HEPATITIS D DEFINITION
Hepatitis D: Liver inflammation due to the hepatitis D virus (HDV), which causes disease only in patients who additionally have the hepatitis B virus. Transmission occurs via infected blood, needles, or sexual contact with an infected person. Symptoms are identical to those of hepatitis B. HDV infection can be prevented with the hepatitis B vaccine and through avoidance of activities that could lead to getting the virus.
HEPATITIS D CAUSES
Only a person who is already infected with hepatitis B can become infected with hepatitis D. It is caused by the virus HDV (Hepatitis D Virus). Infection is through contact with infected blood, unprotected sex, and perforation of the skin with infected needles. The liver of a person with Hepatitis D swells.
HEPATITIS D PATHOPHYSIOLOGY
Hepatitis D virus (HDV) is an RNA virus that is structurally unrelated to hepatitis A(HAV), hepatitis B (HBV), or hepatitis C virus (HCV). It was discovered in 1977. HDV causes a unique infection that requires the assistance of viral particles from HBV to replicate and infect other hepatocytes. 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.
HEPATITIS D SYMPTOMS
The initial phase of hepatitis is called the ACUTE PHASE. The symptoms are like a mild flu, and may include:
Loss of appetite
Muscle or joint aches
Slight abdominal pain
HEPATITIS D DIAGNOSIS
Due to the dependence of HDV on HBV, the presence of HBsAg is necessary for the diagnosis of HDV infection. The additional presence of IgM antibody to hepatitis B core antigen (IgM anti-HBc) is necessary for the diagnosis of acuteHBV/HDV coinfection
HEPATITIS D TREATMENT
The hepatitis D virus (HDV), the smallest virus known to infect man, causes the most severe form of chronic viral hepatitis, hepatitis delta. It is estimated that about 15 to 20 million people are suffering from chronic HDV infection. HDV is a defective satellite virus depending on the hepatitis B surface antigen (HBsAg) for transmission. Chronic hepatitis delta is associated with a rapid progression of liver fibrosis and a high prevalence of liver cirrhosis, even in younger patients. Immunization against hepatitis B virus (HBV) protects from HDV infection, but there is no specific vaccine against HDV available for HBsAg-positive individuals. Treatment options for hepatitis delta patients are limited. So far, only interferon-alpha has shown an antiviral efficacy against HDV. Recent trials showed sustained virological response rates concerning HDV in 25 %-30 % of patients treated with pegylatedinterferons. HDV is dominant over HBV in the majority of cases, but HBV DNA-positive subjects should be treated with HBV polymerase inhibitors. Combination therapy of pegylated interferon-alpha and adefovir showed a more pronounced HBsAg decline, but the exact role of combination therapies in hepatitis delta requires further investigation. Alternative future treatment strategies may include prenylation inhibitors and HBV entry inhibitors, which are in early clinical development.