Page 210 - Medicine and Surgery

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206 Chapter 5: Hepatic, biliary and pancreatic systems

Fatty change is reversible sublethal cell injury. Cells

are swollen pale and vacuolated. This form of change
is seen in those ingesting more than 80 g alcohol per
day (6 units, 1 bottle of wine or 3 pints of beer). Steatosis
Cirrhosis: Repeated damage has led to fibrosis, with

damage to the normal architecture upon which func-
Steatohepatitis
tion is dependent.
(NASH)
Complications Fibrosis
Acute hepatitis may rarely lead to fulminant hepatic fail-
ure. Up to 10% of patients with cirrhosis, secondary to Cirrhosis
alcohol use, develop hepatocellular carcinoma.

Investigations
Patients have deranged liver function tests especially
γ GT, the MCV is also raised. Assessment of severity re-
quires a liver biopsy, as significant liver damage can be Figure 5.10 Non-alcoholic fatty liver disease (NAFLD).
present with a few symptoms or enzyme changes. Ultra-
sound may show significant cholestasis and be mistaken
liver injury, occurring in patients with little or no his-
for extra-hepatic obstructive jaundice.
tory of alcohol consumption. The exact significance of
NAFLD is currently unknown.
Management NAFLD encompasses a histological spectrum that
Abstinence is the best treatment. In late stages patients ranges from fat accumulation in hepatocytes (hepatic
maybeconsideredforlivertransplantiftheyhaveproved steatosis) to hepatic steatosis with hepatic inflamma-
abstinence. tion (nonalcoholic steatohepatitis or NASH) that may
or may not have associated fibrosis, (see Fig. 5.10).
Prognosis NASH may progress to cirrhosis in up to 20% of
Abstinence results in an improved prognosis, but patients.
alcohol-induced liver damage is a progressive disorder
continuing to cirrhosis in many patients despite absti- Aetiology/pathophysiology
nence. The pathogenesis of nonalcoholic fatty liver disease is
Fatty liver is reversible, with complete recovery. not fully understood.

Asymptomatic patients with biopsy-proven alcoholic Hepaticsteatosisresultsfromexcessivetriglycerideac-

hepatitis who continue to drink progress to cirrhosis cumulationintheliverasaresultofincreasedfreefatty
in 90%. However, if they abstain from drinking 90% acid entering the liver, decreased free fatty acid leav-
have a full recovery. ing the liver or impaired beta-oxidation of free fatty
Patientswithestablishedcirrhosiswhopresentwithan acid. Insulin resistance appears to be important in the

acute episode of hepatitis have the poorest prognosis development of hepatic steatosis and steatohepatitis.
(∼60–70% 5-year survival rate). Obesity, type II diabetes and insulin resistance are fre-
quently seen in patients with NAFLD.
Oxidative injury may be required for the develop-
Nonalcoholic fatty liver disease
ment of hepatic inflammation and necrosis. Sug-
Definition gested mechanisms include increased hepatic iron,
Nonalcoholic fatty liver disease (NAFLD) is a condition anti-oxidant deficiencies and intestinal bacterial over-
with histological features resembling alcohol-induced growth.