Evaluation of liver steatosis, measured by controlled attenuation parameter, in patients with hepatitis C-induced advanced liver fibrosis and hepatocellular carcinoma Ashraf O. Abdelaziz a , Hend I. Shousha a , Ebada M. Said c , Zeinab A. Soliman a , Ahmed A. Shehata c , Mohamed M. Nabil a , Ahmed H. Abdelmaksoud b , Tamer M. Elbaz a and Fatma M. Abdelsalam c Introduction Steatosis is a documented feature of chronic hepatitis C (CHC). There is an association between steatosis decrease and fibrosis progression. The association between steatosis and advanced fibrosis versus hepatocellular carcinoma (HCC) development has not been precisely evaluated. The controlled attenuation parameter (CAP) was applied as an immediate and efficient process to detect and quantify hepatic steatosis with adequate accuracy. Aims The aim of this study was to assess the difference in liver steatosis between patients with hepatitis C virus-related advanced hepatic fibrosis versus HCC. Patients and methods This cross-sectional study included 130 patients with HCC, attending the multidisciplinary HCC clinic, Cairo University, and 54 patients with CHC between October 2015 and June 2016. Clinical and laboratory characteristics were recorded. Liver stiffness and CAP were obtained by using the FibroScan 502, touch. Results All included patients had genotype 4. The mean CAP value was significantly lower in HCC (209.5 ± 57.1 dB/m) versus CHC (259.9 ± 54.9 dB/m). Receiver operating characteristic curve revealed an area under the curve of 0.75 for the differentiation between groups. At a cutoff value of 237 dB/m, sensitivity was 72.3%, specificity was 70.7%, positive likelihood ratio was 2.5, and negative likelihood ratio was 0.4 in the differentiation between CHC versus HCC. Logistic regression analysis revealed an odds ratio of 6.4 for the diagnosis of HCC with CAP of less than 237 dB/m. Multivariate analysis, controlling for age, sex, BMI, triglycerides, and cholesterol levels, revealed a significantly increased odds for HCC diagnosis (odds ratio: 4.3, P = 0.006). Conclusion The progression of CHC is associated with a decrease in steatosis, particularly toward advanced fibrosis and HCC. Steatosis reduction less than 237 dB/m is likely to be associated with HCC. Eur J Gastroenterol Hepatol 30:1384–1388 Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved. Introduction Hepatic steatosis is a known histological feature in chronic hepatitis C (CHC). Hepatitis C virus (HCV) induces steatosis through its core protein and nonstructural protein 5A as they induce overproduction of reactive oxygen species and mitochondrial dysfunction in addition to insulin resistance [1]. The prevalence of steatosis ranges from 40 to 86% in CHC and most (78%) patients have mild steatosis [2]. HCV genotype plays a role in inducing steatosis; moderate or severe steatosis is significantly less frequent in genotypes 1 and 4 than in genotype 3. In overweight, nondiabetic patients, moderate or severe steatosis is present in only 10–15% of genotypes 1 or 4 patients, indicating that liver steatosis is mostly associated with metabolic factors in those genotypes [3]. Egypt had the highest HCV burden worldwide as reported in the demographic and health survey 2008, with 90% of patients infected with HCV genotype 4 and the remaining infected with genotype 1 [4,5]. Thereafter, the sero- prevalence of HCV infection has declined to 6.3% in 2015 [6], with an overall estimated 30% reduction in prevalence [7,8]. Steatosis plays a role in fibrosis progression during the early stages of liver disease but steatosis recedes during the transition from advanced fibrosis to cirrhosis [5]. It has been suggested that hepatic steatosis itself adds an onco- genic potential to the liver [6]. The pathways connecting steatosis to hepatocellular carcinoma (HCC) are still under investigations. They include the following: the low-grade inflammatory status, altered adipokines release enhancing insulin resistance, and increased lipogenesis with avail- ability of fatty acids supplying energy for rapidly growing hepatocytes [7]. In addition, there is oxidative stress with lipid peroxidation and mitochondrial damage in CHC induced by HCV core and nonstructural proteins [8,9]. Liver biopsy was considered as the gold standard for the diagnosis and staging of liver steatosis; however, it is an invasive and expensive method with both interobserver and intraobserver variabilities and major possible Departments of a Endemic Medicine, b Diagnostic and Interventional Radiology, Faculty of Medicine, Cairo University, Cairo and c Department of Hepatology, Gastroenterology and Infectious Diseases, Faculty of Medicine, Benha University, Benha, Egypt Correspondence to Hend I. Shousha, MD, Department of Endemic Medicine, Faculty of Medicine, Cairo University, 11562 Cairo, Egypt Tel: + 20 100 573 8455; fax: + 20 225 326 543; e-mail: hendshousha@yahoo.com Received 17 March 2018 Accepted 30 April 2018 European Journal of Gastroenterology & Hepatology 2018, 30:1384–1388 Keywords: advanced liver fibrosis, controlled attenuation parameter, hepatic steatosis, hepatitis C virus genotype 4, hepatocellular carcinoma ’ Original article 0954-691X Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/MEG.0000000000001196 1384 Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.