Journal articles on the topic 'Non-Alcoholic Fatty Liver Disease NASH'
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Byrne, Christopher D. "Hypoxia and non-alcoholic fatty liver disease." Clinical Science 118, no. 6 (December 14, 2009): 397–400. http://dx.doi.org/10.1042/cs20090565.
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NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation.
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Scarlat, Gabriel, Bassil Dona, Mihai Cârstea, and Marilena Stoian. "Insights into Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis." Internal Medicine 19, no. 1 (January 1, 2022): 61–77. http://dx.doi.org/10.2478/inmed-2022-0198.
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Abstract Non-alcoholic fatty liver disease (NAFLD) constitutes a common pathological condition of the liver, the prevalence of which is currently increasing in western countries. NAFLD is frequently diagnosed in males and its incidence is higher in individuals with type 2 diabetes mellitus and obesity. Hence, the disease is considered to be the hepatic manifestation of the metabolic syndrome. A multitude of interconnected risk factors have been described over the years – genetic, hormonal and nutritional, which play important roles in the development of NAFLD. Insulin resistance is considered to be the central pathophysiological condition that promotes the disease in diabetic patients, whereas dyslipidemia and cardiovascular comorbidities (arterial hypertension, ischaemic heart disease) are frequently associated conditions. Although there are currently numerous pathophysiological mechanisms involved in NAFLD that are still unknown or poorly understood, there has been some advancements concerning the pathogenesis of the disease and its progression towards its severe form, known as non-alcoholic steatohepatitis (NASH). In the absence of a clear diagnosis and carefully controlled treatment, NAFLD/NASH may evolve towards liver cirrhosis, liver failure or hepatocellular carcinoma. However, the disease may also generate systemic effects, including the development of chronic kidney disease (CKD). The diagnosis of NAFLD/NASH is based both on its clinical manifestations, revealed by a carefully conducted patient history and physical examination of the patient, and on other investigations; histopathological findings upon liver biopsy, liver ultrasonography and the use of transient elastography (or FibroScan) are some of the most important investigations in NAFLD/NASH. The understanding of the most important risk factors and pathogenic mechanisms of the disease is fundamental for the elaboration of the most efficient treatment, to prevent chronic liver disease or the development of hepatocellular carcinoma.
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Ramai, Daryl, Antonio Facciorusso, Erika Vigandt, Bryan Schaf, Waleed Saadedeen, Aditya Chauhan, Sara di Nunzio, Aashni Shah, Luca Giacomelli, and Rodolfo Sacco. "Progressive Liver Fibrosis in Non-Alcoholic Fatty Liver Disease." Cells 10, no. 12 (December 2, 2021): 3401. http://dx.doi.org/10.3390/cells10123401.
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Non-alcoholic steatohepatitis (NASH) is a chronic and progressive form of non-alcoholic fatty liver disease. Its global incidence is increasing and makes NASH an epidemic and a public health threat. Non-alcoholic fatty liver disease is associated with major morbidity and mortality, with a heavy burden on quality of life and liver transplant requirements. Due to repeated insults to the liver, patients are at risk for developing hepatocellular carcinoma. The progression of NASH was initially defined according to a two-hit model involving an initial development of steatosis, followed by a process of lipid peroxidation and inflammation. In contrast, current evidence proposes a “multi-hit” or “multi-parallel hit” model that includes multiple pathways promoting progressive fibrosis and oncogenesis. This model includes multiple cellular, genetic, immunological, metabolic, and endocrine pathways leading to hepatocellular carcinoma development, underscoring the complexity of this disease.
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Sadikova, D. Sh, F. A. Khaydarova, and D. M. Esimova. "CONSTRUCTION OF COMPUTER MODEL FOR DIAGNOSTICS AND MONITORING OF NON-ALCOHOLIC FATTY LIVER DISEASE." UZBEK MEDICAL JOURNAL 2, no. 2 (February 28, 2021): 9–14. http://dx.doi.org/10.26739/2181-0664-2021-2-2.
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Timely diagnosis and treatment of non-alcoholic fatty liver disease (NAFLD) are essential to prevent the development of steatohepatitis and liver cirrhosis. This is especially true for patients with type 2 diabetes. The aim of our workwas to build a computer model for the diagnosis and monitoring of NAFLD treatment. Materials and methods. The study included more than 55 clinical and laboratory parameters of 233 patients with non-alcoholic steatosis (NAS) and 60 patients with steatohepatitis (NASH). Results. The calculations were based on the levels of systolic blood pressure, erythrocytes, ALT, AST, glutamate dehydrogenase and platelets in persons with type 2 diabetes mellitus with NAS and NASH. The model allows to differentiate NAS andNASH with a sensitivity of 82% and a specificity of 88%
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South, Kathy. "Non-Alcoholic Steatohepatitis (NASH)/Non-Alcoholic Fatty Liver Disease (NAFLD)." Gastroenterology Nursing 29, no. 2 (March 2006): 169. http://dx.doi.org/10.1097/00001610-200603000-00082.
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Byrne, Christopher D., Rasaq Olufadi, Kimberley D. Bruce, Felino R. Cagampang, and Mohamed H. Ahmed. "Metabolic disturbances in non-alcoholic fatty liver disease." Clinical Science 116, no. 7 (March 2, 2009): 539–64. http://dx.doi.org/10.1042/cs20080253.
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NAFLD (non-alcoholic fatty liver disease) refers to a wide spectrum of liver damage, ranging from simple steatosis to NASH (non-alcoholic steatohepatitis), advanced fibrosis and cirrhosis. NAFLD is strongly associated with insulin resistance and is defined by accumulation of liver fat >5% per liver weight in the presence of <10 g of daily alcohol consumption. The exact prevalence of NAFLD is uncertain because of the absence of simple non-invasive diagnostic tests to facilitate an estimate of prevalence. In certain subgroups of patients, such as those with Type 2 diabetes, the prevalence of NAFLD, defined by ultrasound, may be as high as 70%. NASH is an important subgroup within the spectrum of NAFLD that progresses over time with worsening fibrosis and cirrhosis, and is associated with increased risk for cardiovascular disease. It is, therefore, important to understand the pathogenesis of NASH and, in particular, to develop strategies for interventions to treat this condition. Currently, the ‘gold standard’ for the diagnosis of NASH is liver biopsy, and the need to undertake a biopsy has impeded research in subjects in this field. Limited results suggest that the prevalence of NASH could be as high as 11% in the general population, suggesting there is a worsening future public health problem in this field of medicine. With a burgeoning epidemic of diabetes in an aging population, it is likely that the prevalence of NASH will continue to increase over time as both factors are important risk factors for liver fibrosis. The purpose of this review is to: (i) briefly discuss the epidemiology of NAFLD to describe the magnitude of the future potential public health problem; and (ii) to discuss extra- and intra-hepatic mechanisms contributing to the pathogenesis of NAFLD, a better understanding of which may help in the development of novel treatments for this condition.
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Toman, Daniel, Petr Vavra, Petr Jelinek, Petr Ostruszka, Peter Ihnat, Ales Foltys, and Jan Roman. "A review on fatty liver disease or non-alcoholic fatty liver disease and hepatocellular carcinoma." Research Journal of Biotechnology 16, no. 10 (September 25, 2021): 156–62. http://dx.doi.org/10.25303/1610rjbt156162.
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The non-alcoholic fatty liver disease (NAFLD) is the predominant etiological factor for liver disease. There is a risk of the development of hepatocellular carcinoma (HCC) in patients suffering from NAFLD. Non-alcoholic steatohepatitis (NASH) is one of the risk factors for the development of HCC. The aim is to discuss an association of NAFLD and HCC in the adult population. HCC is one of the debilitating complications of NAFLD/NASH and obesity is a causative factor for NAFLD/NASH. Various clinical data suggest that obesity appears to be a causative factor in the progression of NAFLD/NASH to HCC. We searched data from the PubMed/Medline and Google Scholar databases including various studies and review articles. Significantly, an increased number of HCC patients with cryptogenic liver disease had well-differentiated tumors than in HCC patients with chronic viral hepatitis and alcoholism. HCC is one of the debilitating complications of NAFLD/NASH and obesity is a causative factor for NAFLD/NASH. Various preclinical and clinical data suggest that obesity appears to be an important causative factor in the progression of NAFLD/NASH to HCC.
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Doumas, Michael, Konstantinos Imprialos, Konstantinos Stavropoulos, and Vasilios G. Athyros. "What Does the Future Hold for Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis?" Current Vascular Pharmacology 17, no. 5 (August 1, 2019): 425–28. http://dx.doi.org/10.2174/157016111705190703102816.
