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Journal articles on the topic 'Non-Alcoholic fatty liver diseases'

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Author: Grafiati

Published: 22 June 2023

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1

Fujioka, Kazumi. "Link between Non-Alcoholic Fatty Liver Disease and Hypertension: Non-Alcoholic Fatty Liver Disease as a Multisystem Disease." International Journal of Clinical Case Reports and Reviews 10, no. 5 (March 11, 2022): 01–04. http://dx.doi.org/10.31579/2690-4861/203.

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The prevalence and incidence of non-alcoholic fatty liver disease (NAFLD) is increasing due to the epidemics of obesity and type 2 diabetes mellitus (T2DM). Many studies provided the evidence of the decreased flow-mediated vasodilation (FMD), increased carotid intima-media thickness (IMT), and increased brachial ankle pulse wave velocity (baPWV) in patients with NAFLD. Recently, a link between NAFLD and hypertension along with new genetic expression, ADIPOQ C11377G and AGTR1 has been shown. It is putative that NAFLD may induce systemic inflammation, insulin resistance, oxidative stress, and increased vasoconstriction and decreased vasodilation, subsequently leading to hypertension. Under the systemic inflammation, it has been suggested that NAFLD may promote sympathetic nervous system (SNS) and renin-angiotensin system (RAS) activation, and local vasculature and renal inflammation, subsequently leading to hypertension. The author has reviewed the current knowledge of the link between NAFLD and hypertension along with new genetic expression in this article. It plausible that NAFLD is a multisystem disease and is associated with hepatic and extrahepatic disease.

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2

Alp, Hayriye. "Acupuncture and Phytotherapy Applications in Non-Alcoholic Fatty Liver." Gastroenterology Pancreatology and Hepatobilary Disorders 5, no. 2 (June 2, 2021): 01–03. http://dx.doi.org/10.31579/2641-5194/026.

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Phytotherapy, medicinal and aromatic plants, algae, fungi and lichens, or their extracts, such as gum, balsam and resin, extracts, essential oils, candles and fixed oils with herbal preparations prepared in various forms (tea, capsule, tablet, syrup, drop , lozenges, sachets, etc.) to be protected from diseases, to treat diseases or to support treatment. Phytotherapy; It is based on scientific research and clinical studies. Historically, it has been the primary support of doctors in the treatment of diseases. Objective:We offer here; In addition to the treatment of obesity with acupuncture and phytotherapeutically artichoke (Cynara scolymus L.) and thistle (Silybum marianum (L.) Gaertn.), dandelion (Taraxacum officinale FH Wigg.) using antidepressants for many years, the treatment of obesity with impaired obesity and elevated liver enzymes. It is a case where a positive decrease is achieved in liver enzymes by giving mix extract. Methods: Yin-tan, Memory, Kid-3, Liv-3, St-36,24,25 in body acupuncture, Shen-men, stomach, larynx, jerome, kidney points were pinned in ear acupuncture. When patients who apply to the outpatient clinic need phytotherapeutic support, liver enzymes are routinely checked. Results:The patient lost both weight and liver enzymes. Conclusions and Recommendations: The biggest disadvantage of these preparations is their uncontrolled and high-dose use. It is most appropriate to give this kind of support treatments by people who are trained and licensed in this regard, especially under the control of a doctor. For this purpose, the Department of Traditional Complementary Medicine provides the development of physicians and pharmacists who have received phytotherapy training.

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3

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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4

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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5

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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6

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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7

Mitra, Souveek, Arka De, and Abhijit Chowdhury. "Epidemiology of non-alcoholic and alcoholic fatty liver diseases." Translational Gastroenterology and Hepatology 5 (April 2020): 16. http://dx.doi.org/10.21037/tgh.2019.09.08.

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8

Kanda, Tatsuo, Shunichi Matsuoka, Motomi Yamazaki, Toshikatsu Shibata, Kazushige Nirei, Hiroshi Takahashi, Tomohiro Kaneko, et al. "Apoptosis and non-alcoholic fatty liver diseases." World Journal of Gastroenterology 24, no. 25 (July 7, 2018): 2661–72. http://dx.doi.org/10.3748/wjg.v24.i25.2661.

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9

Federico, A., M. Trappoliere, M. V. D'Auria, C. Del Vecchio Blanco, and C. Loguercio. "Diet and non alcoholic fatty liver diseases." Digestive and Liver Disease 38 (April 2006): S95. http://dx.doi.org/10.1016/s1590-8658(06)80254-9.

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10

Lamichaney, Rachna. "Biochemical and Radiological Changes in Non Alcoholic Fatty Liver Diseases Compare with Obesity." Journal of Medical Science And clinical Research 05, no. 05 (May 28, 2017): 22367–73. http://dx.doi.org/10.18535/jmscr/v5i5.177.

