Hepatitis D virus (HDV) was first identified in 1977 in individuals already infected with chronic Hepatitis B. Initially, it was mistakenly believed to be an unrecognized component of HBV. However, further investigation revealed that the HDV nuclear antigen belonged to a distinct pathogen, initially called the delta agent.
HDV is classified as a hybrid virus because it relies on the envelope protein of Hepatitis B surface antigen (HBsAg) to form its viral envelope. This unique characteristic limit its ability to infect only individuals concurrently infected with HBV. Interestingly, HDV infection appears to have a suppressing effect on the replication of HBV within the infected individuals, although the underlying reasons for this phenomenon remain unknown.
Epidemiology
Although the Hepatitis D virus relies on the Hepatitis B virus for its transmission, the geographic distribution of HDV differs from that of HBV. This is partly due to variations in their modes of transmission. HDV is primarily transmitted through the parenteral route, typically by exposure to infected blood or blood products. While sexual transmission of HDV, even among gay men, is rare, vertical transmission from mother to child is uncommon. Most of our understanding regarding the epidemiology of HDV has been derived from studying individuals who are carriers of HBV and have been superinfected with HDV.
About 5% of HBV carriers are estimated to be co-infected with HDV. However, in recent years, there has been a notable decline in the transmission of HDV, primarily attributed to the decreasing incidence of HBV infections. Several factors have contributed to this decline, including improvements in socioeconomic conditions, increased awareness about the transmission of infectious diseases, and higher rates of hepatitis B vaccination.
The prevalence of HDV is highest in specific regions such as the Mediterranean area, Central and Northern Asia, the Amazon basin, East Africa, the Middle East, and certain parts of the Pacific. In Western countries, HDV infection is rare and mainly limited to high-risk populations, including immigrants from regions with high HDV prevalence, intravenous drug abusers, and individuals who have received multiple blood transfusions.
Anatomy
Pathophysiology
Hepatitis D virus (HDV) consists of HDAg, RNA genome, and a lipoprotein envelope derived from HBV. The HDV genome encodes only for the HDAg, which comes in short and long forms. Replication of the virus takes place within liver cells known as hepatocytes. This virus’s reliance on the host RNA polymerase II for transcribing its messenger RNA sets it apart.
The short form of HDAg triggers viral replication by directly binding to the HDV RNA, whereas the long form of HDAg is involved in viral assembly and inhibits replication. The assembly process is completed upon incorporating the HBV envelope, after which the virus is released. Notably, HDV infection can only happen in the occurrence of HBV. In individuals susceptible to HBV, co-infection with both viruses leads to an acute hepatitis D and B infection.
Clinically, this co-infection seems like a typical acute hepatitis B infection but with the distinctive feature of exhibiting two peaks of serum ALT levels, following several weeks later. This biphasic course is observed because HDV replication follows the establishment of HBV infection during the acute co-infection. In some cases, the co-infection can result in more severe illness than acute HBV mono-infection, increasing the risk of liver failure.
Fortunately, most individuals recover from the acute co-infection, with approximately 5% progressing to chronic infection. HDV superinfection is characterized by a more accelerated disease progression and an increased risk of developing hepatocellular carcinoma. The severity of the disease is influenced by several factors, including the genotype of the HDV virus, the genotype of the HBV virus, the immune response of the host, and
There are three well-established HDV genotypes: genotype 1, genotype 2, and genotype 3. While other genotypes have been identified, they have yet to be thoroughly characterized. Genotype 1 is the most prevalent in Western countries. When associated with acute hepatitis D, it tends to have a rapidly deteriorating course. Once the infection becomes chronic, it can worsen pre-existing HBV-related liver disease. It has the potential to progress rapidly toward liver cirrhosis, but it can also manifest as a more indolent, slow-progressing condition.
Etiology
Hepatitis D virus infection is a form of inflammatory liver disease that can occur acutely and chronically. The virus is primarily transmitted through parenteral routes, such as exposure to infected blood. HDV can replicate within hepatocytes independently, but it relies on the presence of hepatitis B surface antigen (HBsAg) for its propagation.
The damage to liver cells can result from the direct cytotoxic effects of the hepatitis D virus itself or an immune response triggered by the host. While perinatal transmission of HDV is rare, certain risk factors, such as blood transfusions and intravenous drug use, can increase the likelihood of infection.