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: Non-Alcoholic Fatty Liver Disease (NAFLD), the most common liver disease, is characterized by accumulation of fat (>5% of the liver tissue), in the absence of alcohol abuse or other chronic liver diseases. Its prevalence is increasing because of obesity, metabolic syndrome or Type 2 Diabetes Mellitus (T2DM). NAFLD can cause liver inflammation and progress to Non-Alcoholic Steatohepatitis (NASH), fibrosis, cirrhosis or Hepatocellular Cancer (HCC). Nevertheless, Cardiovascular Disease (CVD) is the most common cause of morbidity and mortality in NAFLD/NASH patients. Current guidelines suggest the use of pioglitazone both in patients with T2DM and in those without. : The newer antidiabetic drugs such as Glucagon Like Peptide-1 Receptor Agonists (GLP-1 RA), Sodium-Glucose co- Transporter-2 inhibitors (SGLT2i), and statins plus ezetimibe, are considered safe by the guidelines, and may have a beneficial effect on NAFLD/NASH as well as Cardiovascular Disease (CVD) morbidity and mortality. : Future drugs seem to have a potential for holding down the evolution of NAFLD and reduce liver- and CVD-related morbidity and mortality, but they will take some years to be approved for routine use. : Until then pioglitazone, GLP-1 RA, SGLT2i, and statins plus ezetimibe, especially in combination might be useful for treating the huge number of patients with NAFLD/NASH.
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Bentsa, T. M. "The therapeutic aspects of non-alcoholic fatty liver disease." Medicine of Ukraine, no. 8(264) (November 22, 2022): 18–21. http://dx.doi.org/10.37987/1997-9894.2022.8(264).271835.
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Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the developed world. NAFLD is encompasses a spectrum of liver manifestations ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis, which may ultimately progress to hepatocellular carcinoma. NASH is an aggressive form of NAFLD, associated with an increased risk of liver and non-liver-related mortality. Liver-biopsy remains the gold standard for diagnosis, but the majority of patients liver damage can be diagnosed accurately by noninvasive methods.
Early identification and management of patients with intensive dietary and lifestyle modification are essential to prevent the development of advanced liver disease and its complications. Pharmacological therapy should be administered to patients with NASH purposed on the fibrosis inhibition, especially in case of the established predictors of high risk of disease progression (age ˃ 50 years, metabolic syndrome, type 2 diabetes mellitus, or ALT increase), as well as to the patients with active NASH with high inflammatory activity
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Garbuzenko, D. V. "Drug Therapy for Non-Alcoholic Steatohepatitis-Induced Liver Fibrosis." Russian Journal of Gastroenterology, Hepatology, Coloproctology 31, no. 5 (January 2, 2022): 16–24. http://dx.doi.org/10.22416/1382-4376-2021-31-5-16-24.
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Aim. An overview of current pharmacotherapy for non-alcoholic steatohepatitis (NASH)-associated liver fibrosis.Key points. In current clinical recommendations, therapeutic measures in non-alcoholic fatty liver disease should include lifestyle change, body weight normalisation, NASH-associated liver fibrosis-specific drug therapy and treatment for metabolic syndrome-related diseases. Given a lack of approved antifibrotic therapies in NASH, several drugs have nevertheless demonstrated an adequate efficacy and safety in phase 3 clinical trials, also in compensated cirrhosis, which allows their practical validation in phase 4.Conclusion. The understanding of liver fibrosis as an adverse natural consequence of non-alcoholic fatty liver disease clearly attests for an early introduction and wide use of antifibrotic therapy to improve NASH outcomes and avoid associated complications.
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Yefimenko, T. I., and M. R. Mykytyuk. "Non-alcoholic fatty liver disease: time for changes." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 17, no. 4 (August 17, 2021): 334–45. http://dx.doi.org/10.22141/2224-0721.17.4.2021.237350.
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The review contains updated information on the epidemiology, etiology, pathogenesis, diagnosis, treatment and prevention of non-alcoholic fatty liver disease (NAFLD). We searched for terms including NAFLD, non-alcoholic steatohepatitis (NASH), metabolic syndrome and type 2 diabetes mellitus in literature published over the past 5 years using the Scopus, Web of Science, CyberLeninka, PubMed databases. The concept of NAFLD includes two morphological forms of the disease with different prognosis: non-alcoholic fatty hepatosis and NASH. The severity of NASH is quite variable, including fibrosis, cirrhosis and hepatocellular carcinoma. NAFLD, a spectrum of fatty liver disorders of viral, autoimmune, drug-induced, and genetic origin, which are not caused by alcohol abuse, has recently been renamed as metabolic (dysfunction) associated fatty liver disease (MAFLD). The average prevalence of NAFLD is approximately 25 % among the adult population worldwide, and in some regions exceeds 30 %. An increase in the prevalence of this pathology is in parallel with the global epidemic of obesity and type 2 diabetes mellitus in the world. It is time to reach a general consensus in the scientific community on changing the nomenclature and moving from a negative to a positive definition of NAFLD/NASH. The new nomenclature points to the “positive” determinants of the disease, namely the close relationship with metabolic disorders, instead of defining it as what it is not (ie. non-alcoholic). The MAFLD abbreviation more accurately discloses existing knowledge about fatty liver diseases associated with metabolic dysfunction and should replace NAFLD/NASH, as this will stimulate the research community’s efforts to update the disease nomenclature and subphenotype and accelerate the transition to new treatments. It is important that primary care physicians, endocrinologists, and other specialists are aware of the extent and long-term consequences of NAFLD. Early identification of patients with NASH can help improve treatment outcomes, avoid liver transplantation in patients with decompensated cirrhosis. There are currently no effective treatments for NAFLD, so it is important to follow a multidisciplinary approach, which means using measures to improve prognosis, reduce the risk of death associated with NAFLD, the development of cirrhosis or hepatocellular carcinoma. Epidemiological data suggest a close relationship between unhealthy lifestyles and NAFLD, so lifestyle adjustments are needed to all patients. Insulin sensitizers, statins, ezetimibe, a cholesterol absorption inhibitor, hepatoprotectors, antioxidants, incretin analogues, dipeptidyl peptidase 4 inhibitors, pentoxifylline, probiotics, angiotensin-converting enzyme inhibitors, and endocannabinoid antagonists are used in the treatment of NAFLD.
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Prakash, Gnana. "Non-Alcoholic Steatohepatitis (NASH): An Update." International Journal of Research in Pharmaceutical Sciences 13, no. 1 (March 15, 2022): 1–4. http://dx.doi.org/10.26452/ijrps.v13i1.7.
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Non-alcoholic Steatohepatitis (NASH) is a globally rising, multifactorial disease which may be a result of obesity, diabetes (type-2), hypercholesteremia and gut dysbiosis. NASH is characterized by inflammation and fibrosis of liver tissues which further leads to hepatocellular carcinoma or liver failure. Patients with non-alcoholic fatty liver disease (NAFLD) show symptoms of NASH in which the fat accumulation in the liver exceeds 5-10%. Accumulation of this fat in the form of triglyceride in the hepatocytes is the key factor for the development of NASH. This may be caused due to increase in the flow of fatty acid and de novo lipogenesis. This abnormal retention of fat leads to lipotoxicity, which can cause apoptosis, necrosis, inflammation and an increase in oxidative stress. Since the pathological factors associated with NASH are unclear, the treatment to control the progression and management of the disease is cumbersome. Progress is being made in order to understand the cellular and molecular mechanisms associated with the pathogenesis of this condition. With studies reporting that NASH is the most common liver disease after hepatitis C, there is an increase in the demands for medical therapy and diagnosis of NASH. However, no treatment has been proven to be effective for long-term use. Gut dysbiosis, major pathways involved in NASH progression, experimental animal models and the current therapeutic strategies for NASH is discussed in the present review.
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Zhang, Chunye, Shuai Liu, and Ming Yang. "The Role of Interferon Regulatory Factors in Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis." Gastroenterology Insights 13, no. 2 (April 26, 2022): 148–61. http://dx.doi.org/10.3390/gastroent13020016.