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11

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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12

Kerimov, Kh N., S. D. Arutyunov, E. S. Malova, V. G. Morozov, Y. S. Degtyareva, Y. N. Kharakh, I. P. Balmasova, and V. N. Tsarev. "Periodontal diseases and non-alcoholic fatty liver disease." Parodontologiya 27, no. 1 (March 14, 2022): 4–12. http://dx.doi.org/10.33925/1683-3759-2022-27-1-4-12.

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Relevance. Periodontal diseases, being an extremely common, do not only cause tooth loss and significantly affect the patients’ quality of life, but are also a risk factor for many systemic diseases and may subsequently aggravate their course. Non-alcoholic fatty liver disease (NAFLD) is one of the relatively understudied pathologies associated with periodontal diseases.Materials and methods. A non-interventional study analytically reviewed Russian and international scientific publications, which presented the results of independent clinical and laboratory studies on the topic from 2011 to 2021.Results. Scientific literature data evidence that NAFLD manifests by impaired lipid metabolism in liver cells, linked with mechanisms regulated by the liver nuclear receptors (LXR), and leads to such life-threatening conditions as liver cirrhosis and hepatocellular carcinoma. The information on the role of periodontal pathogens in NAFLD development has been accumulated by now. The example of such principal periodontal pathogen as Porphyromonas gingivalis experimentally demonstrated that it can integrate into the intestinal microbiome, migrate through the bloodstream to the liver, survive in hepatocytes and influence the nuclear receptors of these cells affecting the lipid metabolism and contributing to NAFLD development.Conclusion. A detailed study of the link between periodontal disease and non-alcoholic fatty liver disease may contribute to the development of new effective strategies for the diagnosis and treatment of these pathological conditions.

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13

Eguchi, Akiko, and Ariel E. Feldstein. "Extracellular vesicles in non-alcoholic and alcoholic fatty liver diseases." Liver Research 2, no. 1 (March 2018): 30–34. http://dx.doi.org/10.1016/j.livres.2018.01.001.

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14

Mahmood, Kawa Abdullah. "PREVALENCE OF FATTY PANCREAS AMONG PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE IN SULAIMANI." Journal of Sulaimani Medical College 6, no. 2 (December 1, 2016): 107–15. http://dx.doi.org/10.17656/jsmc.10094.

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15

Régnier, Marion, Arnaud Polizzi, Hervé Guillou, and Nicolas Loiseau. "Sphingolipid metabolism in non-alcoholic fatty liver diseases." Biochimie 159 (April 2019): 9–22. http://dx.doi.org/10.1016/j.biochi.2018.07.021.

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16

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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17

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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18

Petrov, I. M., I. V. Medvedeva, I. F. Sholomov, L. V. Chesnokova, Yu A. Petrova, V. A. Snezhitskiy, L. V. Kalatsei, and А. V. Gladkevich. "BIOMARKERS OF CARDIOVASCULAR RISK IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE." Journal of the Grodno State Medical University 18, no. 3 (2020): 236–42. http://dx.doi.org/10.25298/2221-8785-2020-18-3-236-242.

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19

Park, Ji-Won, Sung-Eun Kim, Na Young Lee, Jung-Hee Kim, Jang-Han Jung, Myoung-Kuk Jang, Sang-Hoon Park, et al. "Role of Microbiota-Derived Metabolites in Alcoholic and Non-Alcoholic Fatty Liver Diseases." International Journal of Molecular Sciences 23, no. 1 (December 31, 2021): 426. http://dx.doi.org/10.3390/ijms23010426.

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Chronic liver disease encompasses diseases that have various causes, such as alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut–liver axis. The gut microbiota consists of various microorganisms that play a role in maintaining the homeostasis of the host and release a wide number of metabolites, including short-chain fatty acids (SCFAs), peptides, and hormones, continually shaping the host’s immunity and metabolism. The integrity of the intestinal mucosal and vascular barriers is crucial to protect liver cells from exposure to harmful metabolites and pathogen-associated molecular pattern molecules. Dysbiosis and increased intestinal permeability may allow the liver to be exposed to abundant harmful metabolites that promote liver inflammation and fibrosis. In this review, we introduce the metabolites and components derived from the gut microbiota and discuss their pathologic effect in the liver alongside recent advances in molecular-based therapeutics and novel mechanistic findings associated with the gut–liver axis in ALD and NAFLD.

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20

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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21

Perdomo, Carolina M., Nuria Garcia-Fernandez, and Javier Escalada. "Diabetic Kidney Disease, Cardiovascular Disease and Non-Alcoholic Fatty Liver Disease: A New Triumvirate?" Journal of Clinical Medicine 10, no. 9 (May 10, 2021): 2040. http://dx.doi.org/10.3390/jcm10092040.

