Most HBV infections are subclinical, particularly during childhood, but about one-third of adult infections are icteric. The course of acute viral hepatitis is conventionally divided into three phases: (1) preicteric, (2) icteric, and (3) convalescent. Following a long incubation period of 6-26 weeks in the case of hepatitis B, the preicteric (prodromal) phase commences with malaise, lethargy, anorexia, and commonly nausea, vomiting, and pain in the right upper abdominal quandrant. A minority of patients develop at this time a type of serum sickness characterized by mild fever, urticarial rash, and polyarthritis, resembling a benign, fleeting form of acute rheumatoid arthritis. Any time from 2 days to 2 weeks after the prodromal phase begins, the icteric phase commences, heralded by dark urine (bilirubinuria) closely followed by pale stools and jaundice. The convalescent phase may be long and drawn out, with malaise and fatigue lasting for weeks.
There are a number of possible outcomes (Fig. 22-4). Less than 1% of the icteric cases die of fulminant hepatitis. Most recover uneventfully following complete regeneration of the damaged liver within 2-3 months, but some progress to chronic infection. This may take the form of an asymptomatic carrier state, defined as HBs antigenemia persisting for at least 6 months, or of chronic persistent hepatitis or chronic active hepatitis causing progressive liver damage, which may lead eventually to cirrhosis and/or to primary hepatocellular carcinoma. A proportion of those with chronic persistent or chronic active hepatitis develop manifestations of immune-complex disease, systemic necrotizing vasculitis (polyarteritis nodosa) and membranoproliferative glomerulonephritis being the two most common.
The typical course of the hepatitis B carrier can be divided into high and low replicative phases. In the high replicative phase (or productive phase), the liver is supporting a large amount of viral replication; HBsAg, viral DNA, and HBeAg are found to very high titer in the peripheral compartment. In contrast, the low replicative phase (or restricted phase) is characterized by much lower titers of HBsAg, extremely low levels of viral DNA, absence of HBeAg, but the presence of anti-HBe. This switch from HBeAg to anti-HBe, usually associated with a hepatitic flare, is known as the seroconveraion illness. In a number of carriers, this hepatitic flare is not associated with HBeAg clearance and seroconversion to anti-HBe, and is referred to as an abortive serocomvrsion.
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