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Relevant bibliographies by topics / Alcoholic Fatty Liver

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Academic literature on the topic 'Alcoholic Fatty Liver'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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Journal articles on the topic "Alcoholic Fatty Liver"

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Korobkо, Yuriy Ivanovich. "Non-alcoholic fatty liver disease." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 7 (July 1, 2021): 20–24. http://dx.doi.org/10.33920/med-10-2107-03.

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Fatty degeneration of cells under the influence of various factors is called steatosis; most often this process is observed in the pancreas and liver. Steatosis of the liver refers to its fatty infiltration, in which fatty inclusions appear in the parenchyma of the organ, leading to dysfunction of hepatocytes. Steatosis can be focal and diffuse; in the latter case, fat cells are located over the entire surface of the liver. Until 1980, it was believed that only alcohol abuse can lead to steatosis, while fatty degeneration of the liver was noted in 90 % of alcohol abusers. Subsequently, it was found that alcoholism is not the only reason for the development of this pathological condition, after which it was proposed to divide steatosis into alcoholic and non-alcoholic. Most often, non-alcoholic steatosis develops in women over 45 years old against the background of obesity or diabetes mellitus. Also, the cause of the development of liver steatosis can be malnutrition and diseases of other digestive organs, leading to impaired absorption of nutrients, metabolic disorders, and hormonal disruptions.

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Fitzpatrick, Emer. "PAEDIATRIC NON ALCOHOLIC FATTY LIVER DISEASE: AN EMERGING THREAT." Paediatrics Today 11, no. 1 (March 15, 2015): 1–9. http://dx.doi.org/10.5457/p2005-114.104.

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DELLA CORTE, Claudia. "PEDIATRIC NON-ALCOHOLIC FATTY LIVER DISEASE: A GROWING PROBLEM." Paediatrics Today 11, no. 2 (October 8, 2015): 81–83. http://dx.doi.org/10.5457/p2005-114.114.

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Narayan, Smriti, Sonu Kumar Gupta, Priyanka Singh, Villayat Ali, and Malkhey Verma. "Non-alcoholic fatty liver disease progression and current research." Asian Pacific Journal of Health Sciences 6, no. 1 (March 2019): 189–98. http://dx.doi.org/10.21276/apjhs.2019.6.1.26.

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Singla, Bharti, Gesu Singla, and Harsharan Kaur. "Lipid profile variations in non alcoholic fatty liver disease." Asian Pacific Journal of Health Sciences 6, no. 3 (September 2019): 1–4. http://dx.doi.org/10.21276/apjhs.2019.6.3.1.

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Diehl, Anna Mae. "Recent Events in Alcoholic Liver Disease V. Effects of ethanol on liver regeneration." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 1 (January 2005): G1—G6. http://dx.doi.org/10.1152/ajpgi.00376.2004.

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Liver regeneration is necessary to recover from alcoholic liver injury. Herein, we review evidence that ethanol interferes with liver regeneration. Briefly, alcoholic fatty livers demonstrate increased rates of hepatocyte death. The latter provides a regenerative stimulus. However, unlike mature hepatocytes in healthy adult livers, most surviving mature hepatocytes in alcoholic fatty livers cannot replicate. Therefore, less mature cells (progenitors) must differentiate to replace dead hepatocytes. Little is known about the general mechanisms that modulate the differentiation of liver progenitors in adults. Delineation of these mechanisms and clarification of how ethanol influences them might suggest new therapies for alcoholic liver disease.

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K.C., Geetika. "Diagnosis of Non-alcoholic fatty liver disease." Journal of Pathology of Nepal 6, no. 11 (March 17, 2016): 947–52. http://dx.doi.org/10.3126/jpn.v6i11.15679.

