Porth's Essentials of Pathophysiology, 4e

733

Disorders of Hepatobiliary and Exocrine Pancreas Function

C h a p t e r 3 0

HBsAg (envelope)

Incubation period

Acute illness

Convalescence

Exposure

Viral coat

Double-stranded circular DNA (HBV genome) HBcAg/HBeAg (nucleocapsid)

IgM anti-HAV

HAV

IgG anti-HAV

DNA polymerase

Fecal HAV

A

Onset symptoms Onset recovery

0

12

20

4

8

16

Weeks after exposure FIGURE 30-7. The sequence of fecal shedding of the hepatitis A virus (HAV), HAV viremia, and HAV antibody (IgM and IgG anti-HAV) changes in hepatitis A.

HBsAg

HBeAg

IgG anti-HBc

Exposure

Antibodies to HAV (anti-HAV) appear early in the disease and tend to persist in the serum (Fig. 30-7). The immunoglobulin M (IgM) antibodies (see Chapter 15) usually appear during the first week of symptomatic dis- ease and begin to decline in a few months. 3 Their pres- ence coincides with a decline in fecal shedding of the virus. Peak levels of IgG antibodies occur after 1 month of illness and may persist for years; they provide long- term protective immunity against reinfection. The pres- ence of IgM anti-HAV is indicative of acute hepatitis A, whereas IgG anti-HAV merely documents past infection. A HAV vaccine is available for persons at high risk for HAV exposure. 9 These include international travelers to regions where sanitation is poor and endemic HAV infec- tions are high, children living in communities with high rates of HAV infection, homosexually active men, and users of illicit drugs. A public health benefit also may be derived from vaccinating persons with increased poten- tial for transmitting the disease (e.g., food handlers). The Centers for Disease Control and Prevention (CDC) has recently recommended vaccination of children in states, counties, and communities with high rates of infection. 9 Persons who have been exposed to HAV are advised to receive postexposure prophylaxis with a single dose of HAV vaccine or immune globulin (IgG) as soon as possible. The immune globulin is preferred for persons older than 40 years or younger than 1 year of age and for those who are immunocompromised or have chronic liver disease. Hepatitis B. Hepatitis B is caused by a hepatotropic deoxyribonucleic acid (DNA)-containing Hepadnavirus . The complete hepatitis B virion, also called a Dane par- ticle, consists of an outer envelope and an inner nucleo- capsid that contains the viral DNA and viral polymerase that exhibits both DNA polymerase and reverse tran- scriptase activity (Fig. 30-8). HBV infection can produce acute hepatitis, chronic hepatitis, hepatocellular carci- noma, and fulminant hepatic failure. It also participates in the development of hepatitis D (delta hepatitis). 3,4,10 The virus usually is transmitted through inoculation

Anti-HBs

HBV DNA

IgM anti-HBc

with infected blood or serum. However, the viral anti- gen can be found in most body secretions and can be spread by oral or sexual contact. Hepatitis B has a longer incubation period and rep- resents a more serious health problem than hepatitis A. More than 2 billion people—one third of the world’s population—alive today have been infected with HBV, and of these more than 240 million remain infected. 3,11 The incidence of acute hepatitis B in the United States has dramatically declined since 1990, with the greatest declines in children and adolescents, coincident with HBV vaccination. Worldwide, perinatal (vertical) transmission is the predominant mode of HBV transmission, whereas intra- venous drug use and unprotected sexual intercourse are the main routes of transmission in low-prevalence areas such as the United States. Although the virus can be spread through transfusion or administration of blood products, routine screening methods have appreciably reduced transmission through this route. 12 Three well-defined antigens are associated with the HBV virus: a core antigen, HBcAg; HBeAg, a precore pro- tein; and a surface antigen, HBsAg. These HBV antigens evoke specific antibodies: anti-HBc, anti-HBe, and anti- HBs. The antigens and their antibodies serve as serologic markers for following the natural course of the disease 3,4 (see Fig. 30-8). HBsAg is the viral antigen measured most B FIGURE 30-8. (A) The hepatitis B virus. (B) The sequence of hepatitis B virus (HBV) viral antigens (HBsAg, HBeAg), HBV DNA, and HBV antibody (IgM, IgG, anti-HBc, and anti-HBs) changes in acute resolving hepatitis B. 0 4 8 12 16 20 24 28 32 36 40 52 Weeks