ODP181 Diabetes Mellitus and Advanced Liver Fibrosis – is Cirrhosis Reversible and Who Should We Screen?
Authors: Reda Sarah A , Barjaktarovic Mirjana , Lee Tae Hoon , Saul Shira R , Greenberg Pietra D 
Published: November 2022

Recent evidence shows an association between type 2 diabetes mellitus (T2DM) and liver steatosis, fibrosis, and hepatocellular carcinoma. Studies suggest that improved glycemic control, weight loss, and GLP-1 agonists may halt progression and even improve non-alcoholic fatty liver disease (NAFLD); however, little is known about the extent of improvement these factors have on liver fibrosis. ADA guidelines suggest only patients with T2DM or pre-DM and elevated liver enzymes (or fatty liver on ultrasound) should be evaluated for NAFLD and fibrosis. Three patients ages 65-71 with long-standing T2DM, HLD, obesity, and no history of liver disease or current alcohol use were followed in our diabetic clinic and referred for screening for liver steatosis and fibrosis. The transient elastography method (fibroscan) was used to determine the degree of liver fibrosis. On initial fibroscans, all three patients were found to have F4 scores consistent with liver cirrhosis. The first patient is a 71-year-old male with T2DM (BMI 37.5kg/m 2), treated with semaglutide, empagliflozin, glipizide, and insulin. Over two years, he experienced a 4-lb weight loss and improvement in HbA1c(7.8% to 7.1%). Repeat fibroscan after two years showed improved fibrosis score – F3 (11.6 kPa to 10.2 kPa), consistent with moderate fibrosis. The second patient is a 69-year-old female with T2DM (BMI 37.3kg/m 2) and transient mild LFT abnormalities, found to have cirrhosis on fibroscan – F4 score. She was managed with semaglutide, empagliflozin, metformin, and insulin; weight decreased 9-lbs over two years and HbA1c improved(10.8% to 7.8%). Repeat fibroscan showed improvement in fibrosis score to F2 (15.1 kPa to 8.9 kPa), and her LFT abnormalities resolved. The third patient is a 65-year-old male with T2DM (BMI 35kg/m 2). His initial fibroscan showed cirrhotic liver – F4 score. He was maintained on empagliflozin and dulaglutide- then switched to semaglutide. He experienced a 10-lb weight loss during this time and had a stable HbA1c(6.6%). Repeat fibroscan after one year showed improvement to F0-F1(11.3 kPa to 6.1 kPa) consistent with little to no liver scarring. These cases highlight two important factors: 1) ADA liver screening guidelines should be expanded to include obesity and dyslipidemia; and 2) advanced liver fibrosis in patients with diabetes is, to some degree, reversible. Not all of the patients initially met standard ADA screening criteria, mostly without elevated liver enzymes and no prior abnormal liver imaging. Yet, all were diabetic and obese with dyslipidemia, which are independent risk factors for NAFLD. Additionally, patients with improved glycemic control on GLP-1 treatment as well as some weight loss have promising results on repeat fibroscan. These findings may improve screening and management of diabetes-related liver disease. Further studies are needed to investigate to what extent GLP-1 agonists alone or in combination with glycemic control and weight loss contribute to these improvements.

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