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OP08 NAFLD related HCC is rising dramatically in the North of England
  1. H L Reeves1,
  2. J Graham2,
  3. T Aslam3,
  4. D Chattopadyhay3,
  5. D Das4,
  6. I Patanwala4,
  7. J Rose5,
  8. B Jaques3,
  9. D Manas3,
  10. M Hudson4
  1. 1Northern Institute for Cancer Research, Newcastle University
  2. 2Northern Centre for Cancer Care, Newcastle upon Tyne Hospitals NHS Foundation Trust
  3. 3Department of Surgery, Newcastle upon Tyne Hospitals NHS Foundation Trust
  4. 4The Liver Unit, Newcastle upon Tyne Hospitals NHS Foundation Trust
  5. 5Department of Radiology, Newcastle upon Tyne Hospitals NHS Foundation Trust

Abstract

Introduction A reported increase in hepatocellular cancer (HCC) in western nations has been attributed to the rising prevalence of predisposing hepatitis C (HCV) related chronic liver disease. In parallel, however, the prevalence of the metabolic syndrome has risen markedly, and both a raised BMI and type 2 diabetes, characteristic features of the syndrome, are independently associated with an increased risk of HCC development.

Aim We have assessed the prevalence of the metabolic syndrome in our patients with HCC.

Method 686 consecutive patients with HCC, diagnosed as per EASL guidelines, referred to our unit over a 10-year period (2000 and 2010), have been studied and demographic, laboratory, radiological variables, treatments and survival recorded.

Results The numbers of patients referred from our catchment population of 3.5 million has increased more than 10-fold in 10 years, reaching 133 in 2010. While numbers with underlying hepatitis B, haemochromatosis, autoimmune or cryptogenic cirrhosis have remained constant, those with underlying HCV or ALD have increased fivefold up to 10 and 35 per year respectively. The most dramatic increase, however, has been in those patients with NAFLD, increasing from 1 or 2 to over 30 per year in 2009 and 2010. There has also been an increase in HCC arising in individuals without chronic liver disease, 40 and 65% of which had diabetes and the metabolic syndrome respectively. Patients with NAFLD related HCC were significantly older (median age of 72 yrs vs 65 and 61 for ALD and HCV respectively. While NAFLD HCC cases were less likely to be detected by surveillance, they were more likely to be detected incidentally. Survival was determined by stage at presentation for all etiologies, and was not adversely affected by advanced age in the NAFLD population.

Conclusion NAFLD related HCC now equals that related to ALD in Northern England. The median age at presentation was higher for NAFLD HCC patients, but this did not adversely affect their survival. While relatively few NAFLD HCC cases were detected by surveillance, and the prognosis was particularly poor for those presenting with symptomatic disease (median 8.14 months), this was offset by an increase in incidental HCC detection, largely in diabetic follow-up clinics. The median survival of incidental patients (median 21.2 months) was similar to that of detected by surveillance (18.68 months). A raised awareness of the risk of HCC in older diabetic patients may reduce the numbers of those presenting with advanced symptomatic disease.

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