Clinical Manifestations and Diagnosis

Clinically cirrhosis may be latent (5 to 10 percent of cases), well compensated, or active and decompensated. The clinical features depend on the underlying etiology and the appearance of the two cardinal manifestations, portal hypertension and hepatocellular failure. As cirrhosis usually evolves over a period of several years, the course may be intermittent with therapeutic intervention such as with corticosteroids or with temporary cessation of injury. During the early phase of disease, patients often present with nonspecific symptoms and signs including malaise, lethargy, anorexia, loss of libido, and weight gain. Incidental laboratory findings of abnormal liver function tests, positive hepatitis B serology and hypergammaglobulinemia, and incidental physical findings such as icterus, hepatomegaly, gynecomastia, and spider nevi may point to the presence of cirrhosis. With the progression of disease, portal hypertension and hepatocellular failure invariably supervene. These two complications are interrelated in their pathogenesis, and often represent the initial presentation of many cirrhotics. Esophageal varices, ascites, splenomegaly, and gastrointestinal hemorrhage indicate elevated pressure in the portal venous system. Jaundice and abnormal liver function tests may occur in early and mild hepatocellular failure, which in its severe state is manifested as hepatic encephalopathy and hepatorenal syndrome.

Prognosis need not be poor, as cirrhosis can be checked, for example, in the alcoholic who abstains from alcohol abuse. Treatment can reverse the hepatic fibrosis and improve the outlook of patients with chronic active hepatitis, primary hemochromatosis, or Wilson's disease. On the other hand, after ascites has developed, the 5-year survival rate falls to below 50 percent.

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