hepatic and biliary disorders
Overview of Acute Viral Hepatitis
Diagnosis of Acute Viral Hepatitis
Liver tests (aspartate aminotransferase [AST] and alanine aminotransferase [ALT] elevated out of proportion to alkaline phosphatase, usually with hyperbilirubinemia) Viral serologic testing Prothrombin/international normalized ratio (PT/INR) measurement Acute hepatitis must first be differentiated from other disorders that cause similar symptoms. In the prodromal phase, hepatitis mimics various nonspecific viral illnesses and is difficult to diagnose. Anicteric patients suspected of having hepatitis based on risk factors are tested initially with liver tests, including aminotransferases, bilirubin, and alkaline phosphatase. Acute hepatitis often manifests in the icteric phase and so should be differentiated from other disorders causing Jaundice (see figure Acute hepatitis can usually be differentiated from other causes of jaundice by Its marked elevations of AST and ALT: Typically≥400 IU/L (6.68 microkat/L) ALT is typically higher than AST, but absolute levels correlate poorly with clinical severity. Values increase early in the prodromal phase, peak before jaundice is maximal, and fall slowly during the recovery phase. Urinary bilirubin usually precedes jaundice. Hyperbilirubinemia in acute hepatitis varies in severity, and fractionation has no clinical value. Alkaline phosphatase is usually only moderately elevated; marked elevation suggests extrahepatic cholestasis and prompts imaging tests (eg, ultrasonography). Liver biopsy is usually not needed unless the diagnosis is uncertain. If laboratory results suggest acute hepatitis, particularly if ALT and AST are>1000 IU/L (16.7 microkat/L), PT/INR is measured to assess liver function. Manifestations of Portosystemic Encephalopathy combined with bleeding diathesis or prolongation of INR suggest If acute hepatitis is suspected, efforts are next directed toward identifying its cause. A history of exposure may provide the only clue of drug-induced or toxic hepatitis. The history should also elicit risk factors for viral hepatitis. Prodromal sore throat and diffuse adenopathy suggest infectious mononucleosis rather than viral hepatitis. * Obtain additional laboratory studies for hepatitis A (see table Hepatitis A Serology ), hepatitis B (see table ALT=alanine aminotransferase; anti-HCV=antibody to hepatitis C virus; AST=aspartate aminotransferase; HBsAg=hepatitis B surface antigen; IgM anti-HAV=IgM antibody to hepatitis A virus. In patients with findings suggesting acute viral hepatitis, the following studies are done to screen for hepatitis viruses A, B, and C: IgM antibody to HAV (IgM anti-HAV) Hepatitis B surface antigen (HBsAg) IgM antibody to hepatitis B core (IgM anti-HBc) Antibody to HCV (anti-HCV) Hepatitis C RNA (HCV-RNA) polymerase chain reaction If any are positive, further serologic testing may be necessary to differentiate acute from past or chronic infection (see tables Hepatitis A Serology , If serologically confirmed HBV infection is severe, anti-HDV is measured. If the patient has recently traveled to an endemic area or is immunosuppressed, IgM antibody to HEV (IgM anti-HEV) should be measured if the test is available. Biopsy is usually unnecessary but, if done, usually reveals similar histopathology regardless of the specific virus: Patchy cell dropout Acidophilic hepatocellular necrosis Mononuclear inflammatory infiltrate Histologic evidence of regeneration Preservation of the reticulin framework HBV infection can occasionally be diagnosed based on the presence of ground-glass hepatocytes (caused by HBsAg-packed cytoplasm) and using special immunologic stains for the viral components. However, these findings are unusual in acute HBV infection and are much more common in chronic HBV infection. 