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Non-alcoholic fatty liver disease (NAFLD) is becoming the most common chronic liver disease with many metabolic comorbidities, such as obesity, diabetes, and cardiovascular diseases. Non-alcoholic steatohepatitis (NASH), an advanced form of NAFLD, accompanies the progression of hepatic steatosis, inflammation, cell death, and varying degree of liver fibrosis. Interferons (IFNs) have been shown to play important roles in the pathogenesis of NAFLD and NASH. Their regulating transcriptional factors such as interferon regulatory factors (IRFs) can regulate IFN expression, as well as genes involved in macrophage polarization, which are implicated in the pathogenesis of NAFLD and advanced liver disease. In this review, the roles of IRF-involved signaling pathways in hepatic inflammation, insulin resistance, and immune cell activation are reviewed. IRFs such as IRF1 and IRF4 are also involved in the polarization of macrophages that contribute to critical roles in NAFLD or NASH pathogenesis. In addition, IRFs have been shown to be regulated by treatments including microRNAs, PPAR modulators, anti-inflammatory agents, and TLR agonists or antagonists. Modulating IRF-mediated factors through these treatments in chronic liver disease can ameliorate the progression of NAFLD to NASH. Furthermore, adenoviruses and CRISPR activation plasmids can also be applied to regulate IRF-mediated effects in chronic liver disease. Pre-clinical and clinical trials for evaluating IRF regulators in NAFLD treatment are essential in the future direction.
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Zhang, Chunye, Shuai Liu, and Ming Yang. "The Role of Interferon Regulatory Factors in Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis." Gastroenterology Insights 13, no. 2 (April 26, 2022): 148–61. http://dx.doi.org/10.3390/gastroent13020016.
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Non-alcoholic fatty liver disease (NAFLD) is becoming the most common chronic liver disease with many metabolic comorbidities, such as obesity, diabetes, and cardiovascular diseases. Non-alcoholic steatohepatitis (NASH), an advanced form of NAFLD, accompanies the progression of hepatic steatosis, inflammation, cell death, and varying degree of liver fibrosis. Interferons (IFNs) have been shown to play important roles in the pathogenesis of NAFLD and NASH. Their regulating transcriptional factors such as interferon regulatory factors (IRFs) can regulate IFN expression, as well as genes involved in macrophage polarization, which are implicated in the pathogenesis of NAFLD and advanced liver disease. In this review, the roles of IRF-involved signaling pathways in hepatic inflammation, insulin resistance, and immune cell activation are reviewed. IRFs such as IRF1 and IRF4 are also involved in the polarization of macrophages that contribute to critical roles in NAFLD or NASH pathogenesis. In addition, IRFs have been shown to be regulated by treatments including microRNAs, PPAR modulators, anti-inflammatory agents, and TLR agonists or antagonists. Modulating IRF-mediated factors through these treatments in chronic liver disease can ameliorate the progression of NAFLD to NASH. Furthermore, adenoviruses and CRISPR activation plasmids can also be applied to regulate IRF-mediated effects in chronic liver disease. Pre-clinical and clinical trials for evaluating IRF regulators in NAFLD treatment are essential in the future direction.
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Yoneda, Masato, Satoru Saito, and Atsushi Nakajima. "III. Non-alcoholic Fatty Liver Disease (NAFLD) /Non-alcoholic Steatohepatitis (NASH)." Nihon Naika Gakkai Zasshi 110, no. 4 (April 10, 2021): 729–37. http://dx.doi.org/10.2169/naika.110.729.
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BUGIANESI, E., R. MARZOCCHI, N. VILLANOVA, and G. MARCHESINI. "Non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH): treatment." Best Practice & Research Clinical Gastroenterology 18, no. 6 (December 2004): 1105–16. http://dx.doi.org/10.1016/s1521-6918(04)00086-1.
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Bogomolov, Pavel O., Kseniya Yu Kokina, Aleksander Yu Mayorov, and Ekaterina E. Mishina. "Genetic Aspects of Non-Alcoholic Fatty Liver Disease." Current pediatrics 17, no. 6 (January 31, 2019): 442–48. http://dx.doi.org/10.15690/vsp.v17i6.1974.
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Non-alcoholic fatty liver disease (NAFLD) is the most commonly diagnosed hepatopathy. There is an increase in the incidence of NAFLD in the structure of liver diseases in children and adolescents, which is directly related to the increasing prevalence of obesity. The spectrum of liver tissue changes in NAFLD ranges from benign hepatocellular steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis of the liver, and hepatocellular carcinoma. With the increasing prevalence of NAFLD in children, we can expect an increase in the incidence of adverse outcomes among people of working age. The key problem for NAFLD is the prediction of disease outcomes. In epidemiological and genetic studies, the relationship between the morphological stage of NAFLD and hereditary factors is shown. Currently, there are three genes associated with NAFLD (PNPLA3, TM6SF2, and GCKR), which, together with the genes responsible for insulin resistance, lipid deposition, inflammation and fibrogenesis in hepatocytes, determine the phenotype of fatty liver disease. The article considers the modern understanding of the issues of genetics, development of liver steatosis and progression of NASH. It is expected that this knowledge can transform our risk stratification strategies in patients with NAFLD and help identify new therapeutic goals.
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Sarwanti, Marini Stephanie, and Ria Kodariah. "Role of CD44 in Non-Alcoholic Steatohepatitis (NASH) Progressivity." Majalah Patologi Indonesia 29, no. 2 (May 1, 2020): 71–81. http://dx.doi.org/10.55816/mpi.v29i2.415.
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Non alcoholic Steatohepatitis (NASH) is part of a group of conditions called Non-Alcoholic Fatty Liver Diseases(NAFLD) where it is a chronic disease, which defined after elimination other causes of fatty liver, such as excessivealcohol consumption and other causes of chronic liver diseases. NASH is fatty liver disease which characterized byballooning of hepatocyte and lobular inflammation with or without fibrosis. Histopathology diagnose on NASH can bedefined by performing liver biopsy. The purpose of liver biopsy is to define level and degree of the disease. Cluster ofDifferentiation (CD) 44 is a transmembrane glycoprotein receptor which located on the surface of macrophage cells,lymphocytes and endothelial cells. In studies which conducted on mice and humans, showed that CD44 playsimportant role in the progression of NASH. CD44 regulates inflammation of adipose tissue and liver. CD44 ispresumed as a marker which increase macrophage infiltration and other inflammatory cells on liver. This processleads to ultimate increment on insulin resistance and fatty liver. Deficiency was discovered on mice which injectedwith methionine and choline deficiency diet (MCDD). CD44 is associated with preventive method to prevent livercomplication by reducing macrophage or monocyte and as well as neutrophil accumulation in liver which wasevaluated through reducing numbers of inflammatory focus, expression of inflammatory cytokines: tumor necrosisfactor α (TNFα), interleukin (IL) -1B and nitric oxide synthesis (iNOS), and pro-inflammatory types of macrophage. Inobese patients, number of CD44 is predicted to be increasing.
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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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Dumitrascu, Dan L., and Manuela G. Neuman. "NON-ALCOHOLIC FATTY LIVER DISEASE: AN UPDATE ON DIAGNOSIS." Medicine and Pharmacy Reports 91, no. 2 (April 26, 2018): 147–50. http://dx.doi.org/10.15386/cjmed-993.
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Background and aim. The non-alcoholic fatty liver disease (NAFLD) and its sub-entity, the non-alcoholic steatohepatitis (NASH) represent a field of a tremendous progress in recent years. Clinicians need to remain updated with new data on pathogenesis and therapy. The present mini review aims to present some new scientific reports on the diagnosis of NAFLD and NASH for clinical practitioners.Methods. A systematic literature search of the main international databases was performed. We looked for seminal and innovative papers published in main international languages. A narrative review of the topic was consequently written.Results. This review describes new data on the diagnosis of NAFLD including NASH. Liver punction biopsy remains the gold standard. However many patients and clinicians prefer to use noninvasive methods. We present the serological tests and the imaging methods used to diagnose inflammation and fibrosis occurring in NAFLD and NASH.Conclusions. NAFLD-NASH are multifaceted entities that have to be diagnosed and treated by skilled and informed practitioners.
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Iravani, Farzaneh, Neda Hosseini, and Majid Mojarrad. "Role of MicroRNAs in Pathophysiology of Non-alcoholic Fatty Liver Disease and Non-alcoholic Steatohepatitis." Middle East Journal of Digestive Diseases 10, no. 4 (July 17, 2018): 213–19. http://dx.doi.org/10.15171/mejdd.2018.113.