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Non Alcoholic Fatty Liver Disease is the deposition of fat in liver in absence of excessive of alcohol consumption. Non Alcoholic Fatty Liver Disease ranges from simple steatosis to Nonalcoholic steatohepatitis and cirrhosis. Most cases (90%) of Non Alcoholic Fatty Liver Disease have simple steatosis with benign prognosis. Ten to thirty percent of Non -Alcoholic Fatty Liver Disease progresses to NASH and 25-40% of Nonalcoholic steatohepatitis undergoes progressive liver fibrosis.Ultimately 20-30% of Nonalcoholic steatohepatitis will go into cirrhosis during their lifetime. Nonalcoholic steatohepatitis cirrhosis has higher chances of (2.6% per year) going into hepatocellular carcinoma. There are several risk factors noted for Non Alcoholic Fatty Liver Disease. Some of which includes increasing age, metabolic syndrome, dietary factors etc. Investigations regarding liver function test can be divided into invasive and noninvasive types. Under invasive procedures comes liver biopsy and non-invasive includes radiological tests and various biochemical tests. This article tries to analyze different scoring systems and their significance in diagnosing steatohepatitis and fibrosis.

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Venkatesan, S., Nancy W. Y. Leung, and Timothy J. Peters. "Fatty acid synthesis in vitro by liver tissue from control subjects and patients with alcoholic liver disease." Clinical Science 71, no. 6 (December 1, 1986): 723–28. http://dx.doi.org/10.1042/cs0710723.

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1. Percutaneous liver biopsy specimens were obtained from 11 control subjects, 24 alcoholic patients and six diabetic patients with mild to severe fatty liver and incubated in Krebs–Henseleit buffer containing 3H2O. The incorporation of 3H into fatty acid was measured and the absolute rate of fatty acid synthesis calculated. 2. Fatty acid synthesis rates were significantly lower in alcoholic fatty liver than in controls. 3. Fatty acid synthesis rates were similar in controls and patients with diabetic fatty livers. 4. Addition of 50 mmol/l ethanol did not alter the fatty acid synthesis rates in vitro. It is concluded that enhanced lipogenesis is not the major cause of fatty liver in patients with alcoholic fatty liver.

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Smith, Briohny W., and Leon A. Adams. "Non-alcoholic fatty liver disease." Critical Reviews in Clinical Laboratory Sciences 48, no. 3 (June 2011): 97–113. http://dx.doi.org/10.3109/10408363.2011.596521.

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Maurice, James, and Pinelopi Manousou. "Non-alcoholic fatty liver disease." Clinical Medicine 18, no. 3 (June 2018): 245–50. http://dx.doi.org/10.7861/clinmedicine.18-3-245.

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Dissertations / Theses on the topic "Alcoholic Fatty Liver"

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Bayard, Max, and Jim Holt. "Non-Alcoholic Fatty Liver Disease." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/6495.

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Levene, Adam Phillip. "Steatosis in non alcoholic fatty liver disease." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9691.

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Non-alcoholic fatty liver disease is the commonest cause of chronic liver disease in developed countries. The accurate assessment of steatosis is central to the diagnosis of non-alcoholic fatty liver disease. I compared the assessment of steatosis by histology, biochemical triglyceride assays, digital image analysis, with and without Oil Red-O staining, in mouse livers and human liver biopsies. In each case Oil Red-O digital image analysis was the most reliable technique for quantitating steatosis. I then investigated a potential, non-invasive technique for distinguishing steatosis from steatohepatitis as only the latter causes progressive liver disease. The liver contains fluorophores which can be detected by autofluorescence spectroscopy. The fluorophore levels vary depending on the levels of oxidative stress and fibrosis within the liver. Mouse and human livers, were assessed to measure the fluorescence intensity at different wavelengths and this was compared with the histology. The probe was able to accurately identify biopsies which had inflammation and fibrosis with a high degree of sensitivity and specificity. Autophagocytosis has recently been suggested to play a role in fat metabolism. Using liver differentiated HUH7 cells grown in normal or oleate containing media with or without Rapamycin (an autophagocytosis activator) the role of autophagocytosis was investigated. This involved examining steatosis by Oil Red-O digital image analysis, biochemical triglyceride assays, electron microscopy and confocal immunofluorescence. I concluded that activating autophagocytosis decreased the levels of steatosis within the cells. This work has shown Oil Red-O digital image analysis is the most accurate way of assessing steatosis within the liver, that autofluorescence spectroscopy has the ability to distinguish, in real-time, isolated steatosis from steatohepatitis and that autophagocytosis has a role in fat metabolism within the liver which may be exploited therapeutically.

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De, Alwis Nimantha M. W. "Mitochondrial dysfunction in non alcoholic fatty liver disease." Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493235.

