Hepatitis D is caused by a defective RNA virus (delta agent) that can replicate only in the presence of hepatitis B virus. It occurs uncommonly as a coinfection with acute hepatitis B or as a superinfection in chronic hepatitis B.
Hepatitis D is usually transmitted by parenteral or mucosal contact with infected blood or body fluids. Infected hepatocytes contain delta particles coated with hepatitis B surface antigen (HBsAg).
Prevalence of hepatitis D virus (HDV) varies widely geographically, with endemic pockets in several countries. Parenteral drug users are at relatively high risk, but HDV, unlike hepatitis B virus (HBV) has not widely permeated the homosexual community.
In the initial diagnosis of acute hepatitis, viral hepatitis should be differentiated from other disorders causing jaundice (see Figure: Simplified diagnostic approach to possible acute viral hepatitis.). If acute viral hepatitis is suspected, the following tests are done to screen for hepatitis viruses A, B, and C:
If serologic tests for hepatitis B confirm infection and clinical manifestations are severe, antibody to HDV (anti-HDV) levels should be measured. Anti-HDV implies active infection. It may not be detectable until weeks after the acute illness.
No treatments attenuate acute viral hepatitis, including hepatitis D. Alcohol should be avoided because it can increase liver damage. Restrictions on diet or activity, including commonly prescribed bed rest, have no scientific basis.
Most patients may safely return to work after jaundice resolves, even if AST or ALT levels are slightly elevated.
For cholestatic hepatitis, cholestyramine 8 g po once/day or bid can relieve itching.
No product exists for immunoprophylaxis of hepatitis D. However, prevention of HBV infection prevents HDV infection.