F. HEPATITIS G (HGV) AND GB VIRUS.C
It has long been believed that there is another non-A, non-B, non- C agent
causing hepatitis in humans. The incubation period for post-transfusion hepatitis
is 14 to 145 days, too long for hepatitis B or C. In the United States, about 5%
of chronic liver disease remains cryptogenic (does not appear to be autoimmune
or viral in origin), and half the patients have previously received transfusions.
Thus, a new form of hepatitis (hepatitis G or GBV-C) has been described. They
are two different isolates of the same virus. Autoantibodies are absent. The
clinical significance of this virus remains uncertain. Risk factors are similar to
those for hepatitis C.
Management of Patients With Nonviral Hepatic Disorders
Certain chemicals have toxic effects on the liver and when taken by mouth,
inhaled, or injected parenterally produce acute liver cell necrosis, or toxic
hepatitis.
The chemicals most commonly implicated in this disease are carbon
tetrachloride, phosphorus, chloroform, and gold compounds.
Drug-induced hepatitis, is similar to acute viral hepatitis, but parenchymal
destruction tends to be more extensive. Some medications that can lead to
hepatitis are isoniazide, halothane, acetaminophen, and certain antibiotics,
antimetabolites, and anesthetic agents.
TOXIC HEPATITIS
Resembles viral hepatitis in onset. Obtaining a history of exposure to
hepatotoxic chemicals, medications, or other agents assists in early treatment
and removal of the offending agent.
Anorexia, nausea, and vomiting are the usual symptoms; jaundice and
hepatomegaly are noted on physical assessment.
Recovery from acute toxic hepatitis is rapid if the hepatotoxin is identified early
and removed or if exposure to the agent has been limited.
DRUG-INDUCED HEPATITIS
Drug-induced hepatitis is responsible for 20% to 25% of cases of acute hepatic
failure in the United States.