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Non Alcoholic fatty Liver disease (NAFLD) is the commonest chronic liver disease worldwide and is a spectrum which includes simple fatty liver (simple steatosis), non-alcoholic steatohepatitis (NASH) and cirrhosis. Simple steatosis is a benign condition but NASH may progress to liver fibrosis and cirrhosis. Why only some develop progressive disease is not known and maybe dependant on the pathophysiology.

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Liu, Yang-Lin. "Genomic studies in non-alcoholic fatty liver disease." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3822.

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Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum that spans simple steatosis, through steatohepatitis (NASH) to fibrosis and ultimately cirrhosis. NAFLD is characterised by substantial inter-patient variation in rate of progression and disease outcome: whilst up to 25% of the general population are at risk of progressive disease, only a minority experience associated liver-related morbidity. Inter-patient genetic variation and environment determine severity and progression of NAFLD. This thesis reports a series of studies examining the association of genetic variations in two genes patatin-like phospholipase domain-containing 3 (PNPLA3, rs738409 c.444 C > G, p.I148M) and transmembrane 6 superfamily member 2, (TM6SF2, rs58542926 c.449 C > T, p.E167K) with severity of NAFLD and risk of NAFLD-associated hepatocellular carcinoma (HCC). Addressing first the role of PNPLA3, I demonstrate that the rs738409 variant is associated with steatosis, steatohepatitis and fibrosis in the largest histologically characterised NAFLD cohort of European-Caucasian descent (n=1,005) studied to date. Subsequently, adopting a case-control analyses in a cohort of 100 consecutive Northern European Caucasian patients with NAFLD-associated HCC arising and a cohort of patients with histologically characterised NAFLD, I demonstrate that carriage of the rs738409 minor (G) allele is significantly associated with increased risk of developing NAFLD-associated HCC, independent of potential confounding factors including gender, age at diagnosis, presence of advanced fibrosis/cirrhosis, T2DM and BMI. During my studies, a genome-wide association study identified a SNP in TM6SF2 as a modifier of hepatic triglyceride accumulation measured by MR Spectroscopy. It was therefore pertinent to determine whether this variant also affected risk of steatohepatitis or fibrosis in NAFLD. Using the aforementioned cohorts, I demonstrate for the first time that, in addition to its association with steatosis, the rs58542926 SNP is significantly associated with stage of fibrosis in NAFLD. In contrast to PNPLA3 however, no association with NAFLD-HCC was found. In conclusion, the current thesis confirms the association of PNPLA3 with NAFLD severity and provides new evidence of its association with HCC risk. In addition, itdemonstrates for the first time that TM6SF2 is associated with NAFLD-fibrosis severity. These studies provide important new insights into NAFLD pathogenesis and mandate further functional study.

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Scorletti, Eleonora. "Effect of omega-3 fatty acids in non-alcoholic fatty liver disease." Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/422265/.

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The first chapter (Introduction) of the thesis summarises the pathogenesis of NAFLD and its associated risk factors such as type 2 diabetes and cardiovascular disease. Moreover, it describes: a) the potential beneficial effects of long chain omega-3 fatty acid treatment [docosahexaenoic acid (DHA) plus eicosapentaenoic acid (EPA)] in NAFLD; b) the effect of genotypes patatin-like phospholipase domain-containing protein-3 (PNPLA3 I148M) and the transmembrane 6 superfamily member 2 protein (TM6SF2 E167K), on the level of DHA and EPA enrichment and end of study liver fat percentage after DHA+EPA treatment; and c) the effect of fatty acid desaturase (FADS) and Elongase (ELOVL) polymorphisms influencing omega-3 fatty acid metabolism. The second chapter describes the overall aim of this thesis. The aim of my research was to investigate in patients with NAFLD: a) the effect of long-chain omega-3 fatty acid treatment on liver fat percentage and liver fibrosis biomarkers; b) the effect of genotypes influencing NAFLD severity on treatment with DHA+EPA; and c) the effect of genotypes influencing omega-3 fatty acid metabolism in NAFLD. The third chapter describes in details the design and methods used in my research. Chapter four highlights my novel results from the WELCOME study. This chapter describes the baseline and end of study characteristics of the WELCOME study participants and shows the results of the DHA+EPA treatment on liver fat percentage and liver fibrosis biomarkers. This chapter also describes the association between DHA erythrocyte enrichment and decrease in liver fat percentage after DHA+EPA treatment. Chapter five illustrates the association between PNPLA3 I148M and DHA erythrocyte enrichment percentage and end of study liver fat percentage after DHA+EPA treatment. The chapter shows that PNPLA3 I148M was associated with higher end of study liver fat percentage and lower DHA tissue enrichment. Chapter six shows the negative association between FADS polymorphisms and omega-3 fatty acid metabolism in NAFLD. The chapter also shows that there was a gene-DHA+EPA interaction between the minor allele of the FADS1 rs174556 and Δ-5 desaturase activity after treatment with DHA+EPA. Finally, chapter seven, summarises my results in the context of current evidence and knowledge about the subject matter.