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Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide. It includes wide range of diseases from different subtypes of simple steatosis to non-alcoholic steatohepatitis (NASH), which may be complicated by liver fibrosis, cirrhosis, or hepatocellular carcinoma. Of the epigenetic factors that play a key role in the progression of it, is microRNAs (miRNAs). MiRNAs are short non-coding RNAs of 22-23 nucleotides in length, which regulate a large number of genes that have a critical role in regulation of lipid and cholesterol biosynthesis in hepatocytes. MiRNAs can be used as a very powerful biomarker to diagnosis and follow-up any disorder, such as NAFLD and NASH with a high specificity and sensitivity. The aim of this study was to review the role of different miRNAs in the pathophysiology of NASH and NAFLD.
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Voiculescu, Mihai, Radu M. Nanau, and Manuela G. Neuman. "Non-invasive Biomarkers in Non-Alcoholic Steatohepatitisinduced Hepatocellular Carcinoma." Journal of Gastrointestinal and Liver Diseases 23, no. 4 (December 1, 2014): 425–29. http://dx.doi.org/10.15403/jgld.2014.1121.234.bna.
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Non-alcoholic fatty liver disease (NAFLD) is by far the most common form of chronic liver disease worldwide, affecting adults as well as children. Under the term of NAFLD there is a wide spectrum of diseases ranging from simple steatosis to the non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis and hepatocellular carcinoma (HCC). Several mechanisms have been described to influence the progression of the disease from the benign NAFL to the aggressive NASH. The imbalance between pro- and anti-oxidant mechanisms and between pro- and anti-inflammatory cytokines is thought to play a pivotal role in the pathogenesis of NAFLD and disease progression toward NASH and fibrosis. The present review intends to look at some of the mechanistic biomarkers to be employed in establishing an early diagnosis in HCC derived from NASH.Abbreviations: ANGPT: angiopoietin-2; AFP: α-fetoprotein; ALT: alanine aminotransferase; AST: aspartate aminotransferase; CI: confidence interval; COL: collagen; DCP: des-carboxyprothrombin; γGT: gamma glutamyl transpeptidase; HBV: hepatitis B virus; HCC: hepatocellular carcinoma; HCV: hepatitis C virus; HR: hazard ratio; ITG: integrin; LAM: laminin collagen genes; MMP: matrix metalloproteinase; MS: metabolic syndrome; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; PDGFRA: platelet derived growth factor receptor-α
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Li, Chao, Lihong Cui, Xiaohui Wang, Zhihui Yan, Shaoxin Wang, and Yan Zheng. "Using intestinal flora to distinguish non-alcoholic steatohepatitis from non-alcoholic fatty liver." Journal of International Medical Research 48, no. 12 (December 2020): 030006052097812. http://dx.doi.org/10.1177/0300060520978122.
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Objective To explore specific flora in mouse models of non-alcoholic steatohepatitis (NASH) to improve NASH diagnostic protocols. Methods Sixty mice were divided into normal diet (ND, 20 mice) and high-fat/high-sugar diet (HFSD) groups (40 mice). After 8 weeks of feeding, 10 mice in the ND group and 20 mice in the HFSD group were sacrificed to create the short-term ND and non-alcoholic fatty liver (NAFL) groups, respectively. After 16 weeks of feeding, the remaining mice were sacrificed to create the long-term ND and NASH groups, respectively. We then examined fecal flora, serum biochemical indices, and lipopolysaccharide and tumor necrosis factor-α levels and analyzed liver tissue. Results The relative abundance of Lactobacillus, Desulfovibrio, Ruminiclostridium 9, and Turicibacter differed between NASH and NAFL mice, and the areas under the receiver operating characteristic curve of the four genera for diagnosing NASH were 0.705, 0.734, 0.737, and 0.937. The non-alcoholic fatty liver disease activity score was positively correlated with the relative abundance of Desulfovibrio (r = 0.353), Ruminiclostridium 9 (r = 0.431), and Turicibacter (r = 0.688). Conclusions The relative abundance of Lactobacillus, Desulfovibrio, Ruminiclostridium, and Turicibacter may help distinguish NASH from NAFL.
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Miyake, Teruki, Sakiko Yoshida, Shinya Furukawa, Takenori Sakai, Fujimasa Tada, Hidenori Senba, Shin Yamamoto, et al. "Ipragliflozin ameliorates liver damage in non-alcoholic fatty liver disease." Open Medicine 13, no. 1 (September 14, 2018): 402–9. http://dx.doi.org/10.1515/med-2018-0059.
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AbstractBackgroundThere are few effective medications for non-alcoholic steatohepatitis (NASH). We investigated the efficacy of ipragliflozin (selective sodium-glucose cotransporter-2 inhibitor [SGLT2I]) for the treatment of patients with type 2 diabetes mellitus (T2DM) complicated by non-alcoholic fatty liver disease (NAFLD).MethodsWe prospectively enrolled patients with T2DM complicated by NAFLD treated at our institutions from January 2015 to December 2016. Patients received oral ipragliflozin (50 mg/day) once daily for 24 weeks. Body composition was evaluated using an InBody720 analyzer. We used transient elastography to measure liver stiffness and the controlled attenuation parameter for the quantification of liver steatosis in patients with NASH.ResultsForty-three patients with T2DM and NAFLD were enrolled (12 with biopsy-proven NASH and 31 with NAFLD diagnosed by ultrasonography). After 24 weeks, body weight, hemoglobin A1c (HbA1c), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase, body fat mass, and steatosis were significantly decreased compared to baseline measurements in patients with NASH. However, muscle mass was not reduced, and liver stiffness showed a statistically insignificant tendency to decrease. NAFLD patients also showed a significant reduction in body weight, HbA1c, AST, and ALT compared to baseline measurements. ConclusionIpragliflozin may be effective in patients with T2DM complicated by NAFLD.
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Cano, Ainara, and Cristina Alonso. "Deciphering non-alcoholic fatty liver disease through metabolomics." Biochemical Society Transactions 42, no. 5 (September 18, 2014): 1447–52. http://dx.doi.org/10.1042/bst20140138.
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Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders in industrialized countries. NAFLD develops in the absence of alcohol abuse and encompasses a wide spectrum of disorders ranging from benign fatty liver to non-alcoholic steatohepatitis (NASH). NASH often leads to fibrosis, cirrhosis and, finally, hepatocellular carcinoma (HCC). Therefore the earlier NAFLD is diagnosed, the better the patient's outlook. A tightly connected basic and applied research is essential to find the molecular mechanisms that accompany illness and to translate them into the clinic. From the simple starting point for triacylglycerol (TG) accumulation in the liver to the more complex implications of phospholipids in membrane biophysics, the influence of lipids may be the clue to understand NAFLD pathophysiology. Nowadays, it is achievable to diagnose non-invasively the initial symptoms to stop, revert or even prevent disease development. In this context, merging metabolomics with other techniques and the interpretation of the huge information obtained resembles the ‘Rosetta stone’ to decipher the pathological metabolic fluxes that must be targeted to find a cure. In the present review, we have tackled the application of metabolomics to find out the metabolic fluxes that underlie membrane integrity in NAFLD.
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Phipps, Meaghan, and Julia Wattacheril. "Non-alcoholic fatty liver disease (NAFLD) in non-obese individuals." Frontline Gastroenterology 11, no. 6 (December 13, 2019): 478–83. http://dx.doi.org/10.1136/flgastro-2018-101119.
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Individuals with non-alcoholic fatty liver disease (NAFLD) who lack classical risk factors also have the ability to develop nonalcoholic steatohepatitis (NASH) and progression to more advanced liver disease. The pathophysiology and risk factors for the development of NAFLD in non-obese persons are not fully understood but seem to be closely related to insulin resistance, atherogenic dyslipidaemia and alterations in body composition, with some patients harbouring predisposing genetic polymorphisms. In normal-weight individuals, also called ‘lean’, there is limited potential for effective lifestyle change in disease management. Additionally, biological mechanisms underlying the development of NASH in non-obese individuals may reveal novel targets for intervention. In this review, the authors discuss the clinical, histological and genetic features and risk factors for non-obese NAFLD and highlight gaps in knowledge and areas for future research.
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Teng, Tieshan, Shuai Qiu, Yiming Zhao, Siyuan Zhao, Dequan Sun, Lingzhu Hou, Yihang Li, et al. "Pathogenesis and Therapeutic Strategies Related to Non-Alcoholic Fatty Liver Disease." International Journal of Molecular Sciences 23, no. 14 (July 16, 2022): 7841. http://dx.doi.org/10.3390/ijms23147841.
