Symptoms of viral hepatitis

The preicteric or prodromal phase lasts upto 2 weeks. The varaemia causes the patient to feel unwell with nausea, vomiting, diarrhea, anorexia, headaches, malaise and 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 cholestatis. 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 3-6 weeks.

Extrahepatic complications are failure. Relapses occasionally occur, with the return of jaundice. Rarely the disease may be very severe with fulminant hepatitis, liver coma and death.

Symptoms are few in the acute phase with a mild flu like illness and a rise in serum transferases. Less than 20 percent 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 percent 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 percent within 5-30 years and of these patients about 15 percent will develop hepatocellular carcinoma.

The spectrum of clinical features of chronic hepatitis B is broad, ranging from asymptomatic infection to debilitating disease or even end stage, fatal hepatic failure.

As noted above, the onset of the disease tends to be insidious in most patients, with the exception of the very few in whom chronic disease follows failure of resolution of clinically apparent acute hepatitis B.

Fatigue is a common symptom and persistent or intermittent jaundice is a common feature in sever or advanced cases. Intermittent deepening of jaundice and recurrence of malaise and anorexia as well as worsening fatigue are reminiscent of acute hepatitis.

Such exacerbations may occur spontaneously, often coinciding with evidence of virologic reactivation may lead to progressive liver injury and when superimposed on well established cirrhosis may cause hepatic decompensation.

Complications of cirrhosis occur in end stage chronic active hepatitis and include ascities, edema, bleeding gastroeosophageal varices, hepatic encephalopathy, coagulopathy or hypersplenism.

Occasionally these complications bring the patient to initial clinical attention. Extrahepatic complications of chronic hepatitis B, similar to those seen during the prodromal phase of acute hepatitis B are associated with deposition of circulating hepatitis B, antigen antibody immune complexes.

These include arthralgias and arthritis, which are common and the more rare purpuric cutaneous lesions, immune complex glomerulonephritis and generalized vasculitis.

Clinical features of chronic hepatitis C are similar to those described above for chronic hepatitis B. Generally, fatigue is the most common symptom, jaundice is rare.

Extrahepatic complications of chronic hepatitis C are less common thanthey are in chronic hepatitis B, with the exception of essential mixed cryoglobulinemia.

Laboratory features of chronic hepatitis C are similar to those in patients with chronic hepatitis B but aminotransferase levels tend to fluctuate more and to be lower especially in patients with long standing disease.

An interesting and occasionally confusing finding in patients with chronic hepatitis C is the presence of autoantibodies. Rarely patients with autoimmune chronic active hepatitis and hyperglobulinemia have false positive enzyme immunoassays for anti HCV.

On the other hand a proportion of patients with serologically confirmable chronic hepatitis C have circulating autoantibodies to liver kidney microsomes.

These antibodies are anti-KLM1 as seen in patients with autoimmune chronic active hepatitis type 2 and arre directed against a 33 amino acide sequence of P450 IID6.

The occurrence of anti KLM1 in some patients with chronic hepatitis C may result from the partial sequence homology between the epitope recognized by anti LKM1 and two segments of the HCV polyprotein.

In addition the finding of this autoantibody in some patients with chronic hepatitis C suggests that autoimmunity may be laying a role in the pathogenesis of chronic hepatitis C.

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Clinical Symptoms of viral hepatitis