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Non‐invasive risk scores do not reliably identify future cirrhosis or hepatocellular carcinoma in Type 2 diabetes: The Edinburgh type 2 diabetes study
Author(s) -
Grecian Sheila M.,
McLachlan Stela,
Fallowfield Jonathan A.,
Kearns Patrick K. A.,
Hayes Peter C.,
Guha Neil I.,
Morling Joanne R.,
Glancy Stephen,
Williamson Rachel M.,
Reynolds Rebecca M.,
Frier Brian M.,
Zammitt Nicola N.,
Price Jackie F.,
Strachan Mark W. J.
Publication year - 2020
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/liv.14590
Subject(s) - hepatocellular carcinoma , type 2 diabetes , cirrhosis , medicine , diabetes mellitus , gastroenterology , endocrinology
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 = 1066, 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 Forty‐three out of 1059 participants with no baseline cirrhosis/HCC developed incident disease. All scores were significantly associated with incident liver disease by odds ratio ( P < .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.