What is Prognosis in viral hepatitis

Course and Prognosis:

The prognosis is excellent, with most patients making a complete recovery. The mortality in young adults is 0.1 percent but it increases with age. Death is due to fulminant hepatic nerosis.

During the convalescence 5-15 percent of patients may have relapse of the hepatitis but this settles spontaneously. Occasionally a more severe jaundice with cholestasis will runa prolonged course of 7-20 weeks and is called cholestatic viral hepatitis.

There is no reason to stop alcohol consumption other than for the few weeks when the patient is ill. Patients may complain of debility for several months following resolution of the symptoms and biochemical parameters.

This is known as the posthepatitis syndrome, it is a functional illness. Treatment is by reassurance. HAV never progresses to chronic liver disease.

The majority of patients recover completely, fulminant hepatitis occurring in up to 1%. Some patients go on to develop chronic hepatitis and hepatocellular carcinoma or become asymptomatic carriers.

The outcome depends upon several factors, including the virulence of the virus and the immunocompetence and age of the patient.

Levels of HCV RNA fall in tandem with ALT levels during interferon therapy, but loss of detectable HCV RNA does not preclude relapse. In fact, no single clinical or laboratory feature of chronic hepatitis C has been found which is predictive of responsiveness to interferon.

Responses occur in patients with established cirrhosis, although, some observers report, at a frequency lower than that seen in patients with chronic active hepatitis without cirrhosis.

Some observers report that responsiveness in chronic active hepatitis without cirrhosis. Some observers report that responsiveness in chronic persistent hepatitis exceeds that in chronic active hepatitis.

Although a consensus exists that patients with symptomatic chronic active hepatitis should be treated with interferon, treatment of asymptomatic patients and those with mild chronic persistent hepatitis remains controversial.

Because progression to cirrhosis can occur in an unpredictable proportion of such cases, the potential benefit of therapy should not be dismissed out of hand in these patients. Additional study is needed.

Currently, no authorities advocate treating asymptomatic hepatitis C ‘carriers’ with normal aminotransferase levels or patients with decompensated cirrhosis secondary to chronic hepatitis C. For those with decompensated, end stage disease, liver transplantation is an option.

Although the likelihood of reexpressing detectable anti-HCV after transplantation is low, the likelihood of reinfection of the new liver is almost universal.

Nevertheless, and the occasional exception notwithstanding, most patients who undergo liver transplantation for chronic hepatitis C experience little, if any, morbidity, allograft loss, or mortality associated with recurrent hepatitis C infection.

Autoimmune chronic active hepatitis is a chronic disorder characterized by continuing hepatocellular necrosis and inflammation, usually with fibrosis, which tends to progress to cirrhosis and liver failure.

When fulfilling criteria of severity, this type of chronic active hepatitis may have a 6 month mortality of as high as 40 percent. The prominence of extrahepatic features of autoimmunity as well as seroimmunologic abnormalities in this disorder supports as autoimmune process in its pathogenesis and this concept is reflected in the labels lupoid plasma cell, or autoimmune chronic active hepatitis.

Because auto antibodies and other typical features of autoimmunicty do not occur in all cases, however, a broader, more appropriate designation for this type of chronic active hepatitis is ‘idiopathic’ or cryptogenic.

Cases in which hepatotropic viruses, metabolic / genetic derangements, and hepatotoxic drugs have been excluded merit this designation and probably include a spectrum of heterogenous liver disorders of unknown cause, a proportion of which have characteristic autoimmune features.

The weight of evidence suggests that the progressive liver injury in patients with idiopathic / autoimmune chronic active hepatitis is the result of a cell mediated immunologic attack directed against liver cells, in all likelihood,.

Predisposition to autoimmunity is inherited, while the liver specificity of this injury is triggered by environmental factors. For example, patients have been descried in whom apparently self limited cases of acute hepatitis A or B led to auto immune chronic active hepatitis, presumably because of genetic susceptibility or predisposition.

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