NASH, Metabolic Syndrome, and Diabetes: How Sugar and Fat Increase the Risk of Developing Advanced Liver Disease
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EDITORIAL
NASH, Metabolic Syndrome, and Diabetes: How Sugar and Fat Increase the Risk of Developing Advanced Liver Disease Paul Manka1 · Wing‑Kin Syn2,3,4 Accepted: 15 September 2020 © The Author(s) 2020
Nonalcoholic steatohepatitis (NASH) is on track to become the leading contributor to the global burden of liver disease, in particular due to the finding that NASH is one of the commonest precursors of hepatocellular carcinoma (HCC) [1]. For example in the USA, while the percentage of total liver transplants for recipients with hepatitis C has decreased from 35.3 to 23.6%, the percentage of liver transplants for NASH has increased [2]. Retrospective reviews of two large biopsy databases reported that up to 5% of HCV patients also had NASH [3] and up to one-third of individuals with chronic HCV have type 2 diabetes, which has been associated with worsening outcomes of HCV infection [4]. In this issue of Digestive Diseases and Sciences, Benhammou and colleagues evaluated the effects of NAFLD risk factors including obesity and diabetes on the long-term outcomes of patients with HCV treated with direct-acting antivirals (DAAs) [5]. The authors conducted a retrospective study off 33,003 DAA treated US Veterans between 2013 and 2015. The patients were categorized using the body mass index (BMI); diabetes was identified using ICD 9/10 codes in association with hemoglobin A1c > 6.5% or having an active prescription for diabetes medications. Patients were evaluated for the development of cirrhosis, liver decompensation, or the development of HCC and death with a mean follow-up of 3 years. They found an association between the presence of diabetes and increased mortality * Paul Manka paul.manka@uk‑essen.de 1
Gastroenterology and Hepatology, Essen University Hospital, Hufelandstr 55, 45147 Essen, Germany
2
Division of Gastroenterology and Hepatology, Department of Medicine, Medical University of South Carolina, Charleston, SC, USA
3
Section of Gastroenterology, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, USA
4
Department of Physiology, Faculty of Medicine and Nursing, University of Basque Country UPV/EHU, Vizcaya, Spain
and liver-related adverse outcomes including HCC, even among patients without baseline cirrhosis. Patients who were obese also exhibited a higher risk of developing cirrhosis compared with normal-weight patients although surprisingly they had a lower risk of mortality and of developing HCC. These results underscore the importance of diabetes as an independent risk factor for liver disease, and in particular, HCC development. In contrast to prior experiences with IFN-based treatments, the presence of insulin resistance or type 2 diabetes mellitus did not appear to diminish the rate of sustained virological response (SVR) to DAA treatments [6]. Conversely, while several early studies had suggested that DAA-associated SVR improves the metabolic status, two of those studies did not observe long-term glycemic control [7]. Though the current study did not examine if DAA treat
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