Genetics
Prognostic Factors
Clinical History
Clinical History
The patient’s clinical history includes risk factors associated with hepatitis D transmission. The primary transmission mode for hepatitis D is through contact with infected blood or body fluids. Therefore, a patient may have a history of intravenous drug use, receive blood transfusions or organ transplants before the implementation of strict screening measures, or engage in high-risk sexual behaviors.
In acute hepatitis D infection, symptoms typically appear within two to eight weeks after exposure. The patient may report experiencing fatigue, jaundice, dark urine, pale stools, abdominal pain, nausea, vomiting, and loss of appetite. The duration of symptoms can vary, with some individuals recovering within a few weeks, while others may progress to chronic hepatitis D.
The patient history would have reports of worsening liver function, recurrent bouts of hepatitis flare-ups, or the development of cirrhosis-related symptoms such as fluid retention, bleeding disorders, and hepatic encephalopathy.
Physical Examination
Physical Examination
During the physical examination of a patient with hepatitis D, several characteristic findings may be observed. Jaundice a common sign of liver dysfunction and may be evident during the examination. Palpably hepatomegaly below the right ribcage and potentially detect an enlarged spleen on the left side of the abdomen.
Abdominal tenderness can be present due to inflammation and liver enlargement. In advanced cases of chronic hepatitis D, skin lesions such as spider angiomas, palmar erythema, or purpura may be visible.
Signs of chronic liver disease, including ascites, lower extremity edema, and muscle wasting, may also be apparent. It is important to consider that the physical examination findings can vary depending on the stage and severity of the disease, as well as individual patient factors.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Alcoholic Hepatitis
Cholecystitis
Cholangitis
Liver abscess
Hepatitis B
Hepatitis C
Budd-Chiari Syndrome
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
The available treatment alternatives for hepatitis D are narrow, and the optimal approach is still uncertain. Currently, there are no known specific treatments for acute hepatitis D. However, although not approved by the FDA specifically for chronic hepatitis D, interferon alpha has demonstrated beneficial effects in numerous clinical trials. According to expert guidelines, the pegylated form of IFN alpha is generally recommended as the preferred treatment option.
This treatment is typically administered once a week for a minimum of one year. The primary objective of treatment is to repress the replication of HDV, which is indicated by the absence of detectable HDV RNA in the bloodstream and HDAg in liver tissue. Treatment success is measured by normalizing ALT levels and reducing inflammation observed in liver biopsy results. In cases where hepatitis D advances to cirrhosis then liver transplantation becomes the only practical option for treatment.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
News
Octopus-Inspired Patches Might Be A Pain-Free Alternative to Injections
Posted on
News
Feminist Cancer Care Approach Aims to Save 800,000 Lives Annually
Posted on
News
Breast Lifts Soar in Popularity Among Women
Posted on
News
Researchers Raise Concern on Alcohol Promotion in Sports
Hepatitis D virus (HDV) was first identified in 1977 in individuals already infected with chronic Hepatitis B. Initially, it was mistakenly believed to be an unrecognized component of HBV. However, further investigation revealed that the HDV nuclear antigen belonged to a distinct pathogen, initially called the delta agent.
HDV is classified as a hybrid virus because it relies on the envelope protein of Hepatitis B surface antigen (HBsAg) to form its viral envelope. This unique characteristic limit its ability to infect only individuals concurrently infected with HBV. Interestingly, HDV infection appears to have a suppressing effect on the replication of HBV within the infected individuals, although the underlying reasons for this phenomenon remain unknown.
Although the Hepatitis D virus relies on the Hepatitis B virus for its transmission, the geographic distribution of HDV differs from that of HBV. This is partly due to variations in their modes of transmission. HDV is primarily transmitted through the parenteral route, typically by exposure to infected blood or blood products. While sexual transmission of HDV, even among gay men, is rare, vertical transmission from mother to child is uncommon. Most of our understanding regarding the epidemiology of HDV has been derived from studying individuals who are carriers of HBV and have been superinfected with HDV.
About 5% of HBV carriers are estimated to be co-infected with HDV. However, in recent years, there has been a notable decline in the transmission of HDV, primarily attributed to the decreasing incidence of HBV infections. Several factors have contributed to this decline, including improvements in socioeconomic conditions, increased awareness about the transmission of infectious diseases, and higher rates of hepatitis B vaccination.
