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Inflammatory diseases of the liver are termed hepatitis.
Hepatitis, which may be acute or chronic, has several important causes including viral infections,
autoimmune disorders, drug reactions, and alcohol.
Whatever the cause of acute hepatitis there are similar clinical features and similar histological
appearances on liver biopsy.

Hepatitis A is transmitted by faecal-oral route.
Hepatitis E is clinically similar to Hepatitis A infection.
Viral infection is a common cause of hepatitis.
The main so-called 'hepatitis viruses' are a group of hepato-trophic viruses.
Although all cause a primary hepatitis, they are unrelated and belong to different viral types.
The main viruses are hepatitis A and E (transmitted via a faecal-oral route), and hepatitis B,
C and D (transmitted via a parenteral route).
Several non-hepatotrophic viruses may also cause hepatitis.

Infection with a hepatitis virus may not always be followed by clinical disease, but there is
a range of clinical manifestations. Following initial infection.

Hepatitis B infection is transmitted parenterally and can cause chronic liver disease
Hepatitis B virus (HBV) is a DNA virus of the hepadna group. Infective virus is transmitted in blood,
semen and saliva through close physical contact, inoculation occurring through breaks in skin or
mucous membranes. Hepatitis B can therefore be a sexually transmitted disease. Transmission by
blood transfusion is now uncommon because of the screening of blood donations, but spread of infection
amongst IV drug abusers via shared unsterile needles is an important mode of transmission. Vertical
transmission from mother to child is also seen.

Infection causes five clinical patterns of infection:
1 Acute self-limited hepatitis is a common outcome. Patients recover after an illness with jaundice, malaise
and anorexia, and have lifelong immunity.
2 Fulminant acute hepatitis is very rare and causes massive necrosis of liver cells.
3 Chronic hepatitis affects 5-10% of cases. It may progress to cirrhosis or may recover.
4 Asymptomatic carrier state (may later develop chronic hepatitis).
5 Clinically inapparent asymptomatic infection is a sub-clinical form of infection, but it may progress to
chronic hepatitis, or the patient may become a carrier.

The importance of the chronic carrier states is that patients are at risk of developing
hepatocellular carcinoma. Carrier rates for hepatitis B infection show geographic variation
(0.3% in Western Europe and USA; 20% in Southeast Asia).
In adults, under 10% of patients develop a chronic carrier state, but virtually all neonates
infected with HBV from the mother become chronic carriers,possibly because of an immature immune response.

Hepatitis C is clinically similar to hepatitis B infection
Hepatitis C is an RNA virus that resembles a flavivirus.
Its mode of transmission is the same as that for hepatitis B, and it is an important
cause of post-transfusion hepatitis.
Half of all cases recover after a period of about 2 months; the remaining half have persistently
abnormal liver function tests for over a year, developing a chronic hepatitis with periods
of remission and relapse. Of the latter, about half will develop chronic active hepatitis,
and many cases progress to cirrhosis.
with a risk of hepatocellular carcinoma.

Although it accounts for many cases of sporadic acute hepatitis, often no recognized source of infection can be identified. Hepatitis C infection is responsible for the vast majority of cases of what was formerly termed non-A non-B hepatitis.
There is an incubation period of about 2 months, followed by acute hepatitis with fever, malaise,
anorexia, and jaundice.

Hepatitis may be caused by other viruses
The histology of acute viral hepatitis is similar for all types
Irrespective of the causative virus, the histological
features of acute viral hepatitis are similar:
Hepatocytes are swollen and many undergo death by apoptosis, forming eosinophilic Councilman bodies.
Focal infiltration of liver by lymphoid cells associated with liver cell necrosis.
Increased number of lymphoid cells in portal tracts.
Regeneration of liver cells produces lobular disarray.
Mild cholestasis may be seen.
In severe cases of acute hepatitis, bridging necrosis between central veins develops. Clinical disease
is usually severe but, with survival, regeneration of hepatocytes occurs. In fulminant massive necrosis
the majority of liver cells undergo necrosis.

The liver may be involved in several parasitic diseases
Parasitic infestation of the liver is an important problem worldwide.
Bacterial infection of the liver occurs by three main routes:
Ascending spread from colonization of the biliary tract by bacteria.
This is almost always predisposed by biliary obstruction.
Infection ascending in the portal vessels (portal pyaemia) into the liver from a focus of
sepsis in the abdomen, e.g. abscess caused by complicated appendicitis.
Systemic blood spread in septicaemia. This may cause severe acute liver failure.

An important complication of bacterial infection of the liver is the development of a iver abscess.
This is a very serious condition with a high mortality if it is left untreated.
Infection of the liver by Leptospira causes Weil's disease. There is fever, jaundice,
purpuric skin rash, and renal failure. The liver shows focal hepatocyte necrosis and cholestasis.
Syphilis may affect the liver in congenital infection, causing diffuse fibrosis of the parenchyma.
In tertiary syphilis, gummatous necrosis may develop leading to deep scars (hepar lobatum).
Tuberculous infection of the liver is seen in miliary tuberculosis.

Abscesses are seen as areas of necrosis containing purulent necrotic material.
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