Articles
| Open Access |
https://doi.org/10.55640/
A SYSTEMATIC REVIEW OF FOLLOW-UP DISEASE PROGRESSION IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER
Khamidоva M.I. , Department of Gospital therapy and EndocrinologyAssistant Andijan State Medical Institute.Abstract
Hepatosteatosis is defined as an excessive accumulation of triglycerides in hepatocytes. There are 2 main conditions associated with hepatic steatosis: non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFFLD). In addition, various causes are listed in the pathogenesis of hepatic steatosis, such as metabolic, nutritional, drug (chemotherapy and steroids), and hepatitis C virus (HCV) infection. 1 The natural course of hepatic steatosis varies depending on the etiology and concomitant conditions such as inflammation and fibrosis, which can progress to cirrhosis and liver failure. Therefore, it is important to diagnose and quantify liver steatosis. Liver biopsy is currently the gold standard for evaluating a patient with suspected liver steatosis.[1] However, there are potential drawbacks to liver biopsy, such as sampling error, variability in interpretation, cost, and associated morbidity. Therefore, imaging techniques are commonly used for this purpose. In this article, we will review the etiology, imaging patterns, and quantification of hepatic steatosis using traditional and advanced imaging techniques.
Keywords
Hepatosteatosis, metabolic syndrome, NAFLD, metabolically healthy obesity, ultrasonography
References
Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686–90.
Friedman SL, Neuschwander-Tetri BA, Rinella M, Sanyal AJ. Mechanisms of NAFLD development and therapeutic strategies. Nat Med. 2018;24:908–22
Idilman IS, Ozdeniz I, Karcaaltincaba M. Hepatic Steatosis: etiology, patterns, and quantification. Semin Ultrasound CT MR. 2016;37:501–10.
Molteni M, Gemma S, Rossetti C. The role of toll-like receptor 4 in infectious and noninfectious inflammation. Mediat Inflamm. 2016;2016:6978936.
Csak T, Velayudham A, Hritz I, Petrasek J, Levin I, Lippai D, et al. Deficiency in myeloid differentiation factor-2 and toll-like receptor 4 expression attenuates nonalcoholic steatohepatitis and fibrosis in mice. Am J Physiol Gastrointest Liver Physiol. 2011;300:G433–41.
Hasan ST, Zingg JM, Kwan P, Noble T, Smith D, Meydani M. Curcumin modulation of high fat diet-induced atherosclerosis and steatohepatosis in LDL receptor deficient mice. Atherosclerosis. 2014;232:40–51.
Lee SB, Park GM, Lee JY, Lee BU, Park JH, Kim BG, et al. Association between non-alcoholic fatty liver disease and subclinical coronary atherosclerosis: an observational cohort study. J Hepatol 2018;68:1018-1024.
Jang HR, Kang D, Sinn DH, Gu S, Cho SJ, Lee JE, et al. Nonalcoholic fatty liver disease accelerates kidney function decline in patients with chronic kidney disease: a cohort study. Sci Rep 2018;8:4718. Erratum in: Sci Rep 2021;11(1):11139.
Lee JY, Kim KM, Lee SG, Yu E, Lim YS, Lee HC, et al. Prevalence and risk factors of non-alcoholic fatty liver disease in potential living liver donors in Korea: a review of 589 consecutive liver biopsies in a single center. J Hepatol 2007;47:239-244.
Article Statistics
Downloads
Copyright License

This work is licensed under a Creative Commons Attribution 4.0 International License.