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3. Decline in liver function.
Hepatic synthetic dysfunction develops over time in a majority of subjects who have compensated
NASH related cirrhosis. Albumin declines early and is usually the first laboratory test to become
abnormal. An albumin <3.5 gm/dl was also the most common laboratory evidence of hepatic synthetic
dysfunction (Fig. 3). A decline in albumin levels also heralds clinical decompensation (unpublished
personal observation).
Figure 3. Decline in liver function.
4. Development of HCC.
HCC developed in about 7% of subjects over 10 years in those with compensated cirrhosis due to
NASH. These rates are lower than in those with HCV related cirrhosis [5, 6]. HCC can also occur in
the absence of cirrhosis in subjects with NASH and accounts for up to 50% of HCC due to NASH [7].
Recently, NASH related HCC has been identified to be the second most common etiology for HCC
that requires liver transplantation [8]. The risk factors for the development of HCC in the absence of
cirrhosis in those with NASH remain to be fully elucidated. The consumption of modest amounts of
alcohol (below the threshold above which steatohepatitis cannot be called non-alcoholic) in subjects
with NASH has been linked to the risk of HCC in a retrospective analysis [6].
The International Liver Congress™ 2015 • Vienna, Austria • April 22–23, 2015 105
Hepatic synthetic dysfunction develops over time in a majority of subjects who have compensated
NASH related cirrhosis. Albumin declines early and is usually the first laboratory test to become
abnormal. An albumin <3.5 gm/dl was also the most common laboratory evidence of hepatic synthetic
dysfunction (Fig. 3). A decline in albumin levels also heralds clinical decompensation (unpublished
personal observation).
Figure 3. Decline in liver function.
4. Development of HCC.
HCC developed in about 7% of subjects over 10 years in those with compensated cirrhosis due to
NASH. These rates are lower than in those with HCV related cirrhosis [5, 6]. HCC can also occur in
the absence of cirrhosis in subjects with NASH and accounts for up to 50% of HCC due to NASH [7].
Recently, NASH related HCC has been identified to be the second most common etiology for HCC
that requires liver transplantation [8]. The risk factors for the development of HCC in the absence of
cirrhosis in those with NASH remain to be fully elucidated. The consumption of modest amounts of
alcohol (below the threshold above which steatohepatitis cannot be called non-alcoholic) in subjects
with NASH has been linked to the risk of HCC in a retrospective analysis [6].
The International Liver Congress™ 2015 • Vienna, Austria • April 22–23, 2015 105
