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      Effect of Weight Reduction on Histological Activity and Fibrosis of Lean Nonalcoholic Steatohepatitis Patient

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          Abstract

          Background and Objectives

          Weight reduction has evidenced benefit on attenuation of histological activity and fibrosis of nonalcoholic steatohepatitis (NASH), but there is scarcity of data for lean NASH subgroup. We have designed this study to compare the effects of weight reduction on histological activity and fibrosis of lean and non-lean NASH.

          Methods

          We have included 20 lean and 20 non-lean histologically proven NASH patients. BMI < 25 kg/m2 was defined as non-lean. Informed consent was taken from each subject. All methods were carried out in accordance with the Declaration of Helsinki. Moderate exercise along with dietary restriction was advised for both groups for weight reduction. After 1 year, 16 non-lean and 15 lean had completed second liver biopsy.

          Results

          Age, sex, alanine transaminase (ALT), aspartate aminotransferase (AST), gamma-glutamyltrasferase (GGT), Homeostasis model assessment insulin resistance (HOMA-IR), triglyceride and high density lipoprotein (HDL) was similar in both groups. Steatosis, ballooning, lobular inflammation, nonalcoholic fatty liver disease activity score (NAS) and fibrosis was similar in the two groups. In lean/non-lean group, any amount of weight reduction, ≥ 5% weight reduction and ≥ 7% weight reduction was found in respectively 8/11, 5/6 and 2/6 patients. In both lean and non-lean groups, weight reduction of any amount was associated with significant reduction of steatosis, ballooning and NAS, except lobular inflammation and fibrosis. In both groups, weight reduction of ≥ 5% was associated with significant reduction in NAS only. However, significant improvement in NAS was noted with ≥ 7% weight reduction in non-lean group only.

          Conclusion

          Smaller amount of weight reduction had the good benefit of improvement in all the segments of histological activity in both lean and non-lean NASH.

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          Most cited references23

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          Non alcoholic fatty liver disease and metabolic syndrome.

          Non-alcoholic fatty liver disease (NAFLD) is a clinicopathologic entity increasingly recognized as a major health burden in developed countries. It includes a spectrum of liver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis, and rarely, progression to cirrhosis. Recent studies emphasize the role of insulin resistance, oxidative stress and subsequent lipid peroxidation, proinflammatory cytokines, adipokines and mitochondrial dysfunction in the development and progression of NAFLD. Furthermore, accumulating evidence supports an association between NAFLD and metabolic syndrome. Although the data are mainly epidemiological, the pathogenesis of NAFLD and metabolic syndrome seems to have common pathophysiological mechanisms, with focus on insulin resistance as a key factor. This review summarizes the current knowledge on the epidemiology, pathophysiology and diagnosis of both NAFLD and metabolic syndrome and the findings that strongly support the association of nonalcoholic fatty liver disease as a possible component in the cluster of metabolic syndrome.
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            Histopathology of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.

            Nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of metabolic syndrome, is the most common chronic liver disease, and the prevalence is rapidly increasing worldwide. Nonalcoholic steatohepatitis (NASH), the severe form of NAFLD, can progress to liver cirrhosis and hepatocellular carcinoma (HCC). Although noninvasive clinical scores and image-based diagnosis for NAFLD have improved, histopathological evaluation of biopsy specimens remains the gold standard for diagnosing NAFLD/NASH. Steatosis, lobular inflammation, and hepatocellular ballooning are all necessary components for the diagnosis of NASH; fibrosis is also typically observed. Other histopathological abnormalities commonly observed in NASH include hepatocellular glycogenated nuclei, lipogranulomas, and acidophil bodies. The characteristics of pediatric NAFLD/NASH differ from adult NAFLD/NASH. Specifically, steatosis and portal inflammation are more severe in pediatric NAFLD, while intralobular inflammation and perisinusoidal fibrosis are milder. Although interobserver agreement for evaluating the extent of steatosis and fibrosis is high, agreement is low for intralobular and portal inflammation. A recently reported histological variant of HCC, steatohepatitic HCC (SH-HCC), shows features that resemble non-neoplastic steatohepatitis, and is thought to be strongly associated with underlying NASH. In this report, we review the histopathological features of NAFLD/NASH.
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              Recommendations for Diagnosis, Referral for Liver Biopsy, and Treatment of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis.

              Nonalcoholic fatty liver disease (NAFLD) is the primary cause of chronic liver disease in the United States, afflicting an estimated 80 to 100 million Americans. Nonalcoholic fatty liver disease is a spectrum of liver diseases composed of nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH). Although nonalcoholic fatty liver has a negligible risk of progression, patients with NASH often develop cirrhosis or hepatocellular carcinoma. Although liver biopsy is required to diagnose NASH, only patients with a high risk of NASH or advanced fibrosis require this evaluation. Despite the high prevalence of NAFLD, well-defined screening recommendations are currently lacking. In this review, suggestions for screening, diagnosis, and initial work-up of NAFLD are given on the basis of established guidelines and recent publications. Proposed drug treatments of NASH are also discussed, highlighting the study outcomes, as well as proposed uses and limitations of these drugs. The literature was searched in PubMed using search terms nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, with filters of "English language." A date range of January 1, 2000, to May 1, 2015, was used for the search. The bibliographies of key references were also searched manually, and seminal publications before the year 2000 were included.
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                Author and article information

                Journal
                J Transl Int Med
                J Transl Int Med
                jtim
                jtim
                Journal of Translational Internal Medicine
                Sciendo
                2450-131X
                2224-4018
                September 2019
                12 October 2019
                : 7
                : 3
                : 106-114
                Affiliations
                [1 ]Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Shahbag , Dhaka, Bangladesh
                [2 ]Department of Medicine, Dr. Sirajul Islam Medical College & Hospital , Dhaka, Bangladesh
                [3 ]Shaheed Sayed Nazrul Islam Medical College , Kishoreganj, Bangladesh
                Author notes
                [* ] Dr. Shahinul Alam, MBBS, FCPS, MD., Associate Professor, Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka, Bangladesh. shahinul67@ 123456yahoo.com
                Article
                jtim-2019-0023
                10.2478/jtim-2019-0023
                6795050
                31637181
                60c27c6f-c208-4f73-ab25-ac2a0a51c282
                © 2019 Shahinul Alam, Mohammad Jahid Hasan, Md. Abdullah Saeed Khan, Mahabubul Alam, Nazmul Hasan, published by Sciendo

                This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

                History
                Page count
                Pages: 9
                Categories
                Original Article

                nonalcoholic steatohepatitis,non-alcoholic fatty liver disease,lean nonalcoholic steatohepatitis,steatohepatitis,non-obese nonalcoholic steatohepatitis

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