biopsier ?" Revue Médicale Suisse 1, n. 43 (2005): 2804–8. http://dx.doi.org/10.53738/revmed.2005.1.43.2804.
Ritz, Claire, e Jean Perdrix. "Stéatose hépatique non alcoolique : enfin un traitement possible ?" Revue Médicale Suisse 18, n. 788 (2022): 1334. http://dx.doi.org/10.53738/revmed.2022.18.788.1334.
Bell, Caroline, e Marc Delisle. "Stéatose hépatique non alcoolique secondaire à la clozapine". Canadian Journal of Psychiatry 49, n. 8 (agosto 2004): 575–76. http://dx.doi.org/10.1177/070674370404900817.
Gariani, Karim, e François R. Jornayvaz. "Diabète et [b]stéatose[/b] hépatique non alcoolique". Revue Médicale Suisse 8, n. 344 (2012): 1211–14. http://dx.doi.org/10.53738/revmed.2012.8.344.1211.
Lê, Sylvie, Matthieu Minty, Émile Boyer, Vincent Blasco-Baque, Martine Bonnaure-Mallet e Vincent Meuric. "Microbiote buccal et foie". médecine/sciences 40, n. 1 (gennaio 2024): 42–48. http://dx.doi.org/10.1051/medsci/2023194.
Zampaglione, Lucia, Jacopo Ferrari e Nicolas Goossens. "La stéatopathie dysmétabolique". Schweizer Gastroenterologie 1, n. 3 (settembre 2020): 79–85. http://dx.doi.org/10.1007/s43472-020-00018-8.
Schlienger, J. L. "Quel régime en cas de stéatose hépatique non alcoolique ?" Médecine des Maladies Métaboliques 1, n. 4 (novembre 2007): 55–56. http://dx.doi.org/10.1016/s1957-2557(07)74144-5.
Tesi sul tema "Stéatose hépatique non alcoolique – complications":
Canivet, Clémence. "Étude de deux acteurs dans le développement des complications hépatiques liées à l’obésité : la vitamine D et FNDC5/Irisine". Thesis, Université Côte d'Azur (ComUE), 2019. http://theses.univ-cotedazur.fr/2019AZUR6036.
Non-Alcoholic Fatty Liver Diseases (NAFLD) is a major public health concern with global prevalence of 25%. NAFLD is increasingly recognized as the most common chronic liver disease. The spectrum of the hepatic diseases ranges from steatosis (fatty liver) to nonalcoholic steatohepatitis (NASH) (steatosis, inflammation, liver injury) and subsequently to the activation of fibrogenic pathways, which correlates with a high risk of developing cirrhosis and hepatocellular carcinoma. The treatment of NASH is still limited because of the lack of effective pharmacological treatment as well as lack of effective and practical diagnostic tools. NAFLD is associated with obesity and metabolic syndrome and the presence of type 2 diabetes can increase the risk of liver diseases. Inversely, NAFLD is also a risk factor for many metabolic diseases, including type 2 diabetes and cardiovascular disease. The mechanisms underlying the progression of NAFLD are multifactorial and not well understood. Better understand the pathogenesis of NASH will lead to identify new potential therapeutic targets. One part of my work focused on clinical aspects in a large cohort of obese patients regarding factors that potentially regulate the development of NAFLD. We here reported that: 1) binge eating disorders were associated as expected with obesity but independently of NAFLD severity and 2) the circulating level of vitamin D, well-known to display anti-oxidant and anti-fibrotic properties, was not diminished with NAFLD severity.In parallel, we investigated the expression level and the role of a new "hepatokine", Fibronectin type III domain containing 5 (FNDC5) and its soluble form irisin in NAFLD. We reported that hepatic expression of FNDC5 increased in the presence of hepatic steatosis and liver injury without impacting the systemic level of irisin in mouse models of NAFLD and in obese patients. This local production of FNDC5 was mainly influenced by genotoxic stress and behaved as local protective factor against NAFLD by preventing hepatocyte steatosis and injury. Finally, the single nucleotide polymorphism (SNP) FNDC5 rs3480 was protective of severe steatosis independently of PNPLA3 SNP rs738409, age, female, BMI and type 2 diabetes in a cohort of 613 patients. In conclusion, our human and experimental data strongly suggest that hepatic expression of FNDC5 could dampen the development of NAFL by negatively regulating steatogenesis and hepatocyte death
Nicolas, Anthony. "Polymorphismes du gène de la t-cadhérine (CDH13), récepteur de l'adiponectine, dans les diabètes et leurs complications". Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066232/document.
