A serious liver infection caused by the hepatitis B virus that's easily preventable by a vaccine. This disease is most commonly spread by exposure to infected bodily fluids. Symptoms are variable and include yellowing of the eyes, abdominal pain and dark urine. Some people, particularly children, don't experience any symptoms. In chronic cases, liver failure, cancer or scarring can occur. The condition often clears up on its own. Chronic cases require medication and possibly a liver transplant.

1. HEPATITIS B

2. Etiology
Virus - Hepatitis B virus (HBV: DNA virus, hepadnavirus)
Transmission
i. Sexual
ii. Parenteral
1. Needlestick injury
2. Contaminated instruments and shared needles
3. Contaminated blood products
iii. Perinatal
High-risk groups for HBV infection
■ IV drug users
■ Infants of HBV-positive mothers
■ Professions with exposure to human blood and/or seminal/vaginal fluids
■ Individuals with multiple sex partners or sex partners of HBV-positive people
■ Patients undergoing hemodialysis; organ or blood transfusion recipients
■ Hepatitis C virus (HCV) or HIV-positive individuals

3. Pathophysiology
Acute infection
• Hepatocytes infected by the hepatitis B virus express viral peptides on their surfaces
→ lymphocytes recognize HBV-derived peptides and become activated (CD8+ cytotoxic T cells)
→ lymphocytes attack liver cells (cellular immune response) → hepatic inflammation with
destruction of hepatocytes
• Replication cycle
1. After entering the host cell's nucleus, the viral polymerase completes the positive strand of
2. the virus' partially double-stranded relaxed circular DNA (rcDNA).
3. The rcDNA is converted to covalently closed circular DNA (cccDNA) primarily by host enzymes
4. The cccDNA is then transcribed into viral mRNA by host RNA polymerase.
5. The viral mRNA leaves the nucleus and is translated into HBV core proteins and reverse transcriptase
in the cytoplasm.
6. Viral mRNA and reverse transcriptase are packaged into a capsid, where viral mRNA is then reverse-
transcribed into viral rcDNA.
7. New viral DNA genomes are enveloped and leave the cell as progeny virions

4. Chronic infection
• If clearance of the virus fails
• Persistent hepatic inflammation with necrosis, mitosis, and regeneration processes → cirrhosis,
cellular dysplasia → HCC
• Integration of HBV DNA into the host genome → altered expression
of endogenous genes, chromosomal instability → HCC

5. Pathology
• Acute viral hepatitis
o Eosinophilic single-cell necrosis (Councilman body)
o Kupffer cell proliferation
o Bridging necrosis
• Chronic viral hepatitis
o Formation of lymphoid follicles and mononuclear infiltrates
o Piecemean necrosis: periportal liver cell necrosis with lymphocytic infiltration indicates
chronic active hepatitis and poor prognosis
o Fibrous septa
o Ground glass hepatocytes

6. Clinical Features
Acute infection
➔ Acute HBV infections are defined as infections that were acquired in the past 6 months.
➔ Subclinical hepatitis (70% of cases)
➔ Symptomatic hepatitis (30% of cases)
◆ Fever, skin rash, arthralgias, myalgias, fatigue
◆ Nausea
◆ Jaundice
◆ Right upper quadrant pain
◆ Symptoms usually resolve after 1–3 months
➔ Fulminant hepatitis (∼ 0.5% of cases)
Chronic infection
➔Chronic HBV infections are defined as infections persisting for more than 6 months with detection
of HBsAg and possibly symptoms of liver damage.
➔Most patients are inactive, non-contagious carriers.may be asymptomatic , imitate acute hepatitis,
or result in hepatic failure
➔Cirrhosis, stigmata of chronic liver disease (25% of cases)
➔Extrahepatic manifestations (10–20% of cases)
◆Polyarteritis nodosa
◆Membranous glomerulonephritis

7. Investigations
Hepatitis B surface antigen
• indicator of active infection, and a negative test for HBsAg makes HBV infection very unlikely.
• HBsAg appears in the blood late in the incubation period but before the prodromal phase of acute type B
hepatitis; usually lasts for 3–4 weeks and can persist for up to 5 months.
• The persistence of HBsAg for longer than 6 months indicates chronic infection.
Antibody to HBsAg (anti-HBs)
• appears after about 3–6 months and persists for many years or perhaps permanently.
• Anti-HBs implies either a previous infection, in which case anti-HBc is usually also present, or previous
vaccination, in which case anti-HBc is not present.
Hepatitis B core antigen and antibody
• HBcAg is not found in the blood, but antibody to it (anti-HBc) appears early in the illness and rapidly
reaches a high titre, which subsides gradually but then persists.
• Anti-HBc is initially of IgM type, with IgG antibody appearing later.
Hepatitis B e antigen and antibody
• HBeAg is an indicator of viral replication. In acute hepatitis B it may appear only transiently at the
outset of the illness; its appearance is followed by the production of antibody (anti-HBe). The HBeAg
reflects active replication of the virus in the liver.
Viral load and genotype HBV-DNA can be measured by PCR in the blood

9. Other Laboratory studies
1. Liver function tests
• Transaminases (AST, ALT)
Acute hepatitis: ↑ with AST/ALT ratio of < 1 (> 1 in fulminant infection)
Chronic hepatitis: variable values (usually < 100 U/L; in active infection > 100
U/L) with AST/ALT ratio of ≥ 1
• ↑ γ-GT, bilirubin, GLDH, and/or AP
• In cirrhosis: ↓ albumin, CHE
1. Abdominal ultrasound
a. Acute hepatitis
i. ↑ Brightness of portal vein radicle walls
ii. ↓ Echogenicity of the liver
b. Chronic hepatitis
i. ↓ Brightness and number of portal vein radicle walls
ii. ↑ Liver echogenicity
1. Liver biopsy
1. Test of common coinfections (e.g., hepatitis C/D, syphilis, HIV)

10. Treatment
Acute hepatitis B
• Supportive care, treat liver failure.
Chronic hepatitis B
1. Antiviral treatment
o Reduce HBV DNA below detectable levels
o Seroconversion of HBeAg to anti-HBe
o Reverse liver disease
2. Nucleoside/nucleotide analogs : indicated for patients with both decompensated and
compensated liver disease and nonresponders to interferon treatment
o Tenofovir is commonly the drug of choice
o Entecavir
4. Lamivudine
3. Pegylated interferon alfa (PEG-IFN-a) : especially in younger patients with compensated liver disease
o Regimen is shorter than nucleoside/nucleotide analogs . Coinfection with HDV is best treated
with PEG-IFN-a.
Surgical treatment
• Liver transplantation In cases of end-stage liver disease due to HBV. In cases of fulminant hepatic
failure (emergent transplantation)