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Non-alcoholic fatty liver disease (NAFLD), one of the most common types of chronic liver disease, is strongly correlated with obesity, insulin resistance, metabolic syndrome, and genetic components. The pathological progression of NAFLD, consisting of non-alcoholic fatty liver (NAFL), non-alcoholic steatohepatitis (NASH), and liver cirrhosis, is characterized by a broad spectrum of clinical phenotypes. Although patients with mild NAFL are considered to show no obvious clinical symptoms, patients with long-term NAFL may culminate in NASH and further liver fibrosis. Even though various drugs are able to improve NAFLD, there are no FDA-approved medications that directly treat NAFLD. In this paper, the pathogenesis of NAFLD, the potential therapeutic targets, and their underlying mechanisms of action were reviewed.
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Pár, Gabriella, Gábor Horváth, and Alajos Pár. "Non-alcoholic fatty liver disease and steatohepatitis." Orvosi Hetilap 154, no. 29 (July 2013): 1124–34. http://dx.doi.org/10.1556/oh.2013.29626.
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Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, the hepatic manifestations of metabolic syndrome with close association with inzulin resistance and obesity, are the most common liver diseases, affecting up to a third of the population worldwide. They confer increased risk for hepatocellular carcinoma as well as cardiovascular diseases. The review aims to summarize advances in epidemiology, pathogenesis and clinical management of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis. Besides liver biopsy and biomarkers, a novel non-invasive diagnostic tool the called “controlled attenuation parameter” measuring the attenuation of ultrasound generated by the transient elastography transducer, can quantitatively assess the hepatic fat content and differentiate between steatosis grades. At the same time, liver stiffness (fibrosis) can also be evaluated. The authors present their own results obtained with the latter procedure. In non-alcoholic fatty liver disease, the lifestyle intervention, weight loss, diet and exercise supported by cognitive behavioural therapy represent the basis of management. Components of metabolic syndrome (obesity, dyslipidaemia, diabetes and arterial hypertension) have to be treated. Although there is no approved pharmacological therapy for NASH, it seems that long lasting administration of vitamin E in association with high dose ursodeoxycholic acid may be beneficial. In addition, omega-3 polyunsaturated fatty acid substitution can also decrease liver fat, however, the optimal dose is not known yet. Further controlled clinical studies are warranted to establish the real value of any suggested treatment modalities for non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, although these are in experimental phase yet. Orv. Hetil., 2013, 154, 1124–1134.
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Umaru, Isaac John, and Okoli Chikodiri Emmanuel. "Review on the Role of Fructose in Non-Alcoholic Fatty Liver Diseases." International Journal of Scientific and Management Research 05, no. 02 (2022): 148–89. http://dx.doi.org/10.37502/ijsmr.2022.5212.
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Non-alcoholic fatty liver disease (NAFLD) is a clinical liver condition characterized by accumulation of fat in the liver that can develop into non-alcoholic steatohepatitis (NASH) without any evidence of excessive alcohol consumption. NASH involves liver inflammation, necrosis, fibrosis, cirrhosis, and eventually liver cancer. Excessive intake of fructose is known to promote non-alcoholic fatty liver (NAFLD), because this sugar is both a substrate and an inducer of liver fat regeneration. In addition to the hepatic lipogenic effects, the consumption of fructose can also cause liver inflammation and cellular stress, such as oxidative and endoplasmic stress, which are conducive to the progression of steatosis to non-alcoholic steatohepatitis (NASH). Fructose also has direct and indirect effects on peripheral levels. For example, excessive fructose intake is associated with changes in the gut micro biota, which can lead to a worsening of the disease. Currently, there is no known treatment for NAFLD. Therefore, treatment is based on lifestyle changes, including changes in diet and physical exercise.
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Yamamoto, Mio, Yasukiyo Yoshioka, Tomoya Kitakaze, Yoko Yamashita, and Hitoshi Ashida. "Preventive effects of black soybean polyphenols on non-alcoholic fatty liver disease in three different mouse models." Food & Function 13, no. 2 (2022): 1000–1014. http://dx.doi.org/10.1039/d1fo03541j.
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Non-alcoholic fatty liver disease (NAFLD) and its advanced stage, non-alcoholic steatohepatitis (NASH), are a major health issue throughout the world. Black soybean polyphenols have possibility of preventing NAFLD and NASH.
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Jennison, Erica, Janisha Patel, Eleonora Scorletti, and Christopher D. Byrne. "Diagnosis and management of non-alcoholic fatty liver disease." Postgraduate Medical Journal 95, no. 1124 (May 13, 2019): 314–22. http://dx.doi.org/10.1136/postgradmedj-2018-136316.
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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western industrialised countries. The prevalence of NAFLD is increasing in parallel with the global rise in obesity and type 2 diabetes mellitus. NAFLD represents a spectrum of liver disease severity. NAFLD begins with accumulation of triacylglycerols in the liver (steatosis), and is defined by hepatic fatty infiltration amounting to greater than 5% by liver weight or the presence of over 5% of hepatocytes loaded with large fat vacuoles. In almost a quarter of affected individuals, steatosis progresses with the development of liver inflammation to non-alcoholic steatohepatitis (NASH). NASH is a potentially progressive liver condition and with ongoing liver injury and cell death can result in fibrosis. Progressive liver fibrosis may lead to the development of cirrhosis in a small proportion of patients. With the growing prevalence of NAFLD, there is an increasing need for a robust, accurate and non-invasive approach to diagnosing the different stages of this condition. This review will focus on (1) the biochemical tests and imaging techniques used to diagnose the different stages of NAFLD; and (2) a selection of the current management approaches focusing on lifestyle interventions and pharmacological therapies for NAFLD.
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Lavallard, Vanessa J., and Philippe Gual. "Autophagy and Non-Alcoholic Fatty Liver Disease." BioMed Research International 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/120179.
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Autophagy, or cellular self-digestion, is a catabolic process that targets cell constituents including damaged organelles, unfolded proteins, and intracellular pathogens to lysosomes for degradation. Autophagy is crucial for development, differentiation, survival, and homeostasis. Important links between the regulation of autophagy and liver complications associated with obesity, non-alcoholic fatty liver disease (NAFLD), have been reported. The spectrum of these hepatic abnormalities extends from isolated steatosis to non-alcoholic steatohepatitis (NASH), steatofibrosis, which sometimes leads to cirrhosis, and hepatocellular carcinoma. NAFLD is one of the three main causes of cirrhosis and increases the risk of liver-related death and hepatocellular carcinoma. The pathophysiological mechanisms of the progression of a normal liver to steatosis and then more severe disease are complex and still unclear. The regulation of the autophagic flux, a dynamic response, and the knowledge of the role of autophagy in specific cells including hepatocytes, hepatic stellate cells, immune cells, and hepatic cancer cells have been extensively studied these last years. This review will provide insight into the current understanding of autophagy and its role in the evolution of the hepatic complications associated with obesity, from steatosis to hepatocellular carcinoma.
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Tkach, S. M., and T. L. Cheverda. "Non-alcoholic fatty liver disease and diabetes mellitus: bidirectional relationship." Clinical Endocrinology and Endocrine Surgery, no. 1 (December 6, 2021): 63–69. http://dx.doi.org/10.30978/cees-2021-1-63.
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To date, nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic diffuse liver disease. Under adverse conditions, its natural course involves progression from simple steatosis and nonalcoholic steatohepatitis (NASH) to the development of liver cirrhosis and hepatocellular carcinoma (HCC). In recent years, there has been much convincing evidence that NAFLD is a multisystem disease that contributes to damage to extrahepatic organs and systems, primarily increasing the risk of cardiovascular diseases, type 2 diabetes, chronic kidney disease and other diseases. In particular, numerous studies in recent years indicate that NAFLD increased the risk of diabetes by at least twice. Currently, the complex and bidirectional relationship between NAFLD and type 2 diabetes are well studied. NAFLD, hepatic and systemic insulin resistance, gut dysbiosis and lipotoxicity are the main factors determining the development of diabetes mellitus in predisposed individuals. Once type 2 diabetes manifests clinically, the likelihood of progressive liver damage increases. Non-alcoholic fatty liver disease, which is associated with type 2 diabetes, is thought to be a sign of a severe clinical course with serious clinical consequences in the form of NASH, liver cirrhosis and HCC. This combination requires a more aggressive therapeutic strategy, HCC screening, and long-term follow-up. A vicious circle is formed, which leads to adverse clinical consequences, worsens the prognosis and requires an active diagnostic and treatment strategy.