T-cadherin is a receptor of adiponectin, a protein involved in the pathophysiology of diabetes. In genome-wide association studies, T-cadherin gene (CDH13) polymorphisms are associated with adiponectin concentrations. The aim of our study was to deepen the relationship between polymorphisms of CDH13, plasma adiponectin, and the risk of diabetes and its complications. We selected two polymorphisms in CDH13. Genotyping was performed in D.E.S.I.R., cohort drawn from the French general population, DIABHYCAR (subjects with type 2 diabetes) and three cohorts of patients with type 1 diabetes, GENESIS, GENEDIAB and SURGENE. In the general population, CDH13 polymorphisms were associated with body mass index, HbA1c, Fatty Liver Index, an index of hepatic steatosis, and plasma adiponectin. In a case-control study between D.E.S.I.R. and DIABHYCAR, polymorphisms were associated with the risk of type 2 diabetes. These associations with clinical phenotypes could be due to the beneficial effects of adiponectin. In subjects with type 1 diabetes from GENESIS and GENEDIAB, we observed associations between polymorphisms of CDH13 and the prevalence and the incidence of kidney disease. The analysis in the SURGENE prospective study confirmed these associations. The direction of the relationships observed in this study is in favor of a deleterious role of adiponectin in diabetic nephropathy. In conclusion, these associations may be explained by variations in adiponectin and suggest a causal relationship
Bauvin, Pierre. "Modélisation de la stéatose hépatique (NAFLD) et de ses facteurs de risque par apprentissage sur des données de santé". Thesis, Lille 2, 2020. http://www.theses.fr/2020LIL2S028.
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease which is a combination of simple, slowly progressing steatosis, and non-alcoholic steatohepatitis (NASH), an inflammatory form which accelerates its progression. It is estimated that one in four people in the world is affected by NAFLD, and its prevalence is increasing rapidly, in parallel with the prevalence of its main risk factors: overweight, obesity and type 2 diabetes.This pathology is asymptomatic up to the complications, cirrhosis and liver cancer (hepatocellular carcinoma, HCC), which leads to late diagnosis and a negative impact on the associated morbidity and mortality. Furthermore, the reference diagnosis requires a liver biopsy, an invasive examination that cannot be performed routinely. As a result, the progression of the disease is poorly known and its estimation may suffer from a selection bias, towards patients with significant risk factors, who require a biopsy in the first place. A better understanding would allow the implementation of strategies to reduce its burden.The modelling approach is appropriate to take into account all susceptible patients, without having to carry out a large-scale follow-up study using liver biopsies in patients who are mostly asymptomatic. The objectives of this thesis are to describe and quantify the progression of NAFLD, to predict the associated morbidity and mortality, and to identify the population at risk, using Markov models. To do this, it is necessary to fill in some of the progression parameters via a literature review, to characterise the initial states (population likely to develop NAFLD) and the final states (mortality due to NAFLD), in order to deduce the missing progression parameters between the onset of the disease and mortality, by back-calculation.To exhaustively characterise NAFLD mortality, we identified all patients with cirrhosis or HCC from national hospital databases, representing more than 380,000 patients. We then developed an identification algorithm to determine the etiology underlying the hepatic complication, based on all the stays of the identified patients. This algorithm requires the identification of patients with cirrhosis or HCC of alcoholic or viral origin, to obtain by elimination only NAFLD patients. Once the specific mortality data had been obtained, we estimated the population likely to develop NAFLD, defined as all individuals with overweight or type 2 diabetes, excluding the population of excessive drinkers. We estimated the prevalence and incidence of this population, and modelled its evolution with age and years, based on individual data from surveys representative of the French population.Finally, we quantified the progression of NAFLD, and the impact of risk factors, using two approaches: from the literature, and from biopsy data from more than 1,800 obese patients who were candidates for bariatric surgery, resulting in a tool for predicting the progression of NAFLD in this population. We chose to back-calculate the progression parameters corresponding to the asymptomatic states, which are the most susceptible to selection bias.We obtained a model of the progression of NAFLD, taking into account the dynamic distribution of the population among weight classes and diabetes status, and resulting in the observed statistics of NAFLD deaths. The model takes into account gender, age, year, BMI (body mass index) class, diabetes status and the presence of a genetic polymorphism (PNPLA3 rs738409, C→G) as covariates of progression. It is a tool for assessing the impact of a possible treatment or public health policy on morbidity and mortality
Decoin, Raphaël. "Impact de la stéatohépatite non alcoolique sur le remodelage myocardique et sur les complications cardiovasculaires". Electronic Thesis or Diss., Université de Lille (2022-....), 2023. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2023/2023ULILS066.pdf.