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Non-alcoholic fatty liver disease is a highly prevalent disease worldwide with a renowned relation to cardiovascular disease and chronic kidney disease. These diseases share a common pathophysiology including insulin resistance, oxidative stress, chronic inflammation, dysbiosis and genetic susceptibilities. Non-alcoholic fatty liver disease is especially prevalent and more severe in type 2 diabetes. Patients with non-alcoholic fatty liver disease should have liver fibrosis assessment in order to identify those at the highest risk of adverse outcomes so that appropriate management strategies can be implemented. Early diagnosis and treatment of non-alcoholic fatty liver disease could ameliorate the burden of cardiovascular disease and chronic kidney disease.

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22

Osadchuk, M. A., and E. D. Mironova. "Non-viral liver diseases: pathogenetic approaches to therapy." Medical alphabet 3, no. 20 (November 25, 2019): 30–36. http://dx.doi.org/10.33667/2078-5631-2019-2-20(395)-30-36.

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Alcoholic liver disease and non-alcoholic fatty liver disease are chronic non-communicable diseases with an extremely high prevalence among the world's population. Currently, there is a tendency to a rapid increase in their number with frequent disability of patients and a high need for liver transplantation. Violations of the main metabolic processes in the liver under the influence of exogenous and endogenous factors are the starting point in the development of alcoholic and nonalcoholic liver pathology. This review discusses the main recommendations for non-drug and drug management of patients with liver diseases of non-viral etiology with a detailed description of the main hepatoprotectors with an emphasis on the universal properties of silymarin.

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23

Nelidova, A. V., M. A. Livzan, N. A. Nikolaev, and T. S. Krolevets. "Cardiovascular Diseases and Non-Alcoholic Fatty Liver Disease: Relationship and Pathogenetic Aspects of Pharmacotherapy." Rational Pharmacotherapy in Cardiology 17, no. 6 (January 12, 2022): 880–88. http://dx.doi.org/10.20996/1819-6446-2021-12-14.

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The association of non-alcoholic fatty liver disease (NAFLD) and cardiovascular risk is currently one of the actively studied areas. The incidence of non-alcoholic fatty liver disease continues to grow worldwide. In the structure of mortality rate of patients with non-alcoholic fatty liver disease, the first place is occupied by cardiovascular events: stroke and myocardial infarction. Studies have shown that the presence of severe liver fibrosis (F3-4) in NAFLD not only increases the risk of cardiovascular diseases (CVD), but also increases the risk of overall mortality by 69% due to mortality from cardiovascular causes. The degree of increased risk is associated with the degree of activity of non-alcoholic steatohepatitis (NASH). Despite the large number of works on this topic, we do not have a clear opinion on the impact on cardiovascular risk, interaction and the contribution of various factors, as well as algorithms for managing patients with non-alcoholic fatty liver disease to reduce the risk of cardiovascular diseases. This article describes the pathogenetic factors of formation of cardiovascular risks in patients with non-alcoholic fatty liver disease, proposed the idea of stratification of cardiovascular risks in these patients, taking into account changes in the structure of the liver (fibrosis) and function (clinical and biochemical activity) and also it describes the main directions of drug therapy, taking into account the common pathogenetic mechanisms for non-alcoholic fatty liver disease and cardiovascular diseases. The role of obesity, local fat depots, adipokines, and endothelial dysfunction as the leading pathogenetic factors of increased cardiovascular risk in patients with NAFLD is discussed. Among pathogenetically justified drugs in conditions of poly and comorbidity, hypolipidemic (statins, fibrates), angiotensin II receptor antagonists, beta-blockers, etc. can be considered. According to numerous studies, it becomes obvious that the assessment of cardiovascular risks in patients with NAFLD will probably allow prescribing cardiological drugs, selecting individualized therapy regimens, taking into account the form of NAFLD, and on the other hand, building curation taking into account the identified cardiovascular risks.

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24

Shahi, A., N. Gautam, S. Rawal, U. Sharma, and A. Jayan. "Lipid Profile and Ultrasonographic Grading in Alcoholic and Non Alcoholic Fatty Liver Patients." Kathmandu University Medical Journal 19, no. 3 (September 30, 2021): 334–38. http://dx.doi.org/10.3126/kumj.v19i3.49712.