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Dallio, Marcello, Mario Masarone, Giuseppe Gerardo Caprio, Rosa Di Sarno, Concetta Tuccillo, Ferdinando Carlo Sasso, Marcello Persico, Carmela Loguercio, and Alessandro Federico. "Endocan Serum Levels in Patients with Non-Alcoholic Fatty Liver Disease with or without Type 2 Diabetes Mellitus: A Pilot Study." Journal of Gastrointestinal and Liver Diseases 26, no. 3 (September 1, 2017): 261–68. http://dx.doi.org/10.15403/jgld.2014.1121.263.dal.
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Background & Aims: Non-alcoholic fatty liver disease (NAFLD) is emerging as an independent cardiovascular risk factor. Recently, Endocan has been studied as an early marker of endothelial dysfunction. Our aim was to evaluate Endocan serum levels in patients with NAFLD with or without type 2 diabetes mellitus.Method: We enrolled 56 patients: 19 with NAFLD and 37 with type 2 diabetes mellitus with or without NAFLD, and compared them to 25 healthy controls. Endocan serum level was measured by using the ELISA EndoMark assay.Results: Endocan level was significantly higher in NAFLD subjects, compared to controls (1.23±1.51 vs 0.68±0.4 ng/mL; p=0.016). It was higher in patients with non-alcoholic fatty liver and non-alcoholic steatohepatitis (NASH) (1.12±1.11, 1.49±2.16 and 0.68±0.4 ng/ml vs controls, respectively), independently from presence of type 2 diabetes mellitus. The increase was more marked in patients with NASH and in those with NAFL versus controls (p=0.001 and p=0.004, respectively), but not statistically different between the two groups (p=0.448). Finally, we found a statistically relevant increase of this marker in diabetic NAFLD patients compared to those non diabetic (1.56±0.81 vs 0.72±0.58 ng/ml; p=0.01).Conclusion: We demonstrated an increased Endocan serum level in NAFLD patients, higher in those with type 2 diabetes mellitus and/or NASH because of an endothelial dysfunction in these pathologies.Abbreviations: BMI: Body Mass Index; CCBS: calcium channel blockers; ED: endothelial dysfunction; ELISA: enzyme-linked immunosorbent assay; ESM-1: Endothelial cell-specific molecule-1; HOMA-IR: Homeostasis Model Assessment Insulin Resistance; ICAM: Intercellular Adhesion Molecule; LFA-1: Lymphocyte Function-Associated Antigen 1; NAFL: non-alcoholic fatty liver; NAFLD: Non-alcoholic fatty liver disease; NAS: non-alcoholic fatty liver disease activity score; NASH: non-alcoholic steatohepatitis; ROS: reactive oxigen species; T2DM: type 2 diabetes mellitus; TNF-alpha: tumor necrosis factor-alpha.
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St.Rose, Kristy, Jun Yan, and Jorge Caviglia. "Mouse Model of Non-Alcoholic Fatty Liver Disease That Replicates the Human Disease." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 700. http://dx.doi.org/10.1093/cdn/nzaa050_023.
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Abstract Objectives To develop a mouse model of non-alcoholic fatty liver disease (NAFLD) that replicates the characteristic of the disease in humans, including development of obesity, dysbiosis, fibrosis and liver tumors. Methods Agouti yellow (Ay) mice, which have hyperphagia, were fed a Western diet (WD) (42% kcal from fat, 341 g/Kg sucrose, and 0.2% cholesterol) and a drinking solution containing fructose and glucose equivalent to 42 g/L of high fructose corn syrup (HFCS). Wild-type mice fed a low-fat diet (LFD) (10% kcal from fat) served as lean controls. After 16 weeks of diet treatment, tissues were collected and analyzed. Obesity was evaluated via body weight and body composition. NAFLD was evaluated by histology and confirmed by liver lipid quantification, plasma ALT and AST levels, expression of inflammation-related genes, and fibrosis-specific staining. Gene expression profile was evaluated by RNAseq. Gut microbiota dysbiosis was evaluated by 16S rRNA metagenomics. Results Ay mice fed the Western diet and HFCS for 16 weeks developed obesity and NAFLD. Histological evaluation determined that the mice developed non-alcoholic steatohepatitis (NASH) with steatosis, liver injury, inflammation, and fibrosis. This was confirmed by the following analyses: In these mice, steatosis, quantified by liver TAG content, increased 4X when compared to lean controls. Liver injury, assessed by measuring plasma ALT and AST, increased 11X and 4X, respectively. Inflammation, evaluated by liver mRNA expression of Tnf and CCl2, increased 6X and 12X, respectively. Fibrosis, quantified morphometrically, increased 2.5X. Gene expression profiling showed increases in inflammation- and fibrosis-related pathways, similar to NASH in humans. In addition, these mice developed gut microbiota dysbiosis, with increased Bacteroidetes and Proteobacteria and decreased Firmicutes, as reported in NASH in humans. Finally, 60% of the Ay mice developed liver tumors when fed the WD + HFCS diet for one year. Conclusions Ay mice fed a Western diet and HFCS developed obesity, gut microbiota dysbiosis, and NASH, including fibrosis and tumors, replicating the characteristics of NASH in humans. We present this as a new model for studying NASH physiopathology and testing new therapies. Funding Sources NIH CUNY.
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Papatheodoridi, Margarita, and Evangelos Cholongitas. "Diagnosis of Non-alcoholic Fatty Liver Disease (NAFLD): Current Concepts." Current Pharmaceutical Design 24, no. 38 (February 27, 2019): 4574–86. http://dx.doi.org/10.2174/1381612825666190117102111.
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Nonalcoholic fatty liver disease (NAFLD) ranges from simple hepatic steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis. The majority of NAFLD patients do not progress to NASH and their morbidity risk is low. However, clinical and economic burden of the disease is considerable since the prevalence of the disease is estimated as high as 25% of the general population. Liver biopsy remains the current gold standard for diagnosis, despite limitations regarding sampling variability, invasive nature, and high cost. However, numerous non-invasive biomarkers, including mainly serum markers or imaging modalities, intend to detect the presence of steatosis, NASH or advanced fibrosis. To date, ultrasound is suggested as first-line screening tool for defining steatosis in a selected population, while diagnosis of NAFLD requires exclusion of other chronic liver disease etiology or other steatosis causes. A crucial step in the management of NAFLD patients is the identification of advanced fibrosis, which may be reliably excluded by using NAFLD-Fibrosis score or FIB-4 score or by performing transient elastography. The most robust modalities implement Magnetic Resonance technology and manage to accurately quantify steatosis or identify fibrosis stage, but are not yet applicable in routine practice. The most challenging endpoint has proved to be a non-invasive diagnosis of NASH since no reliable biomarkers have been found to detect or predict inflammation in NAFLD. Lately, research focuses on validating existing markers as robust diagnostic tools for clinical use and investigating novel experimental markers of disease. Current strategies concepts aim to safely diagnose NAFLD patients, aid drug development and finally, guide personalised treatment.
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Chueansuwan, Rachaneeporn. "Vitamin D in non-alcoholic fatty liver disease (NAFLD)." Thai Journal of Hepatology 1, no. 3 (October 1, 2018): 14–19. http://dx.doi.org/10.30856/th.jhep2018vol1iss3_03.
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Vitamin D is increasingly accepted as an important physiological regulator of several organ systems apart from its classical role in skeletal homeostasis. In recent years, new scientific discoveryon vitamin D expands our knowledge of its actions in many aspects such as immune modulation, cell differentiation and proliferation, and inflammatory regulations. Vitamin D deficiency is one of the mostcommon micronutrient deficiencies worldwide. Non-alcoholic fatty liver disease (NAFLD) and vitamin D deficiency often coexist. In addition, epidemiologic evidence has shown that both conditions shareseveral cardio-metabolic risk factors. While pre-clinical experimental data is promising, most clinical trials based on the effect of vitamin D in NASH are under-powered and inconclusive. Further studiesare required to elucidate the beneficial effect of vitamin D or its analogues in NASH. In this article, we provide an overview of the epidemiology and pathophysiology linking NAFLD and vitamin D deficiency,as well as the available evidence on the clinical utility of vitamin D supplementation in NAFLD.
Figure 1 แสดงวิตามินดีเมตาบอลิสม์ (ดัดแปลงจากเอกสารอ้างอิง Hossein-Nezhad and Holick (12))
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Arshad, Tamoore, Pegah Golabi, Linda Henry, and Zobair M. Younossi. "Epidemiology of Non-alcoholic Fatty Liver Disease in North America." Current Pharmaceutical Design 26, no. 10 (April 24, 2020): 993–97. http://dx.doi.org/10.2174/1381612826666200303114934.