Cardiac remodeling is a pathophysiological phenomenon during which the cardiac muscle undergoes structural alterations at both tissue and cellular levels, leading to functional changes. The clinical implications are diverse, including the development of atrial fibrillation and heart failure. Among the numerous risk factors identified, Non-Alcoholic Fatty Liver Diseases (NAFLD) have an emerging role. This liver disease, characterized by steatosis, inflammation, and fibrosis, is associated with the development of myocardial pathologies.In this study, we hypothesize that NAFLD specifically triggers characteristic cardiac remodeling at both histological and functional levels. To explore this hypothesis, we employ a translational approach using various cohorts from the Lille University Hospital, as well as a murine model of NAFLD. Three distinct objectives have been defined: 1) demonstrate an association between atrial remodeling and NAFLD in patients; 2) propose an early diagnostic method for cardiac remodeling; 3) propose mechanistic hypotheses for the liver-heart connection through a translational methodology. Firstly, we characterized atrial cardiac remodeling in a cohort of patients indicated for atrial fibrillation ablation. Among these patients, we observed a positive association between the progression of hepatic pathology (assessed through clinical-biological scores) and, on one hand, dilation and impaired contractility of the left atrium as estimated by echocardiography, and on the other hand, the presence of areas with low extracellular voltages. This remodeling profile was also linked to a poor prognosis of ablation. In a second cohort of patients scheduled for cardiac surgery (POMI-AF), we demonstrated greater fibrosis in the atrial myocardium of patients with a high-risk NAFLD-related fibrosis compared to those without NAFLD. Next, using the same POMI-AF cohort, we showed that quantifying myocardial fat (intracardiomyocytic lipid droplets) using VARPRO MRI sequence is a robust, reliable, and feasible analysis in NAFLD-affected patients. Lastly, in a murine model of NAFLD developed in the laboratory (high-fat, sucrose, and cholesterol diet for 24 weeks), we described the presence of cardiac remodeling. Mice subjected to the NAFLD-inducing diet developed diastolic dysfunction with preserved ejection fraction, assessed by echocardiography, in comparison to the control diet group. This loss of function was associated with concentric left ventricular hypertrophy. Histologically, this hypertrophy was explained by an increase in the cross-sectional diameter of cardiomyocytes, which was also associated with diffuse interstitial fibrosisstarting from a vascular point. These observations were more pronounced with higher hepatic involvement, reinforcing the initial hypothesis. Total ventricular mRNA sequencing revealed a significantly altered transcriptional profile in NAFLD-affected mice, indicating impaired energy metabolism and a profound immune signature. Subsequently, flow cytometry analysis of immune populations revealed macrophage and dendritic cell infiltration in the myocardium, similar to what is observed in NAFLD liver. This macrophage infiltration was also evident in human biopsies from patients with advanced NAFLD.In conclusion, we demonstrate that NAFLD-associated cardiac remodeling affects both the left atrium and the left ventricle. Additionally, we have shown that quantifying cardiac lipid droplet accumulation is feasible using MRI. Finally, the myeloid infiltration observed in the myocardium of NAFLD patients and in our murine model suggests a potential link between hepatic dysimmunity and cardiac remodeling
Leclère, Pierre. "Rôle du facteur de transcription circadien Krüppel-Like Factor 10 (KLF 10) dans le développement des complications hépatiques de l’obésité". Thesis, Université Côte d'Azur (ComUE), 2019. http://theses.univ-cotedazur.fr/2019AZUR6030.