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Spanos, Christos. "Quantitative liver proteomics for biomarker discovery in non-alcoholic fatty liver disease." Thesis, University of Surrey, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616323.

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Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease worldwide. Given that NAFLD can progress from steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and potentially hepatocellular carcinoma, early diagnosis and accurate disease staging are primary clinical concerns. Hypothesizing that a subset of liver proteins will exhibit differential expression in NAFLD and that these proteins may represent candidate disease biomarkers; the aims of this project were to use proteomics to identify differentially expressed proteins both in an in vitro and an in vivo model of NASH. Preliminary studies developed and characterised both models used here; experiments utilized a relative quantitative proteomic approach with isobaric tags for relative and absolute quantitation labelling combined with nano-liquid chromatography and tandem mass spectrometry.

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Hallsworth, Kate. "Physical activity, exercise and non-alcoholic fatty liver disease." Thesis, University of Newcastle upon Tyne, 2012. http://hdl.handle.net/10443/1510.

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Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of liver conditions ranging from hepatic steatosis through steatohepatitis to cirrhosis. Its prevalence has been estimated at between one-in-five and one-in-three of the adult population depending on country and diagnostic criteria used. Prevalence increases with degree of obesity, and is very common in those with Type 2 diabetes (T2DM). Rising prevalence of obesity and T2DM, particularly in younger people, will ensure that NAFLD remains a growing clinical concern for the future. Lifestyle modification, which encompasses diet, weight loss, physical activity, and/or exercise related behaviours, is the primary recommended therapy for NAFLD, especially in the absence of approved pharmaceutical agents. Despite lifestyle modifications being central to the management of NAFLD, the evidence base upon which these guidelines are based is lacking, and this is particularly true for physical activity and exercise. The focus of this thesis is on defining, exploring and developing the evidence for physical activity and exercise in NAFLD with a view to improving clinical care. The work contained within this thesis demonstrates that low levels of physical activity are prominent in people with NAFLD and that targeting this with resistance exercise therapy confers benefits to both liver lipid and the factors promoting its accumulation. It also highlights alterations in cardiac structure and function in people with NAFLD in the absence of overt cardiac disease, which may provide a therapeutic avenue in which to decrease cardiac disease risk in people with fatty liver. Over the duration of the work described in this thesis, the number of studies reporting on exercise and liver fat in people with NAFLD has increased markedly. The new information contained within this thesis contributes to this body of knowledge and, over time, will improve the management of a condition that is an increasing burden to the people of the Western world.

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Cheng, Lik-fai, and 鄭力暉. "Non-alcoholic fatty liver disease in Asia: a systematic review." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45171117.

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Ekstedt, Mattias. "Non-Alcoholic Fatty Liver Disease : A clinical and histopathological study." Doctoral thesis, Linköpings universitet, Gastroenterologi och hepatologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-17220.

