Hepatitis
DIAGNOSTIC SUMMARY
• Prodrome of anorexia, nausea, vomiting, fatigue, flulike symptoms 2 weeks to 1 month before liver involvement depending on incubation period of virus.
• Symptoms may occur abruptly or insidiously.
• Fever, headaches, abdominal discomfort, light stools, diarrhea, myalgia, arthralgia, drowsiness, enlarged and tender liver, jaundice, itching.
• Normal to low white blood cell count, markedly elevated aminotransaminases, elevated bilirubin.
GENERAL CONSIDERATIONS
Causes: drugs, toxic chemicals, bacterial or fungal infections, immune disorders, metabolic diseases, hepatic perfusion and oxygenation problems. Most common cause: virus types A, B, and C.
• Hepatitis A: caused by virus from Picornaviridiae family. It occurs sporadically or in epidemics and is transmitted primarily by fecal contamination from poor hygiene and sanitation.
• Hepatitis B: linked to 50% of viral cases in the United States; transmitted by infected blood or blood products or sexual contact (virus shed in saliva, semen, vaginal secretions).
• Hepatitis C (hepatitis non-A, non-B): linked to hepacivirus and a member of Flaviviridae family. Transmitted by blood contamination and responsible for 90% of all cases of hepatitis through blood transfusions (10% of people receiving blood transfusions in the past developed hepatitis C). However, only 4% of cases of hepatitis C result from transfusions. Most cases are attributable to intravenous drug use; in other cases the source is unclear. The mortality rate (1%-12%) is much higher than for other forms.
• Other viral causes: hepatitis viruses D, E, and G; herpes simplex; cytomegalovirus; and Epstein-Barr virus.
• Acute viral hepatitis: extremely debilitating form requiring bed rest and 2-16 weeks of recovery. Most patients completely recover (9 weeks for type A and 16 weeks for B, C, D, and G). One in 100 will die. Ten percent of hepatitis B and 10%-40% of hepatitis C cases become chronic. Hepatitis C contracted by blood transfusion has a 70%-80% rate of chronicity.
• Symptoms of chronic hepatitis: vary from nonexistent to chronic fatigue, serious liver damage, and even death.
DIAGNOSTIC CONSIDERATIONS
In addition to liver enzymes, hepatitis C is monitored by the presence of hepatitis C viral RNA by polymerase chain reaction (HCV-RNA[PCR]). Hepatitis B serologic findings and their interpretation are listed in the following table.
Suspect hepatitis when typical signs and symptoms are present. Confirm by blood tests for elevated liver enzymes and presence of viral antigens or virus-specific antibodies. The type of virus is determined by identifying specific viral antigens or antibodies. In chronic hepatitis B or C, use serology to monitor progression or clearance. Hepatitis C is monitored by liver enzymes plus HCV-RNA[PCR].
Hepatitis B Serologic Patterns and Interpretations
| HBsAg | Anti-HBs | Anti-HBc | HBeAg | Anti-HBe | Interpretation |
| + | − | IgM | + | − | Acute hepatitis B |
| + | − | IgG | + | − | Chronic active hepatitis B |
| + | − | IgG | − | + | Chronic nonactive hepatitis B |
| + | + | IgG | +/− | +/− | Chronic hepatitis B |
| − | − | IgM | +/− | +/− | Acute hepatitis B |
| − | + | IgG | − | +/− | Recovery from hepatitis B |
| − | + | − | − | − | Vaccinated against hepatitis B |
| − | − | IgG | − | − | False-positive or infection in remote past |
HBsAg, Hepatitis B surface antigen; HBc, hepatitis B core antigen; HBeAg, hepatitis B secretory antigen; IgG, immunoglobulin G; IgM, immunoglobulin M.
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