Hepatitis D 

Hepatitis D virus (HDV) is an RNA virus that is structurally unrelated to hepatitis A, hepatitis B, or hepatitis C virus. It was discovered in 1977. HDV causes a unique infection that requires the assistance of viral particles from hepatitis B virus (HBV) to replicate and infect other hepatocytes.^{[1, 2, 3]} Its clinical course is varied and ranges from acute, self-limited infection to acute, fulminant liver failure. Chronic liver infection can lead to end-stage liver disease and associated complications.^{[4, 5, 6]}

There are 3 known genotypes of hepatitis D. Genotype I has a worldwide distribution; genotype 2 exists in Taiwan, Japan, and northern Asia; and genotype 3 is found in South America.

Simultaneous infection with HBV and HDV is known as coinfection and results in fulminant liver failure in 1% of patients. Complete clinical recovery and clearance of HBV and HDV coinfection is the most common outcome. Chronic infection with HBV and HDV occurs in less than 5% of patients. (See Prognosis and Workup.)

Infection with HDV in a patient who is already positive for the hepatitis B surface antigen (HBsAg) is known as superinfection and results in fulminant liver failure in 5% of patients. Approximately 80-90% develop chronic HDV infection. These patients progress more rapidly to develop cirrhosis and may develop hepatocellular carcinoma. (See Workup.)

A study from The Netherlands suggested HDV may hinder the control of HBV. Xiridou et al used a mathematical model for the transmission of both viruses and calculated the reproduction numbers of single HBV infections and dual HBV/HDV infections.^[3] The investigators looked at the endemic prevalences of both viruses and found that HDV modulates HBV epidemic severity and also hampers impact on HBV interventions. Xiridou et al concluded that in endemic populations with HDV, control programs that ignore HDV presence may lead to underestimation of the HBV epidemic and overestimation of positive results, as control of HBV is dependent on the reproduction numbers of dual HBV/HDV infections.^[3] (See Epidemiology.)

See the following for more information:

• Alcoholic Hepatitis
• Autoimmune Hepatitis
• Dermatologic Manifestations of Hepatitis C
• Hepatitis A
• Hepatitis B
• Hepatitis C
• Hepatitis E
• Viral Hepatitis

Complications

Complications may include the following:

• Liver failure
• Hepatocellular carcinoma
• Autoimmune manifestations, often including antinuclear antibodies and smooth muscle antibodies

Patient education

Modify high-risk behaviors, including intravenous drug use and unsafe sexual practices.

Promote the use of universal precautions for health care workers.

Patients with chronic HDV and HBV infection should not donate blood, share toothbrushes or razors, or consume alcohol. Precautions should be observed.

Hepatitis D virus (HDV) infection is an acute and chronic inflammatory process involving the liver. HDV is transmitted parenterally; it can replicate independently within the hepatocyte, but it requires HBsAg for propagation. Hepatic cell death may occur due to the direct cytotoxic effect of HDV or via a host-mediated immune response.

Risk factors include intravenous drug use and multiple blood transfusions.

Sexual transmission is less efficient than with HBV.

Perinatal transmission is rare; no such cases have been reported in the United States.

In the United States, HDV infection is observed more commonly among patients with a history of intravenous drug use and in persons from the Mediterranean basin.

Approximately 15 million people are infected with HDV worldwide. Areas with the highest prevalence include southern Italy; North Africa; the Middle East; the Amazon Basin; and the American South Pacific islands of Samoa, Hauru, and Hiue. China, Japan, Taiwan, and Myanmar (formerly Burma) have a high prevalence of HBV infection but a low rate of HDV infection.^{[7, 8]}

HDV infection is more common in adults than in children. However, children from underdeveloped, HDV-endemic countries are more likely to contract HDV infection through breaks in the skin, due to the presence of skin lesions.

The prognosis is excellent for patients with coinfection in whom treatment eradicates both viruses.

The prognosis is variable for patients who are superinfected. It depends on the duration and severity of HBV infection, alcohol consumption, comorbid illnesses, and age.

In patients who undergo liver transplantation for chronic liver disease secondary to HBV and hepatitis D virus (HDV) infection, HDV seems to suppress the replication of HBV in the transplanted liver and may help to prolong graft survival. However, fulminant hepatitis from recurrent HBV and HDV infection in the transplanted liver has resulted in patient death or the need to retransplant.