The prevalence of HDV is highest in specific regions such as the Mediterranean area, Central and Northern Asia, the Amazon basin, East Africa, the Middle East, and certain parts of the Pacific. In Western countries, HDV infection is rare and mainly limited to high-risk populations, including immigrants from regions with high HDV prevalence, intravenous drug abusers, and individuals who have received multiple blood transfusions.
Hepatitis D virus (HDV) consists of HDAg, RNA genome, and a lipoprotein envelope derived from HBV. The HDV genome encodes only for the HDAg, which comes in short and long forms. Replication of the virus takes place within liver cells known as hepatocytes. This virus’s reliance on the host RNA polymerase II for transcribing its messenger RNA sets it apart.
The short form of HDAg triggers viral replication by directly binding to the HDV RNA, whereas the long form of HDAg is involved in viral assembly and inhibits replication. The assembly process is completed upon incorporating the HBV envelope, after which the virus is released. Notably, HDV infection can only happen in the occurrence of HBV. In individuals susceptible to HBV, co-infection with both viruses leads to an acute hepatitis D and B infection.
Clinically, this co-infection seems like a typical acute hepatitis B infection but with the distinctive feature of exhibiting two peaks of serum ALT levels, following several weeks later. This biphasic course is observed because HDV replication follows the establishment of HBV infection during the acute co-infection. In some cases, the co-infection can result in more severe illness than acute HBV mono-infection, increasing the risk of liver failure.
Fortunately, most individuals recover from the acute co-infection, with approximately 5% progressing to chronic infection. HDV superinfection is characterized by a more accelerated disease progression and an increased risk of developing hepatocellular carcinoma. The severity of the disease is influenced by several factors, including the genotype of the HDV virus, the genotype of the HBV virus, the immune response of the host, and
There are three well-established HDV genotypes: genotype 1, genotype 2, and genotype 3. While other genotypes have been identified, they have yet to be thoroughly characterized. Genotype 1 is the most prevalent in Western countries. When associated with acute hepatitis D, it tends to have a rapidly deteriorating course. Once the infection becomes chronic, it can worsen pre-existing HBV-related liver disease. It has the potential to progress rapidly toward liver cirrhosis, but it can also manifest as a more indolent, slow-progressing condition.
Hepatitis D virus infection is a form of inflammatory liver disease that can occur acutely and chronically. The virus is primarily transmitted through parenteral routes, such as exposure to infected blood. HDV can replicate within hepatocytes independently, but it relies on the presence of hepatitis B surface antigen (HBsAg) for its propagation.
The damage to liver cells can result from the direct cytotoxic effects of the hepatitis D virus itself or an immune response triggered by the host. While perinatal transmission of HDV is rare, certain risk factors, such as blood transfusions and intravenous drug use, can increase the likelihood of infection.
Clinical History
The patient’s clinical history includes risk factors associated with hepatitis D transmission. The primary transmission mode for hepatitis D is through contact with infected blood or body fluids. Therefore, a patient may have a history of intravenous drug use, receive blood transfusions or organ transplants before the implementation of strict screening measures, or engage in high-risk sexual behaviors.
In acute hepatitis D infection, symptoms typically appear within two to eight weeks after exposure. The patient may report experiencing fatigue, jaundice, dark urine, pale stools, abdominal pain, nausea, vomiting, and loss of appetite. The duration of symptoms can vary, with some individuals recovering within a few weeks, while others may progress to chronic hepatitis D.
The patient history would have reports of worsening liver function, recurrent bouts of hepatitis flare-ups, or the development of cirrhosis-related symptoms such as fluid retention, bleeding disorders, and hepatic encephalopathy.
Physical Examination
During the physical examination of a patient with hepatitis D, several characteristic findings may be observed. Jaundice a common sign of liver dysfunction and may be evident during the examination. Palpably hepatomegaly below the right ribcage and potentially detect an enlarged spleen on the left side of the abdomen.
Abdominal tenderness can be present due to inflammation and liver enlargement. In advanced cases of chronic hepatitis D, skin lesions such as spider angiomas, palmar erythema, or purpura may be visible.
