Hepatitis B: Slideshow
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Hepatitis B is a disease caused by the hepatitis B virus (HBV), discovered in 1965 by Baruch Blumberg at the National Institutes of Health. Millions of people worldwide are infected through unprotected sexual contact, hematogenous spread, or maternal-fetal transmission. Without adequate diagnosis and treatment, these individuals may go on to develop liver failure, hepatocellular carcinoma, or die. Image courtesy of the US Centers for Disease Control and Prevention (CDC).
Hepatitis B is a worldwide healthcare problem. Roughly one third of the global population has been infected with HBV, and approximately 350 million are chronic carriers. However, due to aggressive vaccination plans, screening of blood products, and antiviral therapy, hepatitis B is now mainly a disease of the developing world. Epidemics still exist in parts of Asia and Africa. In high-prevalence areas without vaccination, perinatal transmission is the major mode of transmission. Image courtesy of the CDC.
In the United States, the incidence of acute hepatitis B has steadily fallen after a peak in the mid-1980s, regardless of steady immigration from endemic areas. Although the number of reported acute clinical cases is 4500, the estimated number of new infections is 10-fold more. The majority of these cases are the result of either unprotected sexual intercourse or injection drug use with dirty needles. The annual number of deaths due to hepatitis B complications is approximately 3000. Image courtesy of the CDC.
HBV is a hepadnavirus, highly resistant to extremes of temperature and humidity, that invades liver hepatocytes. The viral genome is a partially double-stranded circular DNA linked to a DNA polymerase. It is surrounded by an icosahedral nucleocapsid and then by a lipid envelope. Embedded within these layers are numerous antigens that are important in disease identification and progression. Within the nucleocapsid are the hepatitis B core antigen (HBcAg) and precore hepatitis B e antigen (HBeAg), and on the envelope is the hepatitis B surface antigen (HBsAg). Image courtesy of Graham Colm and the Wikipedia, and licensed under the Creative Commons Attribution 3.0 Unported license.
Acute HBV infection in most patients is self-limited and clears without intervention. A chronic infection occurs in 50% of newborns and children, termed the immune-tolerant phase in which viral replication occurs without liver injury. Children, and 5% of adults with acute infection, progress to the immune-active phase, when the immune response leads to liver inflammation. These patients may alternate between active disease and an inactive carrier phase. Depending on the age of infection and the duration spent in the active phase, individuals are at risk for cirrhosis and hepatocellular carcinoma. Image courtesy of the National Institutes of Health.
The history and physical examination findings in HBV infection are related to the degree and severity of liver involvement. In early disease, patients may have symptoms of anorexia, nausea, vomiting, or fatigue; however, on physical exam they may have jaundice, hepatosplenomegaly, or a low-grade fever. With more severe disease, patients may also have mental status changes, somnolence, or encephalopathy; however, on exam they may have palmar erythema, spider angiomas, gynecomastia, testicular atrophy, ascites, variceal bleeding, caput medusa, or peripheral edema. Liver enzyme elevations, classically alanine transaminase (ALT) more than aspartate transaminase (AST), indicate active immune-mediated attack of liver hepatocytes. Image courtesy of the Wikipedia and licensed under the Creative Commons Attribution ShareAlike 3.0 License.
Abdominal ascites is the accumulation of excess fluid within the peritoneal cavity, commonly the result of cirrhosis or severe liver disease. In cirrhosis, increased pressure within the portal vein pushes fluid out of the intravascular space leading to an accumulation of low protein fluid. Paracentesis is frequently performed in 1 of several locations (X's) to remove this fluid.
Spider angiomas, or spider nivea, are superficial angiomas found in advanced liver disease. The central arteriole is dilated from a lack of arterial muscular compression due to increased circulating estrogen levels. Compression of the central arteriole blanches the lesion, with rapid refilling after release. The central arteriole and thin-walled radiating vessels look like a spider body with multiple tiny legs.
The hepatitis B antigens and their concomitant antibodies are used in the detection of hepatitis B infection. HBsAg and HBeAg are actively secreted into the blood. HBcAg is not found in the blood, but retained within infected hepatocytes. Anti-Hbe, anti-HBs, and anti-HBc antibodies are eventually produced, and as the antigen levels fall, the antibody levels rise in nonchronic cases. HBV polymerase chain reactions (PCRs) are also used to measure viral load as an indicator of infectivity. Image is public domain and courtesy of Graham Colm and the Wikipedia.
The antigen-antibody blood profile represents a snapshot in time of the body's immune response to the viral infection. Depending on the detection of HBsAg, anti-HBc immunoglobulin (Ig)M, and anti-HBs, clinicians can determine whether a patient is susceptible, immune, actively infected, or chronically infected. As a general rule of thumb, a positive HBeAg indicates infectivity, whereas a positive anti-HBs indicates immunity. Image courtesy of the CDC.
Liver biopsy is not routinely done for cases of acute hepatitis B infection, but may show degenerative-regenerative changes with centrilobular necrosis. Liver biopsy is useful with chronic infection to determine the extent of disease progression. Liver damage is staged on the basis of the degree of fibrosis: portal, periportal, septal bridging, or cirrhosis. In cirrhosis, the normal liver parenchyma is replaced by scar tissue, leaving regenerative nodules of functional tissue surrounded by fibrosis (as shown).
Radiologic studies may be useful in all stages of hepatitis B infection. Ultrasonography, computed tomography (CT), or magnetic resonance imaging (MRI) may exclude biliary obstruction in acute infection. In chronic disease, ultrasound may show nonspecific increased echogenicity of the liver parenchyma. In patients with long-standing disease, imaging may be used to detect cirrhosis or hepatocellular carcinoma (as shown).
Long-standing cirrhosis leads to progressive replacement of liver parenchyma with fibrotic tissue. Over time, the liver contracts and develops a lobulated contour. These changes are readily apparent on cross-sectional imaging. This contrast-enhanced CT scan demonstrates extensive cirrhosis as well as malignant hepatocellular lesions (arrow).
Routine vaccination of infants in the United States is the mainstay of HBV prevention. For patients not vaccinated as infants, detailed schedules are available from the CDC for the vaccination of children, adolescents, and adults. The complete series induces protective antibody levels (anti-HBs) in 95% of recipients. Protection lasts at least 20 years, and is lifelong in most individuals. Image courtesy of the CDC.
For patients with acute HBV infection, the mainstay of therapy is supportive and symptomatic care. For chronic hepatitis B infection, antiviral therapy in the form of interferon alfa or nucleoside analogs, such as lamivudine, are used to suppress the disease, rather than eradicate it. Of note, there is some evidence that interferon may help prevent the progression of acute-to-chronic disease. Image included with permission and copyrighted by First DataBank, Inc.
Patients who fail medical management and develop fulminant hepatic failure or hepatocellular carcinoma may need surgery. Orthotopic liver transplantation, traditionally with a cadaveric whole liver, is the treatment of choice for patients with end-stage liver disease, whereas surgical resection may be possible for those with hepatocellular carcinoma. Recent advances in transplant surgery involve utilizing split livers from living related donors (shown) to increase the pool of potential organ matches.
Hepatitis D virus (HDV) results in hepatitis D, but can only propagate in the presence of HBV. Infection can occur concomitantly with HBV, termed coinfection, or in a person previously infected with HBV, termed superinfection. Depending on the means of infection, patients are at varying risk for acute fulminant hepatitis or cirrhosis. Patients with coinfection typically do not require any treatment, but those with superinfection leading to chronic HDV infection may require antiviral therapy with interferon alfa. Image courtesy of the World Health Organization.