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Background Fatty liver disease (FLD) is a common and major chronic liver disease. It has been implicated that patients have disorders of lipid metabolism and are involved in the pathogenesis of fatty liver. Hence, it was designed to observe the association between lipid profile and fatty liver disease. Objective This study was undertaken to evaluate the association of lipid profile status, hemoglobin and albumin levels with fatty liver disease patients diagnosed based on ultrasonography (USG). Method This Cross-sectional study was undertaken in the Department of Internal Medicine with the collaboration of the Department of Radiology and Department of Biochemistry, Universal College of Medical Sciences-Teaching Hospital (UCMS-TH), Bhairahawa, Nepal from March 2019 to February 2020 in a total of 100 patients diagnosed with fatty liver disease by ultrasonography. The fasting blood was collected for lipid profile and carried out in the automated analyzer following standard protocol. Result In 100 cases, the male to female ratio was 1.8:1. Fifty six percent of the total cases presented with alcoholic fatty liver disease (AFLD) while the remaining 44% with non-alcoholic fatty liver disease (NAFLD). The spectrum of lipid abnormality was observed with increased total cholesterol (TC), Low Density Lipoprotein (LDL), increased triglycerides (TG), Very Low Density Lipoprotein (VLDL) in alcoholic fatty liver disease cases as compared to non-alcoholic fatty liver disease cases. However, it has been observed that TG/HDL and Non-HDL/HDL were higher in non-alcoholic fatty liver disease as compared to alcoholic fatty liver disease. Moreover, a statistically significant difference was observed in HDL between AFLG2 and NAFLG2 (p-value: 0.012). Conclusion Dyslipidemia and decreased HDL have been implicated in fatty liver diseases. USG in conjunction with Non-HDL/HDL, TG/HDL, hemoglobin, and albumin can be useful in early screening and monitoring of dyslipidemia in fatty liver patients.

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25

Mravec, Boris, and Mária Szántová. "Neurobiology of liver diseases." Gastroenterologie a hepatologie 77, no. 2 (April 26, 2023): 103–11. http://dx.doi.org/10.48095/ccgh2023103.

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he nervous system is an important factor that participates in the adaptive and compensatory reactions of the body, not only in physiological but also in pathological processes. Alterations in the activity of the nervous system may contribute to the development of somatic diseases and may also influence their progression. Experimental and clinical studies have shown that the nervous system also plays a role in liver diseases. Depending on the disease and on the mechanisms and pathways, the nervous system can play a positive as well as a negative role in liver diseases. The aim of this review is to describe the mechanisms and pathways through which the nervous system affects the development and progression of the most common liver diseases, such as alcoholic liver damage, non-alcoholic fatty liver disease, cholestatic liver diseases, hepatitis, cirrhosis, and hepatocellular carcinoma. In addition, we also describe the possible therapeutic consequences based on the modulation of signal transmission between the nervous system and the liver. Keywords alcoholic liver damage, autonomic nervous system, cirrhosis, chronic hepatitis, hepatocellular carcinoma, cholestatic liver diseases, neurobiology, fatty liver disease

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26

Aljomah, Ghanim, Susan S. Baker, Wensheng Liu, Rafal Kozielski, Janet Oluwole, Benita Lupu, Robert D. Baker, and Lixin Zhu. "Induction of CYP2E1 in non-alcoholic fatty liver diseases." Experimental and Molecular Pathology 99, no. 3 (December 2015): 677–81. http://dx.doi.org/10.1016/j.yexmp.2015.11.008.

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27

Nemchaninova, O. B., E. Yu Sklyanova, S. G. Lykova, E. N. Makhnovets, O. N. Pozdnyakova, T. B. Reshetnikova, and A. A. Khryanin. "Comorbidity: non-alcoholic fatty liver disease and psoriasis." Experimental and Clinical Gastroenterology, no. 10 (December 23, 2021): 55–60. http://dx.doi.org/10.31146/1682-8658-ecg-194-10-55-60.

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Non-alcoholic fatty liver disease (NAFLD), being a marker of significant changes in the hepatobiliary system against the background of metabolic syndrome and other endocrine pathologies, has a significant impact on the course of psoriatic disease. The presence of common mechanisms in the pathogenesis of these diseases suggests a very close relationship between them. This requires a multidisciplinary approach to studying the mechanisms of the pathogenesis of psoriasis and NAFLD, which will improve the methods of diagnosis and treatment of both diseases.

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28

Clouston, Andrew D., and Elizabeth E. Powell. "Interaction of non-alcoholic fatty liver disease with other liver diseases." Best Practice & Research Clinical Gastroenterology 16, no. 5 (October 2002): 767–81. http://dx.doi.org/10.1053/bega.2002.0329.

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29

Sharma, Satya Priya, Ki Tae Suk, and Dong Joon Kim. "Significance of gut microbiota in alcoholic and non-alcoholic fatty liver diseases." World Journal of Gastroenterology 27, no. 37 (October 7, 2021): 6161–79. http://dx.doi.org/10.3748/wjg.v27.i37.6161.

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30

Sugimoto, Kazushi, and Yoshiyuki Takei. "Clinicopathological features of non-alcoholic fatty liver disease." Hepatology Research 41, no. 10 (September 26, 2011): 911–20. http://dx.doi.org/10.1111/j.1872-034x.2011.00867.x.