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Fatty liver has previously often been associated with excessive alcohol consumption. During the last two decades, the interest in fatty liver occurring in non-drinkers i.e. non-alcoholic fatty liver disease (NAFLD) has increased dramatically. Today, NAFLD is considered as the most common liver disease in the developed world. It is strongly associated with obesity, insulin resistance, and hypertension. Thus, NAFLD is considered as the hepatic manifestation of the metabolic syndrome. The spectrum of NAFLD includes: simple fatty liver without necroinflammatory activity; non-alcoholic steatohepatitis (NASH), a condition characterised by hepatocellular injury, inflammation, and fibrosis; cirrhosis; and in some individuals hepatocellular carcinoma. The degree of steatosis in liver biopsies is usually assessed by a morphological semiquantitative approach in which the pathologist uses a four-graded scale: 0–3 or none, slight, moderate and severe. In this thesis we show that there is a considerable inter- and intraindividual variation in such scoring methods and that a more standardised and quantitative approach is preferable. The area/volume of fat in liver biopsies is greatly overestimated when assessed semiquantitatively. Moreover, the point counting technique has a better reproducibility than visual evaluation and should be preferred in estimates of liver steatosis. The long-term clinical and histopathological course of 129 consecutively enrolled NAFLD patients was studied. Mean follow-up (SD) was 13.7 (1.3) years. Survival of NASH patients was reduced compared with a matched reference population. These subjects more often died from cardiovascular and liver-related causes. Seven patients (5.4%) developed end-stage liver disease, including 3 patients with hepatocellular carcinoma. Most NAFLD patients will develop diabetes or impaired glucose tolerance in the long term. Progression of liver fibrosis is associated with more pronounced insulin resistance and significant weight gain. During follow-up, 17 patients had been prescribed a statin. At follow-up, patients on medication with statins had significantly higher BMI. Diabetes was significantly more common among patients on medication with statins and they had significantly more pronounced insulin resistance. However, they exhibited a significant reduction of liver steatosis at follow-up as opposed to patients not taking statins. Although patients under statin treatment exhibited a high risk profile for progression of liver fibrosis, only four patients on statin treatment progressed in fibrosis stage. It is concluded that statins can be prescribed safely in patients with elevated liver enzymes because of NAFLD. Alcohol consumption was evaluated with a validated questionnaire combined with an oral interview. In a multivariate analysis moderate alcohol consumption, particularly when frequency of heavy episodic drinking was analysed, consistent with the diagnosis of NAFLD to be set, was independently associated with fibrosis progression in NAFLD. The NAFLD activity score (NAS) is a newly proposed system to grade the necroinflammatory activity in liver biopsies of NAFLD patients. We evaluated the usefulness of the NAS in predicting clinical deterioration and fibrosis progression in our cohort of NAFLD patients. Although the NAS was independently associated with future risk of progressive fibrosis in NAFLD, the clinical usefulness of the score was limited due to significant overlap in clinical development between NAS-score groups.

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Alshaalan, Rasha. "Non-invasive diagnostic methods for non-alcoholic fatty liver disease." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119567.

