Inflammation of the LIVER which damages liver cells and may ultimately kill them. Acute injury of the liver is usually followed by complete recovery, but prolonged inflammation after injury may result in FIBROSIS and CIRRHOSIS. Excluding trauma, hepatitis has several causes:
Viral infections by any of hepatitis A, B, C, D, or E viruses and also CYTOMEGALOVIRUS (CMV), EPSTEIN BARR VIRUS, and HERPES SIMPLEX.
Autoimmune disorders such as autoimmune chronic hepatitis, toxins, alcohol and certain drugs including ISONIAZID, RIFAMPICIN and CHLORPROMAZINE.
WILSON'S DISEASE.
Acute viral hepatitis causes damage throughout the liver and in severe infections may destroy whole lobules (see below).
Chronic hepatitis is typified initially by invasion of the PORTAL SYSTEM by white blood cells. If these inflammatory cells invade the body (parenchyma) of the liver tissue, FIBROSIS and then chronic disease or cirrhosis can develop. Cirrhosis may develop at any age and commonly results in prolonged ill health. It is an important cause of premature death, with excessive alcohol consumption the usual underlying cause. Sometimes, cirrhosis may be asymptomatic, but common symptoms are weakness, tiredness, poor appetite, weight loss, nausea, vomiting, abdominal discomfort and production of abnormal amounts of wind. Initially the liver may enlarge, but it later becomes hard and shrunken, though rarely causing pain. Skin pigmentation may occur along with JAUNDICE, the result of failure to excrete the liver product BILIRUBIN. Routine liver-function tests on blood are used to help diagnose the disease and to monitor its progress. Spider telangiectasia (caused by damage to blood vessels – see TELANGIECTASIS) usually develop and these are a significant pointer to liver disease. ENDOCRINE changes occur, especially in men, who lose their typical hair distribution and suffer from atrophy of their testicles. Bruising and nosebleeds occur increasingly as the cirrhosis worsens, and PORTAL HYPERTENSION (high pressure of venous blood circulation through the liver) develops due to abnormal vascular resistance. ASCITES and HEPATIC ENCEPHALOPATHY are indications of advanced cirrhosis.
Treatment of cirrhosis is to tackle the underlying cause, to maintain the patient's nutrition (advising him or her to avoid alcohol), and to treat any complications. The disorder can also be treated by liver transplantation; indeed, 75 per cent of liver transplants are done for cirrhosis. The overall prognosis of cirrhosis is not good, however, especially as many patients attend for medical care late in the course of the disease. Overall, only 25 per cent of patients live for five years after diagnosis, though patients who have a liver transplant and survive for a year (80 per cent) have a good prognosis.
is a type that most commonly occurs in women between 20 and 40 years of age. The cause is unknown and it has been suggested that the disease has several immunological subtypes. Symptoms are similar to other viral hepatitis infections, with painful joints and AMENORRHOEA as additional symptoms. Jaundice and signs of chronic liver disease usually occur. CORTICOSTEROID treatment is life-saving in autoimmune hepatitis, and maintenance treatment may be needed for two years or more. Remissions and exacerbations are typical, and most patients eventually develop cirrhosis, with 50 per cent of victims dying of liver failure if not treated. This figure falls to 10 per cent in treated patients.
The five hepatic viruses (A to E) all cause acute primary liver disease, though each belongs to a separate group of viruses.
Hepatitis A virus (HAV) is an ENTEROVIRUS which is very infectious, spreading by faecal contamination from patients suffering from (or incubating) the infection; victims excrete viruses into the faeces for around five weeks during incubation and development of the disease. Overcrowding and poor sanitation help to spread hepatitis A, which fortunately usually causes only mild disease with full recovery.
Hepatitis B (HBV) is caused by a hepadna virus, and humans are the only reservoir of infection, with blood the main agent for transferring it. Transfusions of infected blood or blood products, and injections using contaminated needles (as part of medical treatment in certain poor countries and from such practices as needle sharing amongst habitual drug abusers in the developed world), are common modes of transfer. Tattooing and ACUPUNCTURE may spread hepatitis B unless high standards of sterilisation are maintained. Sexual intercourse, particularly between male homosexuals, is a significant infection route.
Hepatitis C (HCV) is a flavivirus whose source of infection is usually via blood contacts. Effective screening of blood donors and heat treatment of blood factors should prevent the spread of this infection, which becomes chronic in about 75 per cent of those infected, lasting for life. Although most carriers do not suffer an acute illness, they must practise life-long preventive measures.
Hepatitis D (HDV) cannot survive independently, needing HBV to replicate, so its sources and methods of spread are similar to the B virus. HDV can infect people at the same time as HBV, but it is capable of superinfecting those who are already chronic carriers of the B virus. Acute and chronic infection of HDV can occur, depending on individual circumstances, and parenteral drug abuse spreads the infection. The disease occurs worldwide, being endemic in Africa, South America and the Mediterranean littoral.
Hepatitis E virus (HEV) is excreted in the stools, spreading via the faeco-oral route. It causes large epidemics of water-borne hepatitis and flourishes wherever there is poor sanitation. It resembles acute HAV infection and the patient usually recovers. HEV does not cause chronic infection.
The clinical characteristics of the five hepatic viruses are broadly similar. The initial symptoms last for up to two weeks (comprising temperature, headache and malaise), and JAUNDICE then develops, with anorexia, nausea, vomiting and diarrhoea common manifestations. Upper abdominal pain and a tender enlarged liver margin, accompanied by enlarged cervical lymph glands, are usual.
As well as blood tests to assess liver function, there are specific virological tests to identify the five infective agents, and these are important contributions to diagnosis. The more seriously ill patients may require hospital care, mainly to enable doctors to spot at an early stage those developing acute liver failure. Otherwise-fit patients under 40 with acute viral hepatitis have a mortality rate of around 0.5 per cent; for those over 60, this figure is around 3 per cent. Up to 95 per cent of adults with ACUTE HBV infection recover fully but the rest may develop life-long chronic hepatitis with a 30% chance of liver cirrhosis, particularly those with IMMUNODEFICIENCY. In chronic hepatitis B, patients without cirrhosis can be safely monitored without specific treatment but once cirrhosis is causing symptoms, treatment may be advised using nucleoside analogues such as lamivudine, adefovir, telbivudine, entecavir and tenfovir. People with chronic hepatitis C and cirrhosis can be treated with certain direct antiviral agents. These are generally only available from specialised liver centres and their high cost may lead to them not being made available to all those who might benefit. Infection is best prevented by good living conditions. HAV and HBV can be prevented by active immunisation with vaccines. There is no vaccine available for viruses C, D and E, although HDV is effectively prevented by immunisation against HBV. At-risk groups who should be vaccinated against HBV include:
Injecting drug abusers.
Close contacts of infected individuals such as regular sexual partners and infants of infected mothers.
Men who have sex with men.
Patients undergoing regular haemodialysis.
Certain health professionals, including laboratory staff dealing with blood samples and products.