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Abstract Details
Non-invasive risk scores do not reliably identify future cirrhosis or hepatocellular carcinoma in Type 2 diabetes: The Edinburgh Type 2 Diabetes Study
Sheila M Grecian1, Stela McLachlan1, Jonathan A Fallowfield2, Patrick Ka Kearns3, Peter C Hayes2, Indra Neil Guha4, Joanne R Morling1, Stephen Glancy5, Rachel M Williamson6, Rebecca M Reynolds7, Brian M Frier7, Nicola N Zammitt8, Jackie F Price1, Mark Wj Strachan6
Author information
1Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, UK.
2Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, UK.
3Centre for Clinical Brain Sciences, University of Edinburgh, UK.
4NIHR Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS Trust and the University of Nottingham, Nottingham, UK.
5Department of Radiology, Western General Hospital, Edinburgh, UK.
6Western General Hospital, Edinburgh, UK.
7University/BHF Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, UK.
8Royal Infirmary of Edinburgh, Edinburgh, UK.
Abstract
Background: The incidence of cirrhosis and hepatocellular carcinoma (HCC) is increased in Type 2 diabetes, primarily secondary to non-alcoholic fatty liver disease (NAFLD). European guidelines recommend screening for NAFLD in Type 2 diabetes. American guidelines, while not advocating a screening protocol, suggest using non-invasive markers of fibrosis for risk-stratification and guiding onward referral.
Aims: To test the ability of individual fibrosis scores and the European screening algorithm to predict 11-year incident cirrhosis/HCC in an asymptomatic community cohort of older people with Type 2 diabetes.
Methods: The Edinburgh Type 2 Diabetes Study investigated men and women with Type 2 diabetes (n=1,066, aged 60-75 at baseline). Liver markers were measured at baseline and year 1; steatosis and fibrosis markers were calculated according to independently published calculations. During 11-years of follow-up, cases of cirrhosis and HCC were identified.
Results: 43/1059 participants with no baseline cirrhosis/HCC developed incident disease. All scores were significantly associated with incident liver disease by odds ratio (p<0.05). The ability of the risk-stratification tools to accurately identify those who developed incident cirrhosis/HCC was poor with low positive predictive values (5-46%) and high false negative and positive rates (up to 60% and 77%) respectively. When fibrosis risk scores were used in conjunction with the European algorithm, they performed modestly better than when applied in isolation.
Conclusions: In a cohort with a moderately low incidence of cirrhosis/HCC, existing risk scores did not reliably identify participants at high-risk. Better prediction models for cirrhosis/HCC in people with Type 2 diabetes are required.