Non-alcoholic steatohepatitis (NASH), the progressive form of nonalcoholic fatty liver diseases (NAFLDs), is a global public health problem without approved pharmacological therapy. NAFLD extend from non-pathogenic lipid accumulation, known as hepatic steatosis to hepatocellular carcinoma (HCC) through a wide spectrum of stages including NASH and fibrosis. NASH is featured by hepatic inflammation and hepatocyte cell death. Better understand NASH pathogenic cellular and molecular mechanisms is an important clinical requirement.Circadian timing system (CTS) is the main synchronizer of organismal physiology to environmental light/dark cycles. This CTS is comprised of a central pacemaker in the supra-chiasmatic nucleus of the hypothalamus and peripheral clocks localized in each single cell throughout the brain and body. Western society life style, including junk food consumption and erratic feeding, chronic jet lag, light exposure at night and shift-work, can disrupt the CTS. CTS disruption has been assessed as a risk factor for the development of chronic diseases including metabolic syndrome and cancer. The liver is the most rhythmic organ and evidence for an intricate link between CTS disruption and NAFLD development is most illustrated by (i) the genetic and environmental disruption of the CTS leads to dyslipidemia, hepatic steatosis as well as spontaneous NASH and HCC development (ii) the circadian hepatic transcriptome is rearranged in mice fed high fat diet and displaying hepatic steatosis, showing that metabolic disruption also impacts diurnal oscillation of transcripts. Krüppel-like factor 10 is a circadian transcription factor directly regulated by the circadian clock in the liver and help shaping the hepatic diurnal transcriptome and the control carbohydrate and lipid metabolism homeostasis. Beside from metabolism, this transcription factor has also been shown to regulate two NASH related processes, in very different contexts, namely inflammation and cell death. We thus aimed to evaluate the implication of circadian rhythms and the role of KLF10 during steatohepatitisHere, we show that hepatic steatosis and inflammation display diurnal rhythmicity in mice developing steatohepatitis upon feeding with a methionine and choline deficient diet (MCDD). Core clock gene oscillations remained mostly unaffected but rhythmic Klf10 expression was abolished in this model. Klf10 deficient mice (Klf10-/-) display enhanced liver injury despite the same level of hepatic steatosis and inflammation that control mice upon MCDD challenge. Specific genetic ablation of Klf10 only in hepatocytes phenocopied the phenotype of Klf10-/- mice upon MCDD. Silencing Klf10 in isolated primary hepatocytes also sensitized these cells to apoptosis along with increased caspase 3 activation in response to TNFα. We also show that the hepatic KLF10 expression correlates with liver injury (ALT activity) and the circulating keratin 18 hepatocyte death marker in a cohort of obese patients. Collectively our findings suggest that specific NASH features including steatosis and inflammation display diurnal oscillations and the associated altered circadian expression of Klf10 may aggravate liver injury through hepatocyte sensitization to cell death.Collectively, our results gathered from cellular and animal experiments as well as correlative study in Human indicate that hepatic steatosis and inflammation could be rhythmic during NASH and that KLF10 could be a hepatoprotective factor that could limit NAFLD progression
Fedchuk, Larysa. "Progression et tests diagnostiques de la stéatose hépatique non alcoolique". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066210/document.
Non-alcoholic fatty liver disease (NAFLD) covers a spectrum ranging from isolated steatosis to non-alcoholic steatohepatitis (NASH) and is becoming one of the most frequent causes of chronic liver disease, mainly because of its close association with the worldwide epidemic of diabetes and obesity. Liver steatosis can predict the occurrence of metabolic complications associated with insulin resistance, such as diabetes and cardiovascular events. Our understanding of the natural history of NAFLD is still incomplete. Currently, the explicative model is based on a dichotomy between steatohepatitis, considered the progressive form of the disease, which can lead to cirrhosis and isolated steatosis with or without minimal inflammation, which is considered a non-progressive condition that does not impact overall survival or result in liver-related mortality and morbidity. This dichotomy largely determines the management of NAFLD patients: patients without steatohepatitis usually do not undergo specific monitoring for liver disease progression. Liver biopsy is considered the reference diagnostic method but its implementation in clinical practice remains limited due to procedure complexity, invasiveness, cost, potential complications, sampling error and inter-observer variability. Non-invasive methods of hepatic injury have become a real alternative to liver biopsy for the diagnosis of patients with chronic liver disease in the past decade. The aims of this thesis were: 1) to better understand the histological course of the disease, to better identify patients at risk of histological progression based on initial histological findings and to establish a correlation between histological changes and the course of metabolic co-morbidities often associated with NAFLD : 2) to establish factors associated with short-term variability of repeated measurements of elastometry in patients with chronic liver diseases in order to understand how this non invasive procedure can be used for patient monitoring 3) to determine the diagnostic value and limitations of several steatosis biomarkers using liver biopsy as a reference standard in a large cohort of patients with suspected NAFLD. Our study shows that a fraction of patients with isolated steatosis can unambiguously evolve towards well-defined steatohepatitis, and in some of them, bridging fibrosis. The presence of mild lobular inflammation or any amount of fibrosis substantially increases the risk of histological progression in the mid-term while those with steatosis alone are at lowest risk. Patients with disease progression experienced a deterioration of cardio-metabolic risk factors. Our data if validated by independent studies, allow for better stratification of patients at risk of disease progression. The results of this study favor a change in the practices of monitoring and risk assessment of patients with steatosis but without steatohepatitis
Delacôte, Claire. "Vers une meilleure compréhension de la maladie du foie liée à l'alcool et des facteurs influençant sa progression : approche de modélisation". Thesis, Lille 2, 2020. http://www.theses.fr/2020LIL2S029.