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31

Vakhrushev, Ya M., E. V. Suchkova, and A. P. Lukashevich. "Non - alcoholic fatty liver disease and enteral insufficiency: comorbidity of their development." Terapevticheskii arkhiv 91, no. 12 (December 15, 2019): 84–89. http://dx.doi.org/10.26442/00403660.2019.12.000134.

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The article reflects current literature data on the epidemiology and risk factors of non - alcoholic fatty liver disease. An important aspect is the description of the modern views of combined lesions of the hepatobiliary tract and small intestine. Disorders of the intestinal microbiota play a special role in the development of non - alcoholic fatty liver disease. The value of enterohepatic circulation of bile acids in the development of intestinal and liver diseases was shown. It seems relevant to further study the comorbidity of the development of non - alcoholic fatty liver disease and enteropathy for the development of pathogenetically substantiated therapy.

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32

Statsenko, M. E., S. V. Turkina, M. N. Ustinova, A. V. Tumarenko, O. Yu Sviridenko, and A. O. Sviridenko. "Hyperuricemia as a predictor of non-alcoholic fatty liver disease." South Russian Journal of Therapeutic Practice 3, no. 2 (June 18, 2022): 19–24. http://dx.doi.org/10.21886/2712-8156-2022-3-2-19-24.

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Non-alcoholic fatty liver disease (NAFLD) is currently a widespread disease among the adult population and, being a component of the metabolic syndrome (MS), is often associated with obesity, insulin resistance (IR), type 2 diabetes mellitus (DM2), cardiovascular diseases (CVD). Many authors in scientiﬁc studies have found that hyperuricemia (HU) can be considered as a predictor of non-alcoholic fatty liver disease (NAFLD), as well as other diseases associated with metabolic syndrome (MS).

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33

Didenko, V. I., I. A. Klenina, О. M. Tatarchuk, O. I. Hrabovska, and O. P. Petishko. "Specificities of lipotoxicity of free fatty acids and cytokine profile in patients with chronic diffuse liver diseases." Regulatory Mechanisms in Biosystems 13, no. 1 (December 26, 2021): 3–9. http://dx.doi.org/10.15421/022201.

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Non-alcoholic fatty liver disease is an important cause of global liver disease characterized by diffuse hepatocytes with hepatocellular ballooning, intrahepatic inflammation and progressive fibrosis. A relevant task is the study of the relationship between content of free fatty acids and serum cytokine profile in patients with chronic diffuse liver diseases. A total of 74 people with chronic diffuse liver diseases were examined, including 32 patients with non-alcoholic fatty liver disease, 22 patients with alcoholic liver disease, 20 patients with toxic hepatitis. Chromatographic examination of free fatty acids (FFA) in blood serum was carried out using a Chromatek-Crystal 5000 gas chromatography system. Patients with chronic diffuse liver diseases had a significant increase in the level of unsaturated free fatty acids (USFA) in cases of toxic hepatitis (by 2.92 times, P > 0.05) and a decrease in the level of saturated free fatty acids (SFA) in cases of non-alcoholic fatty liver disease (by 1.52 times, P > 0.05) compared with the control group; the balance between omega-6 and omega-3 PUFA significantly changed due to increase in linoleic acid in patients with alcoholic liver disease and toxic hepatitis (by 1.91 and 2.11 times, respectively) and arachidonic acid in patients with toxic hepatitis (by 1.78 times). The level of interleukin (IL)-6, IL-10, tumor necrosis factor alpha (TNF-α) were determined. In patients suffering chronic diffuse liver diseases there were multidirectional changes in the composition of free fatty acids of blood serum: a significant increase in the level of USFA, levels ІL-6 in toxic hepatitis; a decrease in the level of SFA, levels ІL-6 and TNF-α during non-alcoholic fatty liver disease; increased TNF-α production, ІL-6 during alcoholic liver disease compared with the control group. Significant change occurred in the balance between omega-6 and omega-3 PUFA due to increase in linoleic acid in cases of alcoholic liver disease and toxic hepatitis and arachidonic acid in cases of toxic hepatitis. The revealed correlations support the hypothesis that inflammation and lipotoxicity of FFA of blood serum contribute to the development and progression of structural changes in the liver. However, the pathomechanism of lipid metabolism and cytokine regulation with different etiological factors have their own characteristics, which should be taken into account when treating patients of these groups. Prospects for further research: these parameters may be used for serologic biomarkers of liver disease and development and implementation of the ratio between FFA and cytokines for the differential diagnosis of chronic diffuse liver disease in medical practice.

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Nakashima, Mitsutaka, Kazufumi Nakamura, Takahiro Nishihara, Keishi Ichikawa, Rie Nakayama, Yoichi Takaya, Norihisa Toh, et al. "Association between Cardiovascular Disease and Liver Disease, from a Clinically Pragmatic Perspective as a Cardiologist." Nutrients 15, no. 3 (February 1, 2023): 748. http://dx.doi.org/10.3390/nu15030748.

