Increased No Yes Yes No No Unknown risk of hepatocellular carcinoma dsDNA, Double-stranded DNA; HAV, hepatitis A virus; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis D virus; HEV, hepatitis E virus; HGV, hepatitis G virus; PCR, polymerase chain reaction; RIBA, recombinant immunoblot assay; RT-PCR, reverse transcriptase-polymerase chain reaction; ssDNA/ssRNA, single- stranded DNA/RNA; TTV, transfusion-transmitted virus. *I.e., enterovirus 72.
†Formerly posttransfusion non-A, non-B virus.
‡Formerly enteral non-A, non-B virus.
to blood products, and prenatal transmission from maternal infection. HEV occurs following travel to endemic areas outside of the United States. HGV is prevalent in HIV-infected persons. HBV and HCV cause chronic infection, which may lead to cirrhosis and is a significant risk factor for hepatocellular carcinoma and represents a persistent risk of transmission.
Available @ StudentConsult.com
There is considerable overlap in the characteristic clinical courses of HAV, HBV, and HCV (Fig. 113-1). The preicteric phase, which lasts approximately 1 week, is characterized by headache, anorexia, malaise, abdominal discomfort, nausea, and vomiting and usually precedes the onset of clinically detectable disease. Infants with perinatal acquired HBV may have immune complexes accompanied by urticaria and arthritis before the onset of icterus. Jaundice and tender hepatomegaly are the most common physical findings and are characteristic of the icteric phase. Prodromal symptoms, particularly in children, may abate during the icteric phase. Asymptomatic or mild, nonspecific illness without icterus is common with HAV, HBV, and HCV, especially in young children. Hepatic enzymes may increase 15to 20-fold. Resolution of the hyperbilirubinemia and normalization of the transaminases may take 6 to 8 weeks.
Alanine aminotransferase and aspartate aminotransferase levels are elevated and generally reflect the degree of parenchymal inflammation. Alkaline phosphatase, 5α-nucleotidase, and total and direct (conjugated) bilirubin levels indicate the degree of cholestasis, which results from hepatocellular and bile duct damage. The prothrombin time is a good predictor
Figure 113-1 Clinical course and laboratory findings associated with hepatitis A, hepatitis B, and hepatitis C. ALT, Alanine aminotransferase; HAV, hepatitis A virus; anti-HBc, antibody to hepatitis B core antigen; HBeAg, hepatitis B early antigen; anti-HBe, antibody to hepatitis B early antigen; HBsAg, hepatitis B surface antigen; anti-HBs, antibody to hepatitis B surface antigen; HCV, hepatitis C virus; PCR, polymerase chain reaction.
of severe hepatocellular injury and progression to fulminant hepatic failure (see Chapter 130).