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Nonalcoholic fatty liver disease (NAFLD) is rapidly becoming the most common cause of chronic liver disease worldwide. This is primarily driven by the global epidemic of obesity and diabetes as well as the aging of the general population. Most of the epidemiology data of NAFLD for North America are published from studies originating in the United States (U.S.). The overall prevalence of NAFLD in the U.S. is estimated to be 24%. Hispanic Americans have a higher prevalence of NAFLD, whereas African Americans have a lower prevalence of NAFLD. The exact contributions of genetic and environmental factors on these differences in the prevalence rates have not been determined. From the spectrum of NAFLD, patients with non-alcoholic steatohepatitis (NASH) are at the highest risk of progression to cirrhosis and hepatocellular carcinoma (HCC). The most recent data regarding the progression of NASH suggest a complex pattern of progression and regression of fibrosis. Factors influencing the progression and regression of NASH have not been fully described. More research is needed to better understand NAFLD in Mexico and Canada.
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Akter, Sharmin. "Non-alcoholic Fatty Liver Disease and Steatohepatitis: Risk Factors and Pathophysiology." Middle East Journal of Digestive Diseases 14, no. 2 (April 30, 2022): 167–81. http://dx.doi.org/10.34172/mejdd.2022.270.
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Non-alcoholic fatty liver disease (NAFLD) and its progressive subtype non-alcoholic steatohepatitis (NASH) are the most prevalent liver diseases, often leading to hepatocellular carcinoma (HCC). This review aims to describe the present knowledge of the risk factors responsible for the development of NAFLD and NASH. I performed a literature review identifying studies focusing on the complex pathogenic pathway and risk factors of NAFLD and steatohepatitis. The relationship between NAFLD and metabolic syndrome is well established and widely recognized. Obesity, dyslipidemia, type 2 diabetes, hypertension, and insulin resistance are the most common risk factors associated with NAFLD. Among the components of metabolic syndrome, current evidence strongly suggests obesity and type 2 diabetes as risk factors of NASH and HCC. However, other elements, namely gender divergences, ethnicity, genetic factors, participation of innate immune system, oxidative stress, apoptotic pathways, and adipocytokines, take a leading role in the onset and promotion of NAFLD. Pathophysiological mechanisms that are responsible for NAFLD development and subsequent progression to NASH are insulin resistance and hyperinsulinemia, oxidative stress, hepatic stellate cell (HSC) activation, cytokine/adipokine signaling pathways, and genetic and environmental factors. Major pathophysiological findings of NAFLD are dysfunction of adipose tissue through the enhanced flow of free fatty acids (FFAs) and release of adipokines, and altered gut microbiome that generate proinflammatory signals and cause NASH progression. Understanding the pathophysiology and risk factors of NAFLD and NASH; this review could provide insight into the development of therapeutic strategies and useful diagnostic tools.
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Skvortsov, V. V., M. V. Lunkov, R. Sh Tinaeva, and E. M. Skvortsova. "Phospholipids in non-alcoholic fatty liver disease." Meditsinskiy sovet = Medical Council, no. 6 (April 24, 2022): 92–99. http://dx.doi.org/10.21518/2079-701x-2022-16-6-92-99.
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Non-alcoholic fatty liver disease, or NAFLD – is a pathology that usually has a metabolic cause and is not caused by excessive alcohol consumption. NAFLD is the most frequent chronic liver disease worldwide and is accompanied by a high financial burden for the patient and the healthcare system. NAFLD is generally considered a “benign disease” with low progression to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Nevertheless, due to the large number of affected patients, the prevalence of cirrhosis of the liver has gradually increased, and in fact it represents the third cause of liver transplantation in the world. Moreover, even if the frequency of HCC in patients with NAFLD is lower than in patients with HCV/HBV cirrhosis, the absolute number of HCC associated with NASH is higher due to the higher number of patients with NAFLD. It is likely that the importance of this disease will continue to grow in the future, when new treatments and prevention programs for hepatitis C and B reduce the size of viral liver infections. Many aspects of the disease have yet to be solved. It is very important to understand the mechanisms underlying the occurrence and development of NAFLD, the features of the clinic and diagnosis, as well as the tactics of management and treatment of patients with non-alcoholic fatty liver disease. It is important for patients to get a complete understanding of NAFLD so that they can play an active role in the treatment of their disease.
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Niikura, Toshihiro, Kento Imajo, Anna Ozaki, Takashi Kobayashi, Michihiro Iwaki, Yasushi Honda, Takaomi Kessoku, et al. "Coronary Artery Disease is More Severe in Patients with Non-Alcoholic Steatohepatitis than Fatty Liver." Diagnostics 10, no. 3 (February 26, 2020): 129. http://dx.doi.org/10.3390/diagnostics10030129.
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Non-alcoholic fatty liver disease (NAFLD) is associated with a higher risk of atherosclerotic disease. However, the relationships between the severity of coronary atherosclerosis and pathologic findings in patients with NAFLD remain unknown. We aimed to characterize the coronary artery lesions in patients with NAFLD using coronary computed tomography angiography (CCTA). Overall, 101 patients with liver biopsy-proven NAFLD who had chest pain or electrocardiographic abnormalities underwent CCTA. Coronary artery lesions, including coronary artery stenosis (CAS), calcium score (CACS, Agatston score), and coronary artery non-calcified plaque were assessed using multi-slice CT. Multivariate analysis showed that age, smoking status, prevalence of dyslipidemia (DLP) and non-alcoholic steatohepatitis (NASH), and stage of fibrosis were independent risk factors for CAS. Age, and the prevalence of DM and DLP, were independent risk factors for CACS, and the prevalence of NASH tended to be an independent risk factor. In addition, the prevalence of DLP and NASH were independent risk factors for non-calcified plaques. Coronary artery lesions are more common in patients with NASH than in those with non-alcoholic fatty liver, suggesting a higher risk in patients with NASH. Therefore, patients with NASH should be closely followed, with particular vigilance for coronary artery diseases.
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Rockstroh, Jürgen Kurt. "Non-Alcoholic Fatty Liver Disease (NAFLD) and Non-Alcoholic Steatohepatitis (NASH) in HIV." Current HIV/AIDS Reports 14, no. 2 (March 10, 2017): 47–53. http://dx.doi.org/10.1007/s11904-017-0351-2.
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Perveen, Irin. "Current Management Strategy of Non-Alcoholic Fatty Liver Disease." Journal of Enam Medical College 9, no. 1 (January 25, 2019): 46–56. http://dx.doi.org/10.3329/jemc.v9i1.39906.
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Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide and is becoming the most common indication for liver transplant in the Western world. The disease spectrum varies from steatosis to non-alcoholic steatohepatitis (NASH), advanced fibrosis, cirrhosis and hepatocellular carcinoma. The global prevalence of NAFLD and NASH varies from 24–25% and 1.5–6.45% respectively among general population. Despite the disease burden and adverse outcome of the condition, no highly effective treatment is currently available for NAFLD. Considering its global prevalence and impact clinicians and researchers from different scientific associations worldwide tried hard to develop high-quality international guidelines to improve the management of NAFLD patients in clinical practice. This paper aims to discuss the management options for NAFLD based on five different well-known international guidelines. These guidelines agree on many points and disagree on some points. Notably these guidelines differ in determining alcohol threshold for defining NAFLD, in screening strategies in high-risk patients, the non-invasive test proposed for the diagnosis of NAFLD and advanced fibrosis in patients with NAFLD, in the follow-up protocols and, finally, in the proposed pharmacological treatment strategy.
J Enam Med Col 2019; 9(1): 46-56
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Mortimore, Gerri. "Non-alcoholic fatty liver disease: a global concern." Practice Nursing 33, no. 9 (September 2, 2022): 358–64. http://dx.doi.org/10.12968/pnur.2022.33.9.358.
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Non-alcoholic fatty liver disease is an umbrella term used to describe a build-up of fat in the liver. Gerri Mortimore provides an overview of the condition, its diagnosis, treatment and the role of the practice nurse in health promotion In the early stages of non-alcoholic fatty liver disease (NAFLD), the condition does not cause damage and is reversible. If left untreated, it can develop into the more serious form of non-alcoholic steatohepatitis (NASH), where the liver becomes inflamed, and over time can further develop into fibrosis and cirrhosis. Obesity is associated with the development of NAFLD. Any patient who falls in the obese category and/or has type 2 diabetes or insulin resistance and/or is diagnosed with metabolic syndrome should be tested for NAFLD. Nurses are often in the best position to prompt early investigation. Health promotion in the form of lifestyle advice is the mainstay of treatment, with an emphasis on weight reduction and healthy diet.