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Cardiovascular diseases and liver diseases are closely related. Non-alcoholic fatty liver disease has the same risk factors as those for atherosclerotic cardiovascular disease and may also be a risk factor for atherosclerotic cardiovascular disease on its own. Heart failure causes liver fibrosis, and liver fibrosis results in worsened cardiac preload and congestion. Although some previous reports regard the association between cardiovascular diseases and liver disease, the management strategy for liver disease in patients with cardiovascular diseases is not still established. This review summarized the association between cardiovascular diseases and liver disease. In patients with non-alcoholic fatty liver disease, the degree of liver fibrosis progresses with worsening cardiovascular prognosis. In patients with heart failure, liver fibrosis could be a prognostic marker. Liver stiffness assessed with shear wave elastography, the fibrosis-4 index, and non-alcoholic fatty liver disease fibrosis score is associated with both liver fibrosis in patients with liver diseases and worse prognosis in patients with heart failure. With the current population ageing, the importance of management for cardiovascular diseases and liver disease has been increasing. However, whether management and interventions for liver disease improve the prognosis of cardiovascular diseases has not been fully understood. Future investigations are needed.

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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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Maksimov, Maksim Leonidovich, Albina Airatovna Zvegintseva, and Tatyana Sergeevna Shindina. "Modern approaches to pharmacotherapy of non-alcoholic fatty liver disease." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 2 (February 1, 2021): 48–64. http://dx.doi.org/10.33920/med-10-2102-06.

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According to the forecasts of the World Health Organization, non-alcoholic fatty liver disease (NAFLD) will rank first in the structure of liver diseases by 2020. The article presents the current provisions on the pathogenesis of NAFLD, as well as existing and promising directions in the treatment of non-alcoholic fatty liver disease. A review of the recommendations of the leading hepatological associations for the treatment of non-alcoholic fatty liver disease is carried out. The main directions in the pharmacological treatment of NAFLD are the prescription of drugs that reduce body weight, increase the sensitivity of tissues to insulin, affect oxidative stress, normalize the levels of lipids and blood transaminases, and correct intestinal microflora.

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Kakati, Donny, Evan Raff, Khaleed Rashid, Mohamed Shoreibah, Joseph Bloomer, Yong-Fang Kuo, and Ashwani Singal. "A Validated Clinical Score to Differentiate Non-Alcoholic Fatty Liver Diseases From Alcoholic Liver Disease." American Journal of Gastroenterology 109 (October 2014): S174. http://dx.doi.org/10.14309/00000434-201410002-00594.

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Zhirkov, I. I., A. V. Gordienko, B. A. Chumak, I. M. Pavlovich, V. V. Yakovlev, and D. Yu Serdukov. "Prognostic mathematical models of the development of chronic non-viral liver diseases." Experimental and Clinical Gastroenterology, no. 8 (January 18, 2023): 84–91. http://dx.doi.org/10.31146/1682-8658-ecg-204-8-84-91.

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Chronic non-viral liver diseases are one of the most pressing problems of modern internal medicine. Over the past two decades, there has been a steady increase in diseases of this group due to the widespread prevalence of major risk factors, such as obesity, diabetes mellitus, physical inactivity, alcohol abuse, irrational use of medications, etc. Since most of the patients represent the most able-bodied and active part of the population, this circumstance inevitably leads to significant financial, economic and humanitarian losses, which gives the problem acute social significance. The purpose of the study. To develop mathematical prognostic models of the development of the most common chronic non-viral liver pathology using the most important predictors of these diseases. Material and methods. The contingent included in the study consisted of 412 young and middle-aged men, 138 of them with non-alcoholic fatty liver disease, 50 with alcoholic liver disease, 157 with alcoholic-metabolic fatty liver disease and 67 people without pathology. The subjects were measured anthropometric indicators (height, body weight, calculation of body mass index, waist circumference), determination of the type of alcohol consumption according to the AUDIT questionnaire, the level of physical activity according to the IPAQ questionnaire. In the biochemical study of blood serum, the parameters of alanine and aspartate aminotransferase, total and direct bilirubin, alkaline phosphatase, gamma-glutamyltranspeptidase, glucose, insulin, and lipid spectrum were determined. The study of the qualitative and quantitative composition of the intestinal microbiome was carried out by sowing feces on nutrient media, followed by the determination of the species of microorganisms and the assessment of their quantitative content using microscopy. Ultrasound examination of the hepatobiliary zone included measuring the main sizes of the right and left lobes of the liver, as well as identifying the main signs of diffuse liver damage. To assess steatosis and liver fibrosis, a FibroScan 530 device was used with the functions of evaluating the parameter of controlled attenuation of ultrasound and transient elastography by controlled vibration. Statistical processing and analysis of the results obtained were performed using the StatTech 2.8.8 program. Results. Mathematical prognostic models have been developed to determine the probability of developing non-alcoholic fatty liver disease, alcoholic fatty liver disease and alcoholic-metabolic fatty liver disease. All the regression models obtained were statistically significant with sensitivity and specificity of more than 90%. AUROC diagnostic accuracy values exceeded 0.9 units, which characterizes the quality of diagnostic models as excellent. Conclusions. The use of mathematical prognostic models using publicly available data from objective and laboratory research methods allows optimizing the diagnosis of chronic non-viral liver diseases.

