• Chronic hepatitis B

• Fibrosis

• Cirrhosis

• Portal hypertension

• Decompensated liver disease / liver failure

• Hepatocellular carcinoma

• Fulminant hepatitis / acute liver failure in a small proportion of acute infections

If presenting as Acuter Hepatitis :: think of

• Hepatitis A, C, E

• Drug-induced liver injury

• Alcoholic hepatitis

• Ischemic hepatitis

• Acute biliary obstruction

• Acute exacerbation of chronic HBV

If presenting with Chronic Liver Disease :: think of

\ • Chronic hepatitis C

• Autoimmune hepatitis

• Wilson disease

• Hemochromatosis

• Cirrhosis of other causes

• Hepatocellular carcinoma in advanced disease

• HBV-related HCC can occur even without cirrhosis, although cirrhosis is very common in advanced cases.

*• Liver biopsy in selected cases when diagnosis or staging remains uncertain* 

A slightly organized version:

• CBC

• Serum bilirubin

• AST, ALT, ALP

• Albumin

• PT/INR

• Ultrasonography of liver and spleen 

• HBsAg

• Anti-HBc IgM / total anti-HBc

• Anti-HBs

• HBeAg / anti-HBe

• HBV DNA quantification 

Assessment of chronic liver injury

• APRI / FIB-4 / FibroScan or other elastography

• Liver biopsy if needed for staging or diagnostic clarification 

A useful practical line:::

• Diagnosis is stepwise: routine liver evaluation first, then HBV serology and viral load, followed by fibrosis assessment where indicated.

FibroScan / Elastography

• FibroScan provides noninvasive assessment of liver stiffness (kPa) and steatosis by CAP (dB/m)

• Liver stiffness <10 kPa usually makes advanced chronic liver disease less likely

• 10–15 kPa may suggest advanced fibrosis / compensated advanced chronic liver disease

• ≥15 kPa is strongly suggestive of compensated advanced chronic liver disease

• Interpretation must be correlated with clinical findings, laboratory tests, ultrasound, and disease etiology

Acute hepatitis B

• Lobular hepatitis

• Hepatocyte ballooning

• Spotty necrosis / acidophil bodies

• Lobular disarray

• Cholestatic features in some cases 

Chronic hepatitis B

• Portal mononuclear inflammation

• Interface hepatitis

• Variable lobular activity

• Fibrosis progressing to cirrhosis

• Ground-glass hepatocytes as a classic HBV-associated finding

Microscopic (histologic) description

Acute phase of hepatitis B

Inflammatory cell infiltration

Predominantly lymphocytic infiltrate within the parenchyma and portal tracts (usually perivenular distribution)

Involvement of portal inflammation is variable

Plasma cells may also be prominent and few neutrophils and eosinophils may be present (Liver 1985;5:84)

Compared to acute hepatitis C, acute hepatitis B has periportal inflammation (J Gastroenterol Hepatol 2001;16:209)

Occult infection and mild portal inflammation, focal necrosis, apoptosis and fibrosis may persist following clinical recovery of acute hepatitis B (Hepatology 2003;37:1172)

Hepatocellular damage

Hepatocyte nuclei show prominent nucleoli and a moderate degree of pleomorphism; may show multiple nucleoli

Changes ranging from a minor degree of cell swelling to cell death, most severe in perivenular areas

Ballooning degeneration is seen as more severe degrees