African American Females are More Vulnerable to Develop Biliary Injury in NAFLD (Nonalcoholic fatty liver disease) Patients – A Single Institute Experience

Abstract Introduction/Objective Chronic alcohol exposure alone may take decades to induce severe liver disease, yet when combined with elements such as the Western diet, liver pathogenesis accelerates, resulting in earlier symptoms. Identifying the specific contributions of alcohol, diet, and other factors to liver disease is challenging, despite the availability of diagnostic tools like patient histories, liver enzyme tests, imaging, and biopsies. Methods/Case Report This study seeks to detail the liver disease profile of patients who underwent liver biopsies in 2022. Comprehensive profiles were created by retrieving liver biopsy specimens and associated diagnostic data from electronic medical records. Two independent pathologists analyzed the biopsy slides, looking for liver damage associated with alcohol consumption and Western diet influences. We employed enhanced staining techniques to better associate specific types of liver damage with demographic variables. The data analysis was conducted using GraphPad Prism 9 for robust statistical evaluation. Results (if a Case Study enter NA) The research included 88 participants—41 males and 47 females, with average ages of 56 and 62 respectively. The predominant diagnosis was fatty liver disease, with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) accounting for 26% of cases, and alcoholic liver disease (ALD) making up 10%. The NAFLD/NASH group (n=23) consisted mainly of African Americans (n=15) and Caucasians (n=8). Among these, African Americans showed a significantly greater ductular reaction and portal inflammation (p<0.05). Conversely, no notable differences in portal fibrosis and bile stasis were observed between these groups. Notably, African American females (n=11) demonstrated more severe pathological features compared to Caucasian females (n=6), including elevated levels of ductular reaction, fibrosis, portal inflammation, and bile stasis (p<0.05), suggesting a higher vulnerability to biliary injuries. Conclusion The study highlights the complex interplay between lifestyle factors and liver disease development and emphasizes the need for precise diagnostic strategies that consider these multifactorial influences. Additionally, it reveals ethnic disparities in the pathology of NAFLD, advocating for further research into their causes and implications for clinical management. Future investigations should focus on race and gender-specific factors and adapt local healthcare strategies to effectively manage the escalating burden of liver disease.