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Akhavan Rezayat, Arash, Malihe Dadgar Moghadam, Mohammad Ghasemi Nour, Matin Shirazinia, Hamidreza Ghodsi, Mohammad Reza Rouhbakhsh Zahmatkesh, Mitra Tavakolizadeh Noghabi, Benyamin Hoseini, and Kambiz Akhavan Rezayat. "Association between smoking and non-alcoholic fatty liver disease: A systematic review and meta-analysis." SAGE Open Medicine 6 (January 1, 2018): 205031211774522. http://dx.doi.org/10.1177/2050312117745223.

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Background/aims: Non-alcoholic fatty liver disease is one of the most common chronic liver diseases. Some risk factors are known to influence the development of non-alcoholic fatty liver disease, but the effect of tobacco smoking on the progression of non-alcoholic fatty liver disease is controversial. The main goal of this systematic review and meta-analysis is to investigate the association between smoking and non-alcoholic fatty liver disease. Method: Electronic databases (PubMed, Scopus, and ISI Web of Science) were searched to find published articles on non-alcoholic fatty liver disease and smoking until December 2016. All relevant studies were screened by inclusion and exclusion criteria and compatible studies were chosen. The Newcastle–Ottawa Scale was used to assess the methodological quality of eligible articles. Subsequently, information was gathered based on the following: author, publication year, keywords, country, inclusion and exclusion criteria, main results, study design, conclusion, and confounder variables (age, body mass index, gender, ethnicity, and diabetes). Finally, analyses were performed using Comprehensive Meta-Analysis Software. Results: Data were extracted from 20 observational studies (9 cross-sectional, 6 case-control, 4 cohort studies, and 1 retrospective cohort study). A significant association was observed between smoking and non-alcoholic fatty liver disease with a pooled odds ratio of 1.110 (95% confidence interval, 1.028–1.199), p-value = 0.008. The statistical heterogeneity was medium with an I2 of 40.012%, p-heterogeneity = 0.074. Also there was a significant relation between non-alcoholic fatty liver disease and passive smoking with a pooled odds ratio of 1.380 (95% confidence interval, 1.199–1.588; p-value = 0.001; I2 = 59.41; p-heterogeneity = 0.117). Conclusion: Our meta-analysis demonstrated that smoking is significantly associated with non-alcoholic fatty liver disease. Further prospective studies exploring the underlying mechanisms of this association should be pursued. Also passive smoking increases the risk of non-alcoholic fatty liver disease about 1.38-fold. The effects of smoking cigarettes on active smokers (current smoker, former smoker, and total smoker) are less than passive smokers. Further studies are needed to compare the of effects of passive and active smoking on non-alcoholic fatty liver disease.

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Shabangu, Ciniso Sylvester, Jee-Fu Huang, Hui-Hua Hsiao, Ming-Lung Yu, Wan-Long Chuang, and Shu-Chi Wang. "Liquid Biopsy for the Diagnosis of Viral Hepatitis, Fatty Liver Steatosis, and Alcoholic Liver Diseases." International Journal of Molecular Sciences 21, no. 10 (May 25, 2020): 3732. http://dx.doi.org/10.3390/ijms21103732.

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During the progression from hepatitis to fibrosis, cirrhosis, and liver failure, the accumulation of stressed/damaged hepatocyte elements associated with liver inflammation is critical. The causes of hepatocyte injuries include viral hepatitis infections, alcoholic hepatitis, and non-alcoholic fatty liver disease. Hepatocyte-derived extracellular vesicles (Hep-EVs) released from stressed/damaged hepatocytes are partly responsible for liver disease progression and liver damage because they activate non-parenchymal cells and infiltrate inflammatory cells within the liver, which are in turn are an important source of EVs. This cell-to-cell signaling is prevalent during inflammation in many liver diseases. Accordingly, special emphasis should be placed on liquid biopsy methods for the long-term monitoring of chronic liver diseases. In the present review, we have highlighted various aspects of current liquid biopsy research into chronic liver diseases. We have also reviewed recent progress on liquid biopsies that focus on cell-free DNA (cfDNA), long non-coding RNA (lncRNA), and the proteins in EVs as potential diagnostic tools and novel therapeutic targets in patients with viral hepatitis, fatty liver steatosis, and alcoholic liver diseases.

