Hepatitis C virus

Hev is a single-stranded RNA virus arranged into structural and non-structural regions. There are six subtypes based on differences in the non-structural region. Only types I, II and III are seen in Europe and type IV occurs in the Far East. Immunogenic peptides have been derived from these regions for use in Hev assays’ and are becoming increasingly sensitive. The concentration of viral antigens in the blood is very low.


Symptoms are few in the acute phase with a mild flu-like illness and a rise in serum transferases. Less than 20% of patients develop jaundice and this is mild and self-limiting. Most patients will not be diagnosed until they present, years later, with complications of chronic liver disease. Extrahepatic manifestations are seen, including arthritis, agranulocytosis and aplastic anaemia, as well as diffuse neurological problems. Rarely, fulminant hepatic failure occurs. At least 50% of patients go on to develop chronic liver disease . Histologically, a chronic hepatitis leading to a cirrhotic picture is seen . Cirrhosis develops in about 10-20% within 5-30 years and of these patients about 15% will develop hepatocellular carcinoma.

Hepatitis C virus. A schematic diagram showing single-stranded RNA genome with coding regions.
Hepatitis C virus. A schematic diagram showing single-stranded RNA genome with coding regions.


Antibodies to Hev are found in the serum. The first generation tests using the clOO antigen were relatively insensitive. Second generation tests (enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA) ) include c22 and c33 antigens and are more sensitive and specific. Anti-Ht.V-positive patients should have the presence of viral RNA confirmed by a peR test. This is expensive and not generally available. Patients with a positive peR should have a liver biopsy to detect chronic hepatitis and cirrhosis.


As most patients are not diagnosed in the acute stage, there are no clear guidelines for treatment. However, interferon has been used in some acute cases.


Hepatitis E virus (HEV) is an RNA virus which causes enteral (epidemic or water-borne) hepatitis. Epidemics have been seen in many developing countries. It has a mortality from fulminant hepatic failure of 1-2% which rises to 20% in pregnant women. There is no carrier state and it does not progress to chronic liver disease. Serological tests for HEV are being developed although HEV RNA can be detected in the serum or stools by peR. Prevention and control depend on good sanitation and hygiene.

Other viral hepatitides

Most of the non-A, non-B hepatitides (NANB) have now been identified. The letter F has been occasionally applied to fulminant hepatic failure (although several viruses are implicated) and G to granulomatous hepatitis.


(F H F)

This is defined as severe hepatic failure with encephalopathy developing in less than 8 weeks in a patient with a previously normal liver. Cases that evolve at a slower pace are called subacute or sub fulminant hepatic failure. FHF is a rare but often life-threatening syndrome due to acute hepatitis from any cause (Table 5.6). The causes vary throughout the world; the majority are due to viral hepa titis but paracetamol overdose is common in the UK. Histologically there is massive necrosis of the whole liver lobule. Severe fatty degeneration in FHF is seen in pregnancy, Reye’s syndrome, lymphoma or following i.v. tetracycline administration.

Fulminant hepatic failure-causes.
Fulminant hepatic failure-causes.


Examination shows a jaundiced patient with the signs of hepatic encephalopathy developing usually within 2 weeks. The condition is called sub fulminant if the encephalopathy develops between 2 and 8 weeks. The mental state varies from slight drowsiness, confusion and disorientation (grades I and II) to unresponsive coma (grade IV) with convulsions. Fetor hepaticus is common but signs of chronic liver disease, e.g. ascites and splenomegaly, are rare. The liver size is usually small. Fever, vomiting, hypertension and hypoglycaemia occur. Neurological examination shows spasticity and extension of the arms and legs; plantar responses remain flexor until late. Cerebral oedema is found in 80% of patients who die.
Other complications include bacterial infections, vasodilatory hypotension, gastrointestinal bleeding, respiratory arrest, renal failure (hepatorenal syndrome and acute tubular necrosis) and pancreatitis.


This is as for acute liver disease. The PT is the most useful index of severity and when very high indicates a poor prognosis. The AST is high initially but is not a useful indicator of the course of the disease since it falls with progressive liver damage. The serum albumin falls and an EEG is sometimes helpful in grading the encephalopathy. An isotope scan may show no uptake in the liver.


There is no specific treatment but patients should be managed in an intensive care unit. Supportive therapy as for hepatic encephalopathy  is necessary. Cerebral oedema (which is measured directly) is the major cause of death and when signs of raised intracranial pressure are present 20% mannitol (1 g kg-I body reight) should be infused intravenously; this dose may need to be repeated. Dexamethasone is of no value.

Hypoglycaemia, hypokalaemia and hypocalcaemia should be anticipated and corrected with 10% dextrose infusion (checked by 2-hourly Dextrostix testing), potassium and calcium. Coagulopathy is managed with i.v. vitamin K, platelets, blood or fresh frozen plasma. Haemorrhage may be a problem and patients are given Hj-receptor antagonists to prevent gastrointestinal bleeding. Infection should be treated with suitable antibiotics, and renal and respiratory failure treated as appropriate. Flumazenil, a benzodiazepine receptor antagonist, may give a transient improvement in encephalopathy.
Liver transplantation has been a major advance for patients with FHF. It is difficult to judge the timing or the necessity for transplantation but various transplant centres have developed guidelines depending on prognosis .


In mild cases (grades I and II), two-thirds of the patients will survive. The outcome of severe cases (grades III and IV) is related to the aetiology. In special units 70% of patients with paracetamol overdosage and grade IV coma survive, as do 30-40% of patients with HAV or HBV hepatitis. The survival is extremely poor in patients with HCV hepatitis. In patients with drug reactions and viral hepatitis, poor prognostic variables include aetiology (HCV or drugs), age «10 years and >40 years), time interval from onset of jaundice to encephalopathy (more than 7 days-subfulminant), a serum bilirubin >300 f.Lmol litre:” and a PT over 50 s. In addition, for paracetamol overdose an arterial pH <7.3, a serum creatinine >3 mg dr ‘, a PT > 100 s with grade III-IV encephalopathy indicates a very poor prognosis and need for transplantation.

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