The clinical course of HBV runs similarly to that of Hepatitis
A Virus (HAV), but tends to be more severe and may be associated with
The mildest attacks are asymptomatic and are detectable only by an increase
in serum transaminase levels. Alternatively, patients may be anicteric,
but may suffer from gastrointestinal and influenza-like symptoms. These
patients are likely to remain undiagnosed unless a clear history of exposure
is available. The severity of infection may vary from the asymptomatic
and icteric (from which recovery is typical) through to fulminant, fatal
Icteric attacks in adults are marked by a prodromal period (typically
three to four days, but may last up to two or three weeks) during which
patients feel sickly, suffer from digestive symtoms such as anorexia and
nausea and may, in the later stages, have mild pyrexia. Other common symptoms
are rigors, loss of desire to drink alcohol or smoke, malaise, and occasionally,
severe headaches. The prodromal period is followed by the darkening of
urine and lightening of feces, followed by the development of jaundice.
Cirrhosis can be characterized anatomically by widespread nodules
in the liver combined with fibrosis. These excessive nodules and fibroids
result in the distortion of the normal liver architecture and interfere
with blood flow through the liver. Cirrhosis may also result in the inability
of the liver to perform its functions as abnormalities progressively develop.
This is a rare form of the disease which usually overwhelms
the patient within ten days. This form may develop so quickly that jaundice
is inconspicuous and may be confused with acute psychosis or meningo-encephalitis.
On the other hand, the patient may become deeply jaundiced. Forboding
signs may be repeated vomiting, fetor hepaticus, confusion, and drowsiness.
The 'flapping' tremor may only be transient, but rigidity is usual. These
are then supervened by coma, indicating likely acute liver failure. The
patient's temperature rises, jaundice deepens, and liver shrinks, possibly
accompanied by widespread hemorrhages.
The levels of serum bilirubin and transaminase are poor prognostic indicators
because transaminase levels may actually decrease as the patient's clinical
condition worsens. Prothrombin is the best indicator of prognosis. Frequency
of the fulminant course varies, depending upon the type of viral hepatitis
and prevalence of hepatitis B carriage.
Adult patients feel less-than-perfect for variable spans of
time following acute hepatitis. Typically, this period lasts for a few
weeks, but may extend into months. Common features are anxiety, fatigue,
failure to regain weight, anorexia, alcohol intolerance, and right upper
abdominal discomfort. The edges of the liver may be tender. Serum transaminase
levels may be up to three times that of normal. Hepatic
histology reveals mild, residual portal zone cellularity and fibrosis,
and sometimes fatty changes in the liver cells. These conditions do not
differ from patients found to be recovering normally and who are now symptom-free.
Thus, a liver biopsy should not be done within six months after acute
hepatitis as there may be difficulty in distinguishing the residual changes
from developing chronic hepatitis.
Occasionally, prolonged jaundice is of the cholestatic type.
The onset is acute, and as the jaundice deepens within the first three
weeks, the patient begins to itch. After the first few weeks, the patient
feels well, gains weight, and is asymptomatic apart from icterus and slight
hepatomegaly. Jaundice persists for 8 - 29 weeks, after which recovery
In 1.8% - 15% of cases, some of the original attack is duplicated,
but typically in a milder form. Often, relapse is simply shown by an increase
in serum transaminases and bilirubin. Relapses may be a result of premature
activity or intake of large amounts of alcohol. Multiple relapses may
occur. However, full recovery may follow, though in some patients, relapses
may indicate progression to chronic hepatitis.
Hepatocellular carcinoma is the technical term for liver cancer.
This form of the disease develops after a long time in individuals suffering
from chronic hepatitis B infection. What events trigger the development
of this disease are currently unknown.