The Utility of Noninvasive Scores in Assessing the Prevalence of Nonalcoholic Fatty Liver Disease and Advanced Fibrosis in Type 2 Diabetic Patients Amandeep Singh, MD,* Phuc Le, MD,* Maajid M. Peerzada, MD,* Rocio Lopez, MS, MPH,† and Naim Alkhouri, MD‡§ Goals: The aim of our study is to assess the prevalence of nonalcoholic fatty liver disease (NAFLD) and advanced hepatic fibrosis in patients with type 2 diabetes mellitus (T2DM) using simple noninvasive scores. Background: In individuals with T2DM, there is a very high prev- alence of NAFLD. Moreover, T2DM is a risk factor for advanced disease in NAFLD patients. Study: Using International Classification of Diseases, Ninth Revision codes all patients with the diagnosis of T2DM were reviewed and a retrospective chart analysis was performed on 169,910 patients between the ages of 18 to 80. To predict the prevalence of NAFLD, we calcu- lated the hepatic steatosis index. To estimate the prevalence of advanced fibrosis, NAFLD fibrosis score (NFS), fibrosis-4 index, aspartate aminotransferase (AST) to platelet ratio index (APRI), and AST/alanine aminotransferase (ALT) ratio were calculated. Results: Of the 121,513 patients included in the analysis, 89.4% were above normal weight limit. NAFLD based on Hepatic Steatosis Index > 36 was present in 87.9% of patients. Advanced fibrosis was present in 35.4% based on NFS > 0.676, 8.4% based on fibrosis- 4 > 2.67, 1.9% based on APRI > 1.5, and 16.9% based on AST/ALT > 1.4% indicating advanced fibrosis and high risk of developing cirrhosis related to NAFLD. Conclusions: In this large cohort of patients with T2DM, we detected high prevalence of hepatic steatosis and advanced fibrosis using noninvasive scores. These scores are easy and nonexpensive tools to screen for NAFLD and advanced fibrosis, although the significant variability of the percentage of patients with advanced fibrosis using these scores indicates the need for further validation in diabetic populations. Key Words: fatty liver, noninvasive scores, fibrosis (J Clin Gastroenterol 2017;00:000–000) N onalcoholic fatty liver disease (NAFLD) refers to the presence of hepatic steatosis, demonstrated by histology or imaging, in the absence of signi ficant alcohol consumption and the other known secondary causes. 1 NAFLD encompasses a broad disease spectrum, ranging from simple steatosis pro- gressing through nonalcoholic steatohepatitis (NASH), advanced fibrosis to cirrhosis, and end-stage liver disease. NAFLD has become the most frequent cause of chronic liver disease in the western world and can progress to NASH. NAFLD is predicted to become the leading cause of liver transplantation in coming years. 2 Obesity and insulin resistance are the key pathogenic factors associated with NAFLD, and thus are very prevalent among patients with type 2 diabetes mellitus (T2DM). Recent studies have shown that 49% to 62% of patients with T2DM have NAFLD 3,4 and clinically relevant fibrosis occurs in upto 20% of these patients. 5 T2DM confers a particular risk for development of the progressive form of NAFLD and in addition, is an independent risk predictor of moderate to severe fibrosis. 6,7 T2DM increases the risk of liver-related deaths in NAFLD patients upto 22-fold, as well as overall mortality by 2.6 to 3.3-fold. 8 In addition, the combination of NAFLD and T2DM increases the risk of cardiovascular disease 9 and accelerates the progression of macro and microvascular complications. Given the increase in worldwide prevalence of T2DM, there is a substantial disease burden associated to end-stage liver disease in the future. An early diagnosis and treatment of NAFLD may have a beneficial clinical impact on the survival of diabetic patients. Liver biopsy is the “gold standard” for NAFLD diag- nosis; however, this is invasive and carries intrinsic morbidity risk. 10 Ultrasonography is the recommended first-line imag- ing technique in clinical practice, although it is known to have limited sensitivity. 11 Other noninvasive tools have been developed for diagnosing NAFLD and its severity, such as proton magnetic resonance spectroscopy (1H-MRS), mag- netic resonance elastography, and vibration controlled tran- sient elastography. However, these tools are expensive, time-consuming, and are not considered cost-effective for large-scale NAFLD screening. Recently, noninvasive scores have been developed to predict the presence of suspected NAFLD such as the hepatic steatosis index (HSI). 12 Other scores were developed to predict advanced fibrosis such as the NAFLD fibrosis score (NFS), fibrosis-4 (FIB-4) index, 13 aspartate aminotransferase (AST) to platelet ratio index (APRI), 14 and AST/alanine aminotransferase (ALT) ratio. 15 These scores are simple to calculate, from demographic and laboratory data to be used by both general practitioners and specialists. This could aid in early diagnosis, which further provide opportunities for early interventions in preventing Received for publication March 18, 2017; accepted July 6, 2017. From the *Department of Hospital Medicine, Medicine Institute; †Department of Quantitative Health Sciences, Lerner Research Institute; ‡Department of Gastroenterology, Hepatology and Nutrition, Digestive Diseases and Surgery Institute; Cleveland Clinic Foundation, Cleveland, OH; and §Texas Liver Institute, San Antonio, TX. Presented at European Association of the Study of Liver Disease Conference 2017, Amsterdam, the Netherlands. Clinical trial registration number: CCF-16-018. N.A., A.S.: study concept and design. A.S., M.P.: acquisition of data. N.A., A.S., R.L.: analysis and interpretation of data. A.S., P.L., M.M.P., R.L., N.A.: drafting of the manuscript and critical revision of the manuscript for important intellectual content. L.R., A.S., N.A.: statistical analysis. NA: administrative, technical, or material support, study supervision. The authors declare that they have nothing to disclose. Address correspondence to: Amandeep Singh, MD, Department of Hospital Medicine, M8-Annex, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195 (e-mail: singha4@ccf.org). Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/MCG.0000000000000905 ORIGINAL ARTICLE J Clin Gastroenterol  Volume 00, Number 00, ’’ 2017 www.jcge.com | 1 Copyright r 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. This paper can be cited using the date of access and the unique DOI number which can be found in the footnotes.