Acute Viral Hepatitis Overview

Persistence of acute hepatitis A symptoms and/or biological changes for weeks or months.

A severe form characterized by prolonged, intense jaundice with a greenish tint.

Extremely rare, characterized by massive liver damage and severe complications.

Does not pose a risk to the fetus.

HIV patients may show elevated transaminases, but not more severe disease than others.

Potentially more severe, with a higher chance of fulminant hepatitis compared to those without chronic liver conditions.

Based on epidemiological (contact, travel), clinical (symptoms), and paraclinical (lab tests) evidence.

Similar lab changes occur in different types of acute hepatitis (A, B, C, D, E).

The percentage of people in a population infected with the Hepatitis B virus.

The ways in which HBV can spread from one person to another.

HBV transmission through blood or contaminated blood products, often via medical procedures or sharing needles.

HBV transmission through bodily fluids like saliva and genital secretions, primarily via sexual contact.

HBV transmission from a mother to her baby during pregnancy, birth, or breastfeeding.

People with a higher chance of contracting HBV due to their lifestyle, medical conditions, or exposure.

Protection from HBV infection due to the presence of antibodies, either from previous infection or vaccination.

Antibodies that provide immunity against HBV, produced after either infection or vaccination.

A condition where liver cells are breaking down, leading to increased transaminases (AST, ALT).

Elevated bilirubin levels, sometimes with a predominance of direct bilirubin, leading to jaundice (yellowing of skin/eyes).

A condition where bile flow is blocked, leading to increased serum bilirubin, GGT, ALP, and cholesterol.

Blood abnormalities sometimes seen in severe liver disease, including leukocyte changes and possible blood disorders (thrombocytopenia, anemia).

A blood test showing the time it takes blood to clot. Reduced prothrombin index or increased INR is an early marker of severe liver disease.

Severe liver damage affecting liver functions like protein synthesis, detoxification, and metabolism.

Elevated levels indicate liver injury, with significantly higher values seen with hepatitis A than other types.

Blockage of bile ducts; detected by ultrasound.

Different HBV subtypes classified by specific combinations of epitopes, resulting in distinct geographical distribution and varied disease progression.

HBsAg (hepatitis B surface antigen) can be found in the blood and within infected liver cells.

HBcAg (hepatitis B core antigen) is found exclusively within the infected liver cell, not detectable in the blood.

HBeAg (hepatitis B e antigen) is a soluble form of HBcAg, indicating active viral replication and high infectivity.

The HBV genome is a small, circular, partially double-stranded DNA molecule, coding for various viral proteins.

A unique enzyme in HBV that mediates viral replication through a process similar to retroviruses, including reverse transcription of RNA.

HbxAg (hepatitis B x antigen) is a protein involved in liver cell death and activation of immune cells.

HBV can remain infectious for 7 days on surfaces even without visible blood, and is resistant to some common disinfectants.

Most healthy individuals fully recover from Hepatitis A with no lasting effects. However, older adults, those with existing liver disease, and individuals with weakened immune systems may experience more severe complications and a mortality rate of 0.1-1%.

Preventing Hepatitis A involves ensuring clean water, proper sanitation, practicing food hygiene, and using immunoglobulins or vaccines for pre- and post-exposure prophylaxis.

Multiple commercially available vaccines contain inactivated hepatitis A virus. These are administered by injection and can be monovalent or bivalent, including protection against other diseases like hepatitis B or typhoid fever.

Hepatitis B virus is a DNA virus, unlike other types of hepatitis. It belongs to the Hepadnaviridae family and has three distinct forms of surface antigen: large (″L″), medium (″M″), and small (″S″).

The complete form of HBV, a small (42 nm) particle consisting of an outer envelope and a viral core (nucleocapsid).

The surface antigen present on the envelope of HBV, existing in three forms: large (″L″), medium (″M″), and small (″S″).

The treatment for acute hepatitis A is similar to that of acute hepatitis B, C, and E.

The treatment of acute hepatitis A is similar to that of acute hepatitis B, C and E (see the subsection Treatment of acute hepatitis B).

The virus itself can directly damage liver cells, suggesting that mutations in the viral pre-core region can lead to more severe liver disease.

The incubation period for hepatitis B typically ranges from 60 to 90 days, but can vary from 45 to 180 days.

The prodromal period, lasting 2-3 weeks, is the pre-jaundice stage featuring symptoms similar to other viral hepatitis forms.

This syndrome is a specific symptom at the onset of acute hepatitis B, characterized by joint pain and inflammation.

Symptoms like fever, cough, headache, muscle aches, and weakness are rarely seen in acute HBV. They are more common in acute hepatitis A.

Clinically, jaundice in HBV is usually more intense, longer-lasting, and often has a fluctuating pattern, accompanied by liver pain and enlargement.

This period marks the gradual recovery from HBV, with the disappearance of general symptoms but ongoing liver enlargement and mild liver cell damage.

In 90% of cases, the HBV infection resolves on its own within a few weeks.