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Background: NAFLD is one of the most common causes of liver disease worldwide. It is a spectrum of disease characterized by macrovesicular steatosis of the liver that ranges from simple fatty liver (steatosis), to non-alcoholic steatohepatitis (NASH). NASH may eventually evolve to cirrhosis and end stage complication. Liver biopsy has long been considered the gold standard of reference to diagnose NAFLD but it is costly and invasive. Recently, non-invasive methods have been proposed. Aims and methods: The aim of this study was to investigate the accuracy of non-invasive methods including (Ultrasound, computed tomography scan, Xenon-133 scan, Hepatic steatosis index, Fibroscan, NAFLD fibrosis score, APRI index, and FIB-4 index) and their combination to diagnose steatosis and to diagnose significant liver fibrosis (>F2) and cirrhosis (F4) as compared to liver biopsy. We conducted a retrospective study of 114 NASH patients (79 males, mean age 49.6±10.6). All had adequate liver histology. Results: The distribution of fibrosis stage was as follows: F0-F1= 50%, F2=16.8%, F3=19.2%, F4=14%. The distribution of steatosis grade was as follows: grade 0-1=16%, grade2=53.3%, grade3=30.7%. The following tests correlated with fibrosis: APRI index (r=0.554), FIB-4(r=0.555), NAFLD fibrosis score (r=0.473), Fibroscan(r=0.586) and Hepatic Steatosis Index (HSI) (r=0.245). The FIB-4 and APRI index showed the best diagnostic accuracy for significant fibrosis as indicated by an Area Under the Curve (AUC) of 0.801 and 0.782, respectively. The FIB-4 showed the best AUC= 0.886 for cirrhosis. None of the following tests US, CT, HSI, and xenon-133 scan were considered correlated significantly. The best combination algorithm for the detection of cirrhosis was gender and FIB-4 with an AUC of 0.8937. Conclusion: this study demonstrates that non-invasive methods for liver fibrosis are accurate to diagnose >F2 and F4. Severe steatosis cannot be reliably diagnosed by non-invasive methods. Notably, a combination of FIB-4 and gender significantly improves the performance of the single method for cirrhosis. These methods may help reducing the number of liver biopsies stratifying NASH patients that should start a screening program for HCC and esophageal varices.
Contexte : La stéatose hépatique non alcoolique (SHNA) est l'une des causes les plus répandues des maladies du foie à l'échelle mondiale. Il s'agit d'un spectre de maladies qui se caractérise par une stéatose hépatique macrovésiculaire allant de la stéatose hépatique simple (stéatose) à la stéatohépatite non alcoolique (NASH). La NASH peut éventuellement évoluer vers une cirrhose et des complications en phase terminale. La biopsie du foie a longtemps été considérée comme la norme de référence par excellence pour le diagnostic de la SHNA, mais elle est coûteuse et invasive. Des méthodes non invasives ont récemment été proposées. Objectifs et méthodes : La présente étude avait pour objectif d'évaluer la précision de certaines méthodes non invasives (notamment les ultrasons [US], la tomographie par ordinateur [TO], la scintigraphie au xénon 133, l'indice de stéatose hépatique (ISH), la technique Fibroscan, le score de fibrose de SHNA, l'indice de ratio entre l'aspartate aminotransférase et les plaquettes [APRI] et l'indice FIB-4) et de l'utilisation combinée de ces méthodes pour le diagnostic de la stéatose et pour le diagnostic d'une fibrose hépatique significative (> F2) et de la cirrhose (F4), par comparaison à la biopsie du foie. Nous avons réalisé une étude rétrospective sur 114 patients atteints de NASH (79 patients de sexe masculin, âge moyen de 49,6 ans ± 10,6). Tous ces patients présentaient une histologie hépatique adéquate.Résultats : La répartition des stades de fibrose était la suivante : F0 F1 = 50 %, F2 = 16,8%, F3 = 19,2 %, F4 = 14 %. La répartition des stades de stéatose était la suivante : stade 0-1 = 16 %, stade 2 = 53,3 %, stade 3 = 30,7 %. Les tests suivants ont été mis en corrélation avec la fibrose : l'indice APRI (r = 0,554), l'indice FIB-4 (r = 0,555), le score de fibrose de SHNA (r = 0,473), la technique Fibroscan (r = 0,586) et l'indice de stéatose hépatique (r = 0,245). L'indice FIB-4 et l'indice APRI ont offert la meilleure précision diagnostique en ce qui concerne la fibrose significative, comme l'indiquent la surface sous la courbe (SSC) de 0,801 et la SSC de 0,782 respectivement. L'indice FIB-4 a présenté la meilleure SSC, soit 0,886, pour ce qui est de la cirrhose. Aucun des tests suivants, c'est à dire les tests aux US, la TO, l'ISH, et la scintigraphie au xénon 133, n'était considéré comme étant corrélé significativement. Le meilleur algorithme de combinaison pour le dépistage de la cirrhose était le sexe et l'indice FIB-4 avec une surface sous la courbe de 0,8937. Conclusion: cette étude démontre que les méthodes non invasives de diagnostic de la fibrose hépatique sont précises en ce qui concerne les stades > F2 et F4. La Stéatose sévère ne peut être diagnostiqué de façon fiable par des méthodes non invasives Notamment, une combinaison de l'indice FIB-4 et du sexe améliore considérablement le rendement de la méthode unique en ce qui a trait à la cirrhose. Ces méthodes pourraient aider à réduire le nombre de biopsies du foie visant à stratifier les patients atteints de NASH qui devraient entreprendre un programme de dépistage du carcinome hépatocellulaire (CHC) et des varices œsophagiennes.

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Books on the topic "Alcoholic Fatty Liver"

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Farrell, Geoffrey C., Arthur J. McCullough, and Christopher P. Day, eds. Non-Alcoholic Fatty Liver Disease. Oxford, UK: Wiley-Blackwell, 2013. http://dx.doi.org/10.1002/9781118556153.

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Bugianesi, Elisabetta, ed. Non-Alcoholic Fatty Liver Disease. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6.

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Chalasani, Naga, and Gyongyi Szabo, eds. Alcoholic and Non-Alcoholic Fatty Liver Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0.