Signs of chronic liver disease, including ascites, lower extremity edema, and muscle wasting, may also be apparent. It is important to consider that the physical examination findings can vary depending on the stage and severity of the disease, as well as individual patient factors.
Differential Diagnoses
Alcoholic Hepatitis
Cholecystitis
Cholangitis
Liver abscess
Hepatitis B
Hepatitis C
Budd-Chiari Syndrome
The available treatment alternatives for hepatitis D are narrow, and the optimal approach is still uncertain. Currently, there are no known specific treatments for acute hepatitis D. However, although not approved by the FDA specifically for chronic hepatitis D, interferon alpha has demonstrated beneficial effects in numerous clinical trials. According to expert guidelines, the pegylated form of IFN alpha is generally recommended as the preferred treatment option.
This treatment is typically administered once a week for a minimum of one year. The primary objective of treatment is to repress the replication of HDV, which is indicated by the absence of detectable HDV RNA in the bloodstream and HDAg in liver tissue. Treatment success is measured by normalizing ALT levels and reducing inflammation observed in liver biopsy results. In cases where hepatitis D advances to cirrhosis then liver transplantation becomes the only practical option for treatment.
medtigo
Hepatitis D
Updated :
May 12, 2023
Hepatitis D virus (HDV) was first identified in 1977 in individuals already infected with chronic Hepatitis B. Initially, it was mistakenly believed to be an unrecognized component of HBV. However, further investigation revealed that the HDV nuclear antigen belonged to a distinct pathogen, initially called the delta agent.
HDV is classified as a hybrid virus because it relies on the envelope protein of Hepatitis B surface antigen (HBsAg) to form its viral envelope. This unique characteristic limit its ability to infect only individuals concurrently infected with HBV. Interestingly, HDV infection appears to have a suppressing effect on the replication of HBV within the infected individuals, although the underlying reasons for this phenomenon remain unknown.
Although the Hepatitis D virus relies on the Hepatitis B virus for its transmission, the geographic distribution of HDV differs from that of HBV. This is partly due to variations in their modes of transmission. HDV is primarily transmitted through the parenteral route, typically by exposure to infected blood or blood products. While sexual transmission of HDV, even among gay men, is rare, vertical transmission from mother to child is uncommon. Most of our understanding regarding the epidemiology of HDV has been derived from studying individuals who are carriers of HBV and have been superinfected with HDV.
About 5% of HBV carriers are estimated to be co-infected with HDV. However, in recent years, there has been a notable decline in the transmission of HDV, primarily attributed to the decreasing incidence of HBV infections. Several factors have contributed to this decline, including improvements in socioeconomic conditions, increased awareness about the transmission of infectious diseases, and higher rates of hepatitis B vaccination.
The prevalence of HDV is highest in specific regions such as the Mediterranean area, Central and Northern Asia, the Amazon basin, East Africa, the Middle East, and certain parts of the Pacific. In Western countries, HDV infection is rare and mainly limited to high-risk populations, including immigrants from regions with high HDV prevalence, intravenous drug abusers, and individuals who have received multiple blood transfusions.
Hepatitis D virus (HDV) consists of HDAg, RNA genome, and a lipoprotein envelope derived from HBV. The HDV genome encodes only for the HDAg, which comes in short and long forms. Replication of the virus takes place within liver cells known as hepatocytes. This virus’s reliance on the host RNA polymerase II for transcribing its messenger RNA sets it apart.
The short form of HDAg triggers viral replication by directly binding to the HDV RNA, whereas the long form of HDAg is involved in viral assembly and inhibits replication. The assembly process is completed upon incorporating the HBV envelope, after which the virus is released. Notably, HDV infection can only happen in the occurrence of HBV. In individuals susceptible to HBV, co-infection with both viruses leads to an acute hepatitis D and B infection.
Clinically, this co-infection seems like a typical acute hepatitis B infection but with the distinctive feature of exhibiting two peaks of serum ALT levels, following several weeks later. This biphasic course is observed because HDV replication follows the establishment of HBV infection during the acute co-infection. In some cases, the co-infection can result in more severe illness than acute HBV mono-infection, increasing the risk of liver failure.
