Parenchymal liver disease

The most common cause worldwide is viral hepatitis. Parenchymal liver disease can be divided into acute and chronic forms.


Acute parenchymal liver damage can be caused by many agents (Fig. 5.10). If there is widespread damage of hepatocytes, the normal liver architecture may collapse. The extent of hepatocellular damage may be extremely variable.


Although some histological features are suggestive of the aetiological factor, most of the changes are essentially similar whatever the cause. Hepatocytes show degenerative changes (swelling, cytoplasmic granularity, vacuolation), undergo necrosis (becoming shrunken, eosinophilic Councilman bodies) and are rapidly removed. The distribution of these changes varies somewhat with the aetiological agent, but necrosis is usually maximal in zone 3.
The extent of the damage is very variable between individuals affected by the same agent: at one end of the spectrum, single and small groups of hepatocytes die (spotty or focal necrosis), while at the other end multiple acini are destroyed (massive hepatic necrosis) resulting in fulminant hepatic failure. Between these extremes there is limited confluent necrosis of hepatocytes with collapse of the reticulin framework resulting in linking (bridging) between the central veins, the central veins and portal tracts, and between the portal tracts. Centriacinar cholestasis is common, but fatty change is usually absent apart from certain types of hepatitis due to toxins such as alcohol or that seen in pregnancy. The extent of the inflammatory infiltrate is also variable, but portal tracts and lobules are infiltrated mainly by lymphocytes.


This will be discussed under the individual aetiological factors.


The differing features of the common forms of viral hepatitis are summarized. In HAV the damage is due to the virus itself, but in HBV infection it is due to an immunological reaction to the virus.

Hepatitis A


This is the commonest type of viral hepatitis and causes 20-40% of clinically apparent hepatitis. It occurs world wide, often in epidemics. The disease is commonly seen in the autumn and affects children and young adults. Spread of infection is mainly by the faecal-oral route and arises from the ingestion of contaminated food (e.g. shellfish, clams) or water. Overcrowding and poor sanitation facilitate spread. There is no carrier state.

Hepatitis A virus

HAV is a picornavirus; its structure is shown. It has a single serotype as only one epitope is immunodominant. It is excreted in the faeces of infected persons for about 2 weeks before the onset of the illness and for up to 7 days after. The disease is maximally infectious just before the onset of jaundice. HAV particles can be demonstrated in the faeces by electron microscopy.

An algorithm for the investigation of jaundice. Viral causes are rarer in the elderly, CBD, common bile duct; ERCP, endoscopic retrograde cholangiopancreatography.
An algorithm for the investigation of jaundice. Viral causes are rarer in the elderly, CBD, common bile duct; ERCP, endoscopic retrograde cholangiopancreatography.


The preicteric or prodromal phase lasts up to 2 weeks. The viraemia causes the patient to feel unwell with nausea, vomiting, diarrhoea, anorexia, headaches, malaise and a distaste for cigarettes. Fever is usually mild and there may be upper abdominal discomfort. There are few physical signs at this stage; the liver is tender but not enlarged initially.
After 1 or 2 weeks the patient becomes icteric (although some may never do so) and symptoms often improve. The appetite returns and the patient feels better. As the jaundice deepens the urine becomes dark and the stools pale owing to intrahepatic cholestasis. The liver is moderately enlarged and the spleen is palpable in about 10% of patients. Occasionally, tender lymphadenopathy is seen, with a transient rash in some cases. Thereafter the jaundice lessens and in the majority of cases the illness is over within 3–{5weeks. Extrahepatic complications are rare but include arthritis, vasculitis, myocarditis and renal failure. Relapses occasionally occur, with the return of jaundice. Rarely the disease may be very severe with fulminant hepatitis, liver coma and death. The sequence of events after HAY exposure is shown.

Some causes of acute parenchymal damage.
Some causes of acute parenchymal damage.


Liver biochemistry

In the prodromal stage the serum bilirubin is usually normal. However, there is bilirubinuria and increased urinary urobilinogen. A raised serum AST, which can sometimes be very high, precedes the jaundice. In the icteric stage the serum bilirubin reflects the level of jaundice. Serum AST reaches a maximum 1-2 days after the appearance of jaundice, and may rise above 500 IV litre-I. Serum AP is usually less than 300 IV litre “,
After the jaundice has subsided, the AST may remain elevated for some weeks and occasionally up to 6 months.

Haematological tests

There is leucopenia with a relative lymphocytosis. Very rarely there is a Coombs’ -positive haemolytic anaemia or an associated aplastic anaemia. The PT is prolonged in severe cases. The erythrocyte sedimentation rate (ESR) is raised.

Some features of hepatitis viruses.
Some features of hepatitis viruses.
(a) The hepatitis A (HAV) virion consists probably of four polypeptides (VP1-VP4) which form a tight protein shell, or capsid, containing the RNA. The major antigenic component is associated with VP1. (b) Arrangement of HAV genome.
(a) The hepatitis A (HAV) virion consists probably of four polypeptides (VP1-VP4) which form a tight protein shell, or capsid, containing the RNA. The major antigenic component is associated with VP1. (b) Arrangement of HAV genome.

Viral markers

ANTIBODIES TO HAV. IgG antibodies are common in the general population over the age of 50 years but an anti-HAY IgM means an acute infection.

Other tests

ULTRASOUND. This should be performed if bile duct obstruction is suspected and always in an older patient.

LIVER BIOPSY. This is only indicated when there is doubt about the diagnosis.


This is from all other causes of jaundice but, in particular, from other types of viral and drug-induced hepatitis.

Hepatitis A virus-sequence of events after exposure.
Hepatitis A virus-sequence of events after

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