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Farrell, Geoffrey C., Arthur J. McCullough, and Christopher Paul Day. Non-alcoholic fatty liver disease: A practical guide. Chichester, West Sussex: John Wiley & Sons, 2013.

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Taylor-Robinson, Simon D., and Roger Williams. Clinical dilemmas in non-alcoholic fatty liver disease. Chichester, West Sussex: John Wiley & Sons Inc., 2016.

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Williams, Roger, and Simon D. Taylor-Robinson, eds. Clinical Dilemmas in Non-Alcoholic Fatty Liver Disease. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924938.

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Buko, V. U. Prostaglandiny pri alkogolʹnom porazhenii pecheni. Minsk: "Navuka i tėkhnika", 1991.

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U, Leuschner, James O. F. W, and Dancygier Henryk, eds. Steatohepatitis: NASH and ASH. Dordrecht: Kluwer Academic, 2001.

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Fitzpatrick, Emer. Non-alcoholic fatty liver disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0061.

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The chapter on non-alcoholic fatty liver disease includes the risk factors for this ever-increasing condition, the pathophysiology, as well as the differential of hepatic steatosis. Finally it includes the most current principles of its management.

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Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Fatty liver disease in children. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0055.

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Demographics 406Pathophysiology 406Differential diagnoses 407Presenting features 407Investigation 408Management 409Fatty liver disease is now increasingly recognized in children, particularly in the setting of obesity.The term non-alcoholic steatohepatitis (NASH) was first coined in 1980 by Ludwig to describe a pattern of liver injury in adults in which the liver histology was consistent with alcoholic hepatitis, but in whom significant alcohol consumption was denied. NASH can be considered as part of a broader spectrum of non-alcoholic fatty liver disease that extends from simple steatosis through steatohepatitis that is characterized by the potential to progress to fibrosis, cirrhosis and subsequent end stage liver disease....

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Book chapters on the topic "Alcoholic Fatty Liver"

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Alcoholic Fatty Liver." In Encyclopedia of Molecular Mechanisms of Disease, 58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8719.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Alcoholic Fatty Liver Disease." In Encyclopedia of Molecular Mechanisms of Disease, 58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8720.

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Awai, Hannah I., Kimberly P. Newton, and Jeffrey B. Schwimmer. "Nonalcoholic Fatty Liver Disease in Children." In Alcoholic and Non-Alcoholic Fatty Liver Disease, 339–62. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0_17.

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Arteel, Gavin E., and David W. Crabb. "Pathogenesis of Alcoholic Liver Disease." In Alcoholic and Non-Alcoholic Fatty Liver Disease, 41–69. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0_3.

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Petrasek, Jan, and Gyongyi Szabo. "Treatment of Alcoholic Liver Disease Including Emerging Therapies, Novel Targets, and Liver Transplantation." In Alcoholic and Non-Alcoholic Fatty Liver Disease, 291–311. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0_15.

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Xu, Jun, and Hidekazu Tsukamoto. "Animal Models of Alcoholic Liver Disease." In Alcoholic and Non-Alcoholic Fatty Liver Disease, 103–19. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0_5.

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Hardy, Timothy, and Christopher P. Day. "Non-Alcoholic Fatty Liver Disease." In Sherlock's Diseases of the Liver and Biliary System, 540–60. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119237662.ch28.

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Bugianesi, Elisabetta. "Non-Alcoholic Fatty Liver Disease." In Frontiers of Gastrointestinal Research, 1–14. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000258249.

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Caldwell, Stephen H., and Curtis K. Argo. "Non-alcoholic fatty liver disease." In Clinical Dilemmas in Non-Alcoholic Fatty Liver Disease, 1–7. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924938.ch1.

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Marjot, Thomas, and Jeremy Cobbold. "Non-alcoholic Fatty Liver Disease." In In Clinical Practice, 111–29. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43126-0_7.

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Conference papers on the topic "Alcoholic Fatty Liver"

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Male, E., H. Liaquat, N. Agrawal, A. J. Mamary, K. Carney, T. Bronzell-Wynder, G. J. Criner, and P. Mulhall. "Non-Alcoholic Fatty Liver Disease in Lung Transplant." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4744.

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Jagtap, N., R. Kalapala, A. Katakwar, H. Kanakagiri, S. Darisetty, and DN Reddy. "Endoscopic Sleeve Gastroplasty for non-alcoholic Fatty Liver Disease." In ESGE Days 2021. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1724306.

