Imaging has a limited direct role in hepatitis, with laboratory studies and biopsy being bulwarks of diagnosis. Magnetic resonance, however, is of potential value. Among patients with proven chronic hepatitis, histopathology in about two thirds of those with patchy enhancement on early postgadolinium MRI revealed a macrophage infiltrate, hepatocyte necrosis, and steatosis. Prominent linear enhancement on delayed postgadolinium MRI is found with fibrosis.
Hepatitis has no specific imaging findings, with imaging generally performed to exclude other disorders. Necrosis and regeneration on precontrast CT appear as hypodense regions. Periportal edema is seen as periportal hypodense regions on CT and hyperintense regions on T2-weighted MRI. Ultrasonography is usually
normal, although at times a heterogeneous hyperechoic appearance is found. During the initial stage of severe acute hepatitis, a transient decrease in portal blood velocity is followed by a rebound, but in chronic viral hepatitis decreased portal blood velocity correlates with the degree of fibrosis.

Viral An unusual cause of acute hepatitis is measles virus infection. Viral hepatitis is common throughout the world, with the highest prevalence in East Asia. Currently viruses A through G have been identified. At least one other type of enterically transmitted hepatotropic virus probably exists. Hepatotropic viruses A through E induce hepatocellular damage either through a direct cytotoxic effect or through some yet undefined mechanisms. The common end point is hepatocellular necrosis. Co-infection is not uncommon, especially in end-stage disease.
Fat ingestion normally results in gallbladder constriction. In some patients with acute hepatitis, fat results in paradoxical gallbladder dilation, a useful imaging finding. Some patients with acute viral hepatitis present with what clinically appears to be acute cholecystitis. They recover with conservative medical management. Gallbladder US in these patients reveals considerable gallbladder wall thickening, but the gallbladder returns to normal thickness with clinical recovery.
Hepatitis A Humans appear to be the only host for hepatitis A virus. This infection has decreased in prevalence, especially in East Asia. It is an acute infection and does not lead to a chronic carrier state. Effective immunization exists against hepatitis A virus. Some patients with hepatitis A virus infection develop acute renal failure and nephrotic syndrome, presumably due to hepatitis A virus– triggered immune-mediated renal injury in genetically susceptible individuals. Acute viral hepatitis A can progressed to autoimmune hepatitis.
Hepatitis B
In many patients hepatitis B virus (HBV) infection is subclinical; others, however, become chronic carriers, serve as a reservoir for further spread, and develop chronic liver disease, including cirrhosis. A direct relationship exists between chronic hepatitis B infection and hepatocellular carcinoma. Thus in South African blacks, those positive for hepatitis B surface antigen had a 23-fold increased risk of developing a hepatocellular carcinoma; those positive for hepatitis C serology had a sevenfold increased risk,while those with both hepatitis B and C markers had a relative risk of 82. The study estimates that HBV causes about 43%
of hepatocellular carcinomas in South African blacks, hepatitis C 5%, and co-infection with both 20%. Hepatitis B infection probably is a factor in China, while hepatitis C virus plays a similar role in Southern Europe and Japan. Hepatitis B virus is also suspected to have a role in other cancers.
Hepatitis B infection is transmitted vertically from mother to child. Infection in some infants progresses to fibrosis and eventual cirrhosis. A histologic finding of hepatocyte loss, cholestasis, periportal fibrosis, and inflammation is called fibrosing cholestatic hepatitis. It is a variant of HBV infection, and affected patients have a high rate of liver failure. Immunization against HBV is available.
Hepatitis C
Hepatitis C virus (HCV) infection is believed to cause at least 90% of previously called non-A,
non-B hepatitis. In the United States approximately 1.4% of the population is infected. Infection is acquired by either blood product transfusions or intravenous drug abuse. It is a common infection in hemophiliacs. In some patients the mode of transmission is not known. Vertical and sexual transmission is uncommon. Hepatitis during the acute phase is invariably mild and often subclinical, but most infections become chronic. The clinical course of hepatitis C infection is unpredictable.A rough estimate of mean time between initial infection and diagnosis of chronic hepatitis is 10 years, 10 years more for cirrhosis to develop, and another 10 years before hepatocellular carcinoma is discovered, although considerable individual variation exists. Even with advanced disease, half the patients are asymptomatic.Normal biochemical tests do not exclude viral replication in anti- HCV–positive individuals. Different viral genotypes are associated with different severity of liver disease. For instance, HCV type 1b is overrepresented in patients developing cirrhosis and hepatocellular carcinoma and influences the carcinoma risk in cirrhosis.
An association exists between HCV infection and autoimmune diseases. Infection leads to autoimmune hepatitis, membranoproliferative glomerulonephritis, thyroiditis, and such skin disorders as porphyria cutanea tarda and possibly lichen planus.A relationship with Sjögren’s syndrome and possibly even Behçet’s syndrome is suspected. An association with Guillain-Barré syndrome (an acute demyelinating neuropathy believed to have an autoimmune basis) has been suggested. It has been implicated in periarteritis nodosa.
Unlike many other human viruses, hepatitis C virus is an RNA virus and does not appear to be integrated into host cell genome. Carcinogenesis of HCV infection is generally explained by its ability to cause hepatic inflammation, regeneration, fibrosis, and eventual cirrhosis, yet some patients appear to progress from chronic hepatitis directly to carcinoma without developing cirrhosis.
An interesting association appears to exist between HCV serology and primary hepatic lymphoma. Hepatitis C virus is both hepatotropic and lymphotropic and in some patients results in a mixed essential cryoglobulinemia, a lymphoproliferative condition that on occasion evolves into non-Hodgkin’s lymphoma. The
virus is detected in some lymphoma tissue. Anti–hepatitis C virus antibodies are detected in almost half of B-cell non-Hodgkin’s lymphoma patients. Likewise, an occasional patient with chronic HCV infection develops reactive lymphoid hyperplasia (pseudolymphoma),with imaging suggesting a focal hepatocellular carcinoma; biopsy should be diagnostic. Gray-scale US findings do not correlate with liver biopsy findings in patients with chronic HCV infection. Imaging does detect perihepatic lymphadenopathy, however, with number and size related to HCV activity. Gray-scale US can document the response to therapy. Lymph nodes appear hyperintense relative to the liver on T2-weighted MRI. No current immunization is available against this virus. Interferon is the treatment of choice for chronic HCV infection, but relapse rate is high.
Hepatitis D Humans are probably the only host for hepatitis D virus. Its major focus in the United States is in drug addicts. It progresses to chronic hepatitis and cirrhosis.
Hepatitis E
Hepatitis E has a worldwide distribution and is a cause of considerable morbidity and mortality in the developing world. This virus is spread through contaminated water. Infected individuals develop cholestatic jaundice, generally with few sequelae, although in pregnancy it has led to fulminant hepatic failure.
Hepatitis G Hepatitis G virus (HGV) is a RNA virus in the family Flaviviridae and is transmitted by blood transfusion. Both acute and chronic infections occur, but its role in hepatitis is uncertain. Parenteral transmission appears common, and IV drug users, hemodialysis patients, and hemophiliacs are prone to this infection, often in association with HBV and HCV infections. Hepatitis G virus appears to be sensitive to interferon therapy.
Epstein-Barr Virus Infectious mononucleosis (Epstein-Barr virus infection) is a rare cause of hepatitis; it has led to fulminant hepatic failure.
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