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Roeb, Elke. "Non-alcoholic fatty liver diseases: current challenges and future directions." Annals of Translational Medicine 9, no. 8 (April 2021): 726. http://dx.doi.org/10.21037/atm-20-3760.

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Ansari, J. A., Mateen Sayyed, and Faizan Sayeed. "Management of Non Alcoholic Fatty Liver Diseases and their Complications." International Journal of Pharmacology 7, no. 5 (June 15, 2011): 579–88. http://dx.doi.org/10.3923/ijp.2011.579.588.

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Assy, Nimer. "Nutritional recommendations for patients with non-alcoholic fatty liver diseases." World Journal of Gastroenterology 17, no. 29 (2011): 3375. http://dx.doi.org/10.3748/wjg.v17.i29.3375.

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Ahn, J. S., D. H. Sinn, Y. W. Min, S. N. Hong, H. S. Kim, S. H. Jung, S. Gu, et al. "Non-alcoholic fatty liver diseases and risk of colorectal neoplasia." Alimentary Pharmacology & Therapeutics 45, no. 2 (November 18, 2016): 345–53. http://dx.doi.org/10.1111/apt.13866.

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Livzan, M. A., T. S. Krolevets, T. V. Kostoglod, and A. V. Kostoglod. "Non-Alcoholic Fatty Liver Disease: How to Avoid Mistakes in Patient’s Curation." Effective Pharmacotherapy 17, no. 4 (April 18, 2021): 62–67. http://dx.doi.org/10.33978/2307-3586-2021-17-4-62-67.

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The high prevalence of non-alcoholic fatty liver disease and its association with diseases of the metabolic profile causes the interest of doctors of various specialties in the management of patients with this pathology. Due to the accumulation of data on risk factors and disease progression, approaches and attitudes about previously harmless pathology have evolved to understand its potential danger. The formation of the correct approach to the management of patients with non-alcoholic fatty liver disease is a priority task. In this publication, we have analyzed and systematized data from literature concerning the most common problems (mistakes) in the curation of patients with non-alcoholic fatty liver disease.

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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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Hajduch, Eric, Floriane Lachkar, Pascal Ferré, and Fabienne Foufelle. "Roles of Ceramides in Non-Alcoholic Fatty Liver Disease." Journal of Clinical Medicine 10, no. 4 (February 16, 2021): 792. http://dx.doi.org/10.3390/jcm10040792.

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Non-alcoholic fatty liver disease is one of the most common chronic liver diseases, ranging from simple steatosis to steatohepatitis, fibrosis, and cirrhosis. Its prevalence is rapidly increasing and presently affects around 25% of the general population of Western countries, due to the obesity epidemic. Liver fat accumulation induces the synthesis of specific lipid species and particularly ceramides, a sphingolipid. In turn, ceramides have deleterious effects on hepatic metabolism, a phenomenon called lipotoxicity. We review here the evidence showing the role of ceramides in non-alcoholic fatty liver disease and the mechanisms underlying their effects.

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Pinte, Larisa, Daniel Vasile Balaban, Cristian Băicuş, and Mariana Jinga. "Non-alcoholic fatty pancreas disease – practices for clinicians." Romanian Journal of Internal Medicine 57, no. 3 (September 1, 2019): 209–19. http://dx.doi.org/10.2478/rjim-2019-0005.

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Abstract Obesity is a growing health burden worldwide, increasing the risk for several diseases featuring the metabolic syndrome – type 2 diabetes mellitus, dyslipidemia, non-alcoholic fatty liver disease and cardiovascular diseases. With the increasing epidemic of obesity, a new pathologic condition has emerged as a component of the metabolic syndrome – that of non-alcoholic fatty pancreas disease (NAFPD). Similar to non-alcoholic fatty liver disease (NAFLD), NAFPD comprises a wide spectrum of disease – from deposition of fat in the pancreas – fatty pancreas, to pancreatic inflammation and possibly pancreatic fibrosis. In contrast with NAFLD, diagnostic evaluation of NAFPD is less standardized, consisting mostly in imaging methods. Also the natural evolution of NAFPD and its association with pancreatic cancer is much less studied. Not least, the clinical consequences of NAFPD remain largely presumptions and knowledge about its metabolic impact is limited. This review will cover epidemiology, pathogenesis, diagnostic evaluation tools and treatment options for NAFPD, with focus on practices for clinicians.

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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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Dr Ajay Kumar Nandmer, Dr Vijay Kumar Nandmer,. "Pattern of Non Alcoholic Fatty Liver Disease in Coronary Artery Atherosclerosis in Central India." Journal of Medical Science And clinical Research 05, no. 02 (February 19, 2017): 17759–66. http://dx.doi.org/10.18535/jmscr/v5i2.93.

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