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Zhelezniakova, Natalia, Oleg Babak, and Tetiana Aleksandrova. "MODERN METHODS OF DIAGNOSIS AND SCREENING OF NON-ALCOHOLIC FATTY LIVER DISEASE AND ITS STAGES: review." Inter Collegas 8, no. 4 (May 21, 2022): 226–31. http://dx.doi.org/10.35339/ic.8.4.226-231.
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The review is devoted to the problem of diagnosing one of the most common pathologies of the modern world – non-alcoholic fatty liver disease (NAFLD). Data from experimental and clinical studies on the importance of various instrumental and biochemical methods of non-invasive diagnosis ofnon-alcoholic steatohepatitis (NASH) and liver fibrosis (LF) are presented. New non-invasive diagnostic methods of NASH and LF are considered.
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Kamal, Mostafa, Fazal Karim, Md Robed Amin, MH Sarder, and KAK Azad. "Risk Factors of Non-Alcoholic Fatty Liver Disease in Bangladeshi Population." Journal of Medicine 14, no. 2 (July 24, 2014): 143–48. http://dx.doi.org/10.3329/jom.v14i2.19665.
Full textAbstract:
Background: Non-alcoholic fatty liver disease (NAFLD) is becoming a public health problem with increasing incidence and it has been shown to be associated with diabetes, dyslipidemia, obesity and metabolic syndrome and ultimately puts more than half the worlds population at risk of developing NAFLD/NASH/cirrhosis in the coming decades. The importance of detection of patients with NAFLD is to intervene the associated factors and avoid transformation to more severe forms of the disease.Methods: An observational case control study was carried out at Medicine Department, Dhaka Medical College Hospital (DMCH), Dhaka, during the period of August, 2011 to June, 2012. A total number of 100 consecutive patients and 100 healthy controls was approaches DMCH were enrolled in this study. Out of 100 NAFLD patients only 20 patients gave consent for liver biopsy to see the extent of liver damage.Result: Less physical activity, Obesity, mean blood pressure, Diabetes, TG, TC were significantly (P<0.05) higher in NAFLD. Metabolic syndrome was 64% in NAFLD. According to NASH Activity Scoring system definite NASH (score >5) was found in 9(45%) of the NAFLD group.Conclusion: Significant proportion of NAFLD patient suffers from NASH which is alarming and they have potential for the development of advanced liver disease. So recognition of these risk factors in patients of NAFLD can help in early implementation of strategies that halt the progression of this disease. DOI: http://dx.doi.org/10.3329/jom.v14i2.19665 J Medicine 2013, 14(2): 143-148
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Soret, Pierre-Antoine, Julie Magusto, Chantal Housset, and Jérémie Gautheron. "In Vitro and In Vivo Models of Non-Alcoholic Fatty Liver Disease: A Critical Appraisal." Journal of Clinical Medicine 10, no. 1 (December 24, 2020): 36. http://dx.doi.org/10.3390/jcm10010036.
Full textAbstract:
Non-alcoholic fatty liver disease (NAFLD), including non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH), represents the hepatic manifestation of obesity and metabolic syndrome. Due to the spread of the obesity epidemic, NAFLD is becoming the most common chronic liver disease and one of the principal indications for liver transplantation. However, no pharmacological treatment is currently approved to prevent the outbreak of NASH, which leads to fibrosis and cirrhosis. Preclinical research is required to improve our knowledge of NAFLD physiopathology and to identify new therapeutic targets. In the present review, we summarize advances in NAFLD preclinical models from cellular models, including new bioengineered platforms, to in vivo models, with a particular focus on genetic and dietary mouse models. We aim to discuss the advantages and limits of these different models.
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Alam, Shahinul, Mahabubul Alam, Sheikh Mohammad Noor E. Alam, Ziaur Rahman Chowdhury, and Jahangir Kabir. "Prevalence and Predictor of Nonalcoholic Steatohepatitis (NASH) in Nonalcoholic Fatty Liver Disease (NAFLD)." Journal of Bangladesh College of Physicians and Surgeons 32, no. 2 (December 23, 2015): 71–77. http://dx.doi.org/10.3329/jbcps.v32i2.26034.
Full textAbstract:
Fatty liver is a common cause of chronic liver disease in developed as well as developing countries.We have designed this study to estimate the prevalence and predictors for non alcoholic steatohepatitis (NASH) in non alcoholic fatty liver disease (NAFLD). We have included 493 patients with sonographic evidence of fatty change in liver and 177 of them had done liver biopsy for histopathological study. Other causes of liver disease and alcohol consumption were excluded. Metabolic syndrome and biochemical and anthropometric evaluation was done. Females were predominating 250 (57.0 %). Centrally obese 422 (96.2 %) was more than over all obesity330 (75.1%). NASH was absent in 10 (5.6%) cases and diagnostic of NASH was 75 Journal of Bangladesh College of Physicians and Surgeons Vol. 32, No. 2, April 2014 (42.4 %).Presence of diabetes could significantly (p = 0.001) predicted NASH. Age, sex, BMI, waist circumference, Serum HDL,triglyceride, insulin resistance index, hypertension, metabolic syndrome could not predict NASH. Serum GGT level was significantly (p = 0.05) higher in NASHwith a sensitivity of 45 % and specificity of 68 % only. Serum ALT and AST level could not detect NASH. Females were predominant sufferer of NAFLD in Bangladesh. Prevalence of NASH was much higher42.4%. Diabetes was the main predictor of NASH. GGT was the only biochemical indicator of NASH. We recommend liver biopsy in NAFLD with diabetes and raised GGT.J Bangladesh Coll Phys Surg 2014; 32: 71-77
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Francque, Sven M. "The Role of Non-alcoholic Fatty Liver Disease in Cardiovascular Disease." European Cardiology Review 9, no. 1 (2014): 10. http://dx.doi.org/10.15420/ecr.2014.9.1.10.
Full textAbstract:
Non-alcoholic fatty liver disease (NAFLD) has become the most prevalent chronic liver disease in western countries and is closely related to the metabolic syndrome. When NAFLD is associated with hepatocellular damage and inflammation (non-alcoholic steatohepatitis [NASH]) it can lead to severe liver disease. However, it has become clear that NAFLD is also associated with an increased risk of cardiovascular disease (CVD), independently of classical known risk factors for the latter. In the current review we briefly summarise the current clinical evidence on the role of NAFLD in CVD and discuss the potential mechanisms by which NAFLD can be linked to the pathophysiology of CVD.
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Jahn, Daniel, Monika Rau, Julia Wohlfahrt, Heike M. Hermanns, and Andreas Geier. "Non-Alcoholic Steatohepatitis: From Pathophysiology to Novel Therapies." Digestive Diseases 34, no. 4 (2016): 356–63. http://dx.doi.org/10.1159/000444547.
Full textAbstract:
Non-alcoholic fatty liver (NAFL) disease is defined by an accumulation of liver fat exceeding 5% of its weight in the absence of significant alcoholic intake. In 5-20%, there is a progression from NAFL to non-alcoholic steatohepatitis (NASH). Until now, it is not well understood why only some patients develop NASH, and currently, no drugs are licensed for this indication. Different T-cell populations such as T-regulatory, Th1 and Th17 cells play a central role in the immunopathogenesis of fatty liver disease and open the option of future interleukin (IL)-17-based therapeutics. The inflammatory process underlying NASH is furthermore characterized by elevated expression of pro-inflammatory cytokines such as TNFα and IL-1β. Anakinra, a recombinant version of IL-1Ra shows promising metabolic effects with improved hyperglycemia and beta-cell secretory function in a double-blind placebo controlled randomized trial in type 2 diabetic patients but such studies are still in their preliminary stages for NASH. Several studies point out that bile acid farnesoid X receptor (FXR)-mediated signals (such as the enterohepatic hormone fibroblast growth factor 15/19) are involved in the regulation of triglyceride and glucose metabolism. Recent clinical trials have revealed a beneficial impact of the FXR agonist obeticholic acid on body weight, insulin sensitivity and liver histology in patients with NASH. Further potential novel therapeutic targets in NASH are currently in phase II clinical development.