Evaluation of Histological Liver Changes in Obese Patients Compared with Normal-Weight Individuals

Saif kamel  Mohammed

doi:10.51699/cajmns.v7i4.3336

Authors

Saif kamel Mohammed Department of Anatomy, College of Medicine, Tikrit University, Iraq

DOI:

https://doi.org/10.51699/cajmns.v7i4.3336

Keywords:

Obesity, Histopathology, Non-Alcoholic Fatty Liver Disease (NAFLD), Hepatic Steatosis, Liver Fibrosis

Abstract

Background: Obesity is one of the most important health risk factors globally and is known to be one of the most important risk factors for the occurrence of non-alcoholic fatty liver disease (NAFLD) and its histopathological complications. Hepatic lipid accumulation, chronic inflammation and hepatocellular damage and fibrosis, which result from excessive adiposity, represent the risk factors for cirrhosis and liver failure. Objective: To perform comparative and evaluative analysis of the histological changes in liver of obese patient vs. normal weight patient and the correlation between the severity of liver histological changes and obesity. Materials and methods: This was a comparative observational histopathological study that was carried out for two years (May 2024 – May 2026) in the histopathology department of Baghdad Teaching Hospital, Medical city, Baghdad, Iraq. Five hundred pieces of liver were obtained, 50 of which were obese, and 50 normal weight patients. Standard histological methods were used for processing tissue specimens and they were stained with Hematoxylin and Eosin (H&E) and Masson's Trichrome stains and then observed with light microscopy. Histopathological evaluation comprised of macrovesicular steatosis, microvesicular steatosis, hepatocellular ballooning, lobular inflammation, portal inflammation, hepatocyte necrosis, sinusoidal dilatation, glycogenated nuclei, fibrosis stage and Non-alcoholic Fatty Liver Disease Activity Score (NAS). Statistic analysis (SPSS version 27.0) and significance (P < 0.05) were used. The prevalence and severity of macrovesicular steatosis, microvesicular steatosis, hepatocellular ballooning, lobular inflammation, portal inflammation, hepatocyte necrosis, sinusoidal dilatation and glycogenated nuclei were significantly increased in obese compared with normal weight patients (all P < 0.05). Fibrosis and non-alcoholic steatohepatitis (NASH) were also significantly increased in obese patients compared with normal weight patients (P < 0.05). Furthermore, obese patients had significantly increased grades of steatosis, stage of fibrosis and NAS. The liver injury was progressive and all severity parameters of the liver was positively correlated with BMI on histopathology. Finally, the present study confirms the close association between obesity and liver damage, manifested as steatosis, inflammation, hepatocellular degeneration and fibrosis. These results further confirm previous reports indicating that liver biopsy continues to be the standard of care to assess severity of NAFLD and how it progresses to NASH. Early detection of the histo-pathological changes that occur with obesity may facilitate early therapeutic intervention and prevent end-stage liver disease, fibrosis and cirrhosis.

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