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Singh, I., V. Leone, X. Li, D. Pfister, M. Stadler, E. Kotsiliti, S. Rössler, et al. "Dysregulated epigenetic factors in non-alcoholic fatty liver disease and triggered liver cancer." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677184.

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Shi, Ivy, and Takuya Sakaguchi. "Abstract 2111A: Molecular genetics of non-alcoholic fatty liver disease." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2111a.

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Malnick, Stephen. "5 Non-alcoholic fatty liver disease (NAFLD) -underdiagnosed but overtreated." In Preventing Overdiagnosis Abstracts, December 2019, Sydney, Australia. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/bmjebm-2019-pod.111.

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Абрамян, Мария Владимировна, Алина Викторовна Свиридова, and Елена Николаевна Веселова. "HELICOBACTER PYLORI INFECTION AND ITS ROLE IN THE PATHOGENESIS OF NONALCOHOLIC FATTY LIVER DISEASE." In Наука. Исследования. Практика: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Февраль 2021). Crossref, 2021. http://dx.doi.org/10.37539/srp295.2021.30.76.006.

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Abstract:

Велика ли роль инфекции Helicobacter pylori на патогенез неалкогольной жировой болезни печени (НАЖБП)? Последние данные свидетельствуют о наличии их взаимосвязи [1, 2]. Однако до сих пор данная тема остается под вопросом. Цель данной работы - исследовать возможную связь и клиническое значение Helicobacter pylori в патогенезе неалкогольной жировой болезни печени. Is the role of Helicobacter pylori infection on the pathogenesis of non-alcoholic fatty liver disease (NAFLD) significant? Recent data indicate the presence of their relationship [1, 2]. However, until now, this topic remains in question. The aim of this work is to investigate the possible relationship and clinical significance of Helicobacter pylori in the pathogenesis of non-alcoholic fatty liver disease

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Choi, Changhoon, Wonseok Choi, Jeesu Kim, and Chulhong Kim. "Photothermal strain imaging for diagnosis of non-alcoholic fatty liver disease." In Photons Plus Ultrasound: Imaging and Sensing 2020, edited by Alexander A. Oraevsky and Lihong V. Wang. SPIE, 2020. http://dx.doi.org/10.1117/12.2544552.

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Byrne, CD. "4 Diagnosis and management of non-alcoholic fatty liver disease (NAFLD)." In Abstracts from the Fellowship of Postgraduate Medicine Centenary Conference 2018: Transforming Health and Health Care. The Fellowship of Postgraduate Medicine, 2018. http://dx.doi.org/10.1136/postgradmedj-2018-fpm.4.

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Tirikova, O. V., N. M. Kozlova, A. YU Tarasov, S. M. Eliseev, and S. V. Lunenok. "Epidemiology of non-alcoholic fatty liver disease in the Baikal region." In Scientific achievements of the third millennium. SPC "LJournal", 2021. http://dx.doi.org/10.18411/scienceconf-03-2021-11.

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Hohmann, N., WE Haefeli, S. Mueller, H. Seitz, F. Schröder, H. Teng, B. Moreira, and T. Bruckner. "Clomethiazole improves alcoholic fatty liver in patients admitted to the hospital for alcohol detoxification therapy." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402136.

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Reports on the topic "Alcoholic Fatty Liver"

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Zhang, Tiefeng, Duan Han, Tianqi Zhang, Cai Jing, and Jianguang Sun. Complementary and alternative therapies for non-alcoholic fatty liver disease: A Bayesian network meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2020. http://dx.doi.org/10.37766/inplasy2020.12.0136.

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Zhang, Jing, Yiting Wang, and Xinyi Xia. Incidence of Breast cancer among Non-alcoholic fatty liver disease patients: a systematic review and meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0046.

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Liu, Wen-juan. Association between non-alcoholic fatty liver and acute cerebral infarction: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0102.

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Liu, Su-tong, Kai-qi Su, Li-hui Zhang, Ming-hao Liu, and Wen-xia Zhao. Hypoglycemic agents for non-alcoholic fatty liver disease with type 2 diabetes mellitus: A protocol for systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2020. http://dx.doi.org/10.37766/inplasy2020.7.0016.

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