Illness Script: Liver disease

Component Alcoholic Liver Disease

Pathophysiology Alcohol can produce a wide spectrum of liver disease from fatty
change to hepatitis and cirrhosis
Fatty liver:
– metabolism of alcohol invariably produces fat in the liver
– This is minimal with small amounts of alcohol, but with
larger amounts the cells become swollen with fat
(steatosis). There is no liver cell damage. The fat
disappears on stopping alcohol. Steatosis is also seen in
non-alcoholic fatty liver disease
– Alcohol directly affects stellate cells, transforming them
into collagen-producing myofibroblast cells
Alcoholic hepatitis:
– With fatty liver, there is infiltration by
polymorphonuclear leucocytes and hepatocyte necrosis
Alcoholic cirrhosis

Epidemiology
Time Course
Clinical Features Fatty liver
– There are often no symptoms or signs. Vague abdominal
symptoms of nausea, vomiting and diarrhoea are due to
the more general effects of alcohol on the
gastrointestinal tract.

Alcoholic hepatitis
The clinical features vary in degree:
– The patient may be well, with few symptoms, the
hepatitis only being apparent on the liver biopsy in
addition to fatty change.
– Mild to moderate symptoms of ill-health, occasionally
with mild jaundice, may occur. Signs include all the
features of chronic liver disease. Liver biochemistry is
deranged and the diagnosis is made on liver histology.
– In the severe case, often superimposed on alcoholic
cirrhosis, the patient is ill, with jaundice and ascites.
Abdominal pain is frequently present, and a high fever is
associated with the liver necrosis. On examination, there
is deep jaundice, hepatomegaly, sometimes
splenomegaly, and ascites with ankle oedema

Alcoholic cirrhosis
– This represents the final stage of liver disease from
alcohol use. Nevertheless, patients can be very well with
few symptoms. On examination, there are usually signs of
chronic liver disease, but need a liver biopsy.
Diagnosis + Investigations Fatty liver
Illness Script: Liver disease
– An elevated MCV often indicates heavy drinking. Liver
biochemistry shows mild abnormalities with elevation of
both serum aminotransferase enzymes. The γ-GT level is
a useful test for determining whether the patient is
taking alcohol. With severe fatty infiltration, marked
changes in all liver biochemical parameters can occur.
Ultrasound or CT will demonstrate fatty infiltration, as
will liver histology.

Alcoholic hepatitis
Investigations show a leucocytosis with markedly deranged
liver biochemistry and elevated:
– serum bilirubin
– serum AST and ALT
– serum alkaline phosphatase
– prothrombin time.
– A low serum albumin may also be found. Rarely,
hyperlipid-aemia with haemolysis ( Zieve syndrome ) may
occur.
– Liver biopsy , if required, is performed by the transjugular
route because of the prolonged prothrombin time.

Alcoholic cirrhosis
Investigations are as for cirrhosis in general.
Management General management
All patients should stop drinking alcohol. Delirium tremens
(a withdrawal symptom) is treated with diazepam.
Intravenous thiamine should be given empirically to prevent
Wernicke–Korsakoff encephalopathy. Bed rest is necessary,
along with a diet high in protein and vitamin supplements.
Dietary protein sometimes needs to be limited because of
encephalopathy. Patients must be advised to participate in
alcohol cessation programmes.

Fatty liver
– The patient is advised to stop drinking alcohol; the fat will
disappear and the liver biochemistry usually returns to
normal. Small amounts of alcohol can be drunk
subsequently, as long as patients are aware of the
problems and can control their consumption.

Alcoholic hepatitis
– In severe cases, the patient requires admission to
hospital. Nutrition must be maintained with enteral
feeding, if necessary, and vitamin supplementation given.
Steroid therapy has been widely used in patients with a
Illness Script: Liver disease
discriminant function score of >32 but a recent
multicentre UK study, which included over 1000 patients,
suggested that there was no survival benefit.
Alcoholic Cirrhosis
– Ursodeoxycholic acid (10–15 mg/kg) improves bilirubin
and aminotransferase levels. It should be given early in
the asymptomatic phase, as these patients benefit,
whereas no benefit is achieved in advanced disease.
– Steroids improve biochemical and histological disease but
cause osteoporosis and other side-effects, and so should
not be used.
– Malabsorption of fat-soluble vitamins (A, D and K) occurs
and supplementation is required.
– Bisphosphonates are required for osteoporosis. Despite
raised serum lipid concentrations, PBC is not associated
with an increased cardiovascular disease risk and
strategies for prevention of vascular events should be
tailored to the individual.
– Pruritus (itchy skin) is difficult to control; colestyramine is
helpful, although unpalatable. Rifampicin , and naloxone
and naltrexone (opioid antagonists) have been shown to
be of benefit. Intractable pruritus can be relieved by
plasmapheresis or a molecular absorbent recirculating
system (MARS).
– The lack of effective medical therapy has made PBC a
major indication for liver transplantation