In France, excessive alcohol consumption is the leading cause of cirrhosis and hepatocellular carcinoma (HCC), ahead of viral hepatitis and metabolic syndrome. In 2016, there were nearly 10,500 deaths by cirrhosis or HCC, despite a significant decrease in per capita alcohol consumption since 1960 (26L in 1960, 11.7L in 2017).Alcohol drinkers are at risk of developing alcohol-related liver disease (ALD). It progresses from the initial stage of steatosis to more advanced stages of fibrosis and cirrhosis, which may lead to complications: decompensation and HCC. ALD is an asymptomatic disease prior to the onset of complications, and many patients are diagnosed late with life-threatening consequences.Implementing early actions targeting excessive alcohol drinkers could help to reduce liver morbidity and mortality through the avoidance or earlier diagnosis of complications. The evaluation of the possible benefit of such public health actions requires, on the one hand, knowledge of the different stages leading to the development of complications and, on the other hand, knowledge of the impact of risk factors on progression, in order to be able to determine the populations to target. Among the risk factors identified, the metabolic syndrome plays an important role. Thus, in order to understand the mechanisms of evolution of ALD, it is necessary to study in parallel those leading to non-alcoholic fatty liver disease (NAFLD).The natural history of ALD is still poorly described, especially for the stages preceding cirrhosis. Mathematical modeling provides a conceptual framework to overcome the ethical issues that would arise from a cohort study of the evolution of ALD.The main objective of this work is to mathematically reconstruct the natural history of ALD and to predict the associated morbidity and mortality. The secondary objectives are to estimate the incidence of this pathology and to identify the at-risk population. For this purpose, we developed a Markov model that simulates the trajectory of cohorts of individuals from the moment they start at-risk alcohol consumption until their death. It integrates the main risk factors described as associated with the progression of ALD in the literature (sex, age, overweight and obesity, amount of alcohol, genetic polymorphism). Unknown parameters of progression are estimated by a back-calculation method.Three steps were necessary to supply and calibrate this model : 1) characterize mortality by decompensated cirrhosis and HCC related to alcohol consumption or metabolic syndrome from data provided by the French National Hospital Discharge database; 2) set up a Markov model on hospitalization data of excessive consumers to estimate the progression of fibrosis; 3) implement a Markov model on survey data from the general French population to estimate the process of entry into at-risk alcohol consumption or the onset of overweight and obesity.In conclusion, this work is the first to characterize the progression of ALD in the general French population. It is based on robust epidemiological data to which new insights are provided. The developed tools could be used to test the impact of public health policies that could be implemented in populations most likely to develop liver damage
Jegatheesan, Prasanthi. "Stéatose hépatique non-alcoolique : intérêt d’un apport nutritionnel en acides aminés". Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB096.
Nonalcoholic fatty liver disease (NAFLD) is a manifestation of the metabolic syndrome whose prevalence is constantly growing. Therapeutic strategies are either difficult to implement or of limited effectiveness. We studied a nutritional approach with three specific amino acids: glutamine, arginine and citrulline (Cit) for their pharmaconutrient properties. In a model of moderate fructose-induced NAFLD, citrulline alone (1 g/kg/day) improved lipid metabolism. However, the study of the kinetics of NAFLD suggested a protective effect of nitrogen supply by itself. The specific effect of Cit compared to that of nitrogen (NEAAs) has been determined in a model of 8 week fructose diet-induced NAFLD. This has confirmed the protective effect of Cit and NEAAs. However, Cit exerted a specific effect on the expression of Fas and SREBP1c and improves peripheral Arg availability, an important component of insulin sensitivity. Steatosis was associated with loss of lean mass, suggesting AA oxidation at the expense of muscle anabolism, and lipid accumulation causing steatosis and visceral fat gain; Cit and NEAAs by acting on NAFLD would prevent this effect of fructose. We then evaluated the effects of Cit in a model of more severe steatosis induced by western diet. Cit improved liver function (reduced fat and liver inflammation) and protected the liver-gut axis (restoration of Bacteroides/Prevotella group in the colonic mucosa, decreased intestinal inflammation and increased expression of claudin 1) but did not prevent all western diet-induced alterations. It would be interesting to assess the dose/effect relationship and the effectiveness of Cit in combination with other treatments. Furthermore, the cellular mechanisms remain to be elucidated
Perazzo, Pedroso Barbosa Hugo. "Marqueurs non-invasifs de stéatose et fibrose hépatique". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2014. http://tel.archives-ouvertes.fr/tel-00989999.
Trak, Smayra Viviane. "La stéatose hépatique non-alcoolique et la NASH : approche diagnostique et modèles murins". Paris 7, 2011. http://www.theses.fr/2011PA077247.