Fortunately, most individuals recover from the acute co-infection, with approximately 5% progressing to chronic infection. HDV superinfection is characterized by a more accelerated disease progression and an increased risk of developing hepatocellular carcinoma. The severity of the disease is influenced by several factors, including the genotype of the HDV virus, the genotype of the HBV virus, the immune response of the host, and
There are three well-established HDV genotypes: genotype 1, genotype 2, and genotype 3. While other genotypes have been identified, they have yet to be thoroughly characterized. Genotype 1 is the most prevalent in Western countries. When associated with acute hepatitis D, it tends to have a rapidly deteriorating course. Once the infection becomes chronic, it can worsen pre-existing HBV-related liver disease. It has the potential to progress rapidly toward liver cirrhosis, but it can also manifest as a more indolent, slow-progressing condition.
Hepatitis D virus infection is a form of inflammatory liver disease that can occur acutely and chronically. The virus is primarily transmitted through parenteral routes, such as exposure to infected blood. HDV can replicate within hepatocytes independently, but it relies on the presence of hepatitis B surface antigen (HBsAg) for its propagation.
The damage to liver cells can result from the direct cytotoxic effects of the hepatitis D virus itself or an immune response triggered by the host. While perinatal transmission of HDV is rare, certain risk factors, such as blood transfusions and intravenous drug use, can increase the likelihood of infection.
Clinical History
The patient’s clinical history includes risk factors associated with hepatitis D transmission. The primary transmission mode for hepatitis D is through contact with infected blood or body fluids. Therefore, a patient may have a history of intravenous drug use, receive blood transfusions or organ transplants before the implementation of strict screening measures, or engage in high-risk sexual behaviors.
In acute hepatitis D infection, symptoms typically appear within two to eight weeks after exposure. The patient may report experiencing fatigue, jaundice, dark urine, pale stools, abdominal pain, nausea, vomiting, and loss of appetite. The duration of symptoms can vary, with some individuals recovering within a few weeks, while others may progress to chronic hepatitis D.
The patient history would have reports of worsening liver function, recurrent bouts of hepatitis flare-ups, or the development of cirrhosis-related symptoms such as fluid retention, bleeding disorders, and hepatic encephalopathy.
Physical Examination
During the physical examination of a patient with hepatitis D, several characteristic findings may be observed. Jaundice a common sign of liver dysfunction and may be evident during the examination. Palpably hepatomegaly below the right ribcage and potentially detect an enlarged spleen on the left side of the abdomen.
Abdominal tenderness can be present due to inflammation and liver enlargement. In advanced cases of chronic hepatitis D, skin lesions such as spider angiomas, palmar erythema, or purpura may be visible.
Signs of chronic liver disease, including ascites, lower extremity edema, and muscle wasting, may also be apparent. It is important to consider that the physical examination findings can vary depending on the stage and severity of the disease, as well as individual patient factors.
Differential Diagnoses
Alcoholic Hepatitis
Cholecystitis
Cholangitis
Liver abscess
Hepatitis B
Hepatitis C
Budd-Chiari Syndrome
The available treatment alternatives for hepatitis D are narrow, and the optimal approach is still uncertain. Currently, there are no known specific treatments for acute hepatitis D. However, although not approved by the FDA specifically for chronic hepatitis D, interferon alpha has demonstrated beneficial effects in numerous clinical trials. According to expert guidelines, the pegylated form of IFN alpha is generally recommended as the preferred treatment option.
This treatment is typically administered once a week for a minimum of one year. The primary objective of treatment is to repress the replication of HDV, which is indicated by the absence of detectable HDV RNA in the bloodstream and HDAg in liver tissue. Treatment success is measured by normalizing ALT levels and reducing inflammation observed in liver biopsy results. In cases where hepatitis D advances to cirrhosis then liver transplantation becomes the only practical option for treatment.
Free CME credits
Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.
Digital Certificate PDF
On course completion, you will receive a full-sized presentation quality digital certificate.
medtigo Simulation
A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.
medtigo Points
medtigo points is our unique point redemption system created to award users for interacting on our site. These points can be redeemed for special discounts on the medtigo marketplace as well as towards the membership cost itself.
Community Forum post/reply = 5 points
*Redemption of points can occur only through the medtigo marketplace, courses, or simulation system. Money will not be credited to your bank account. 10 points = $1.
All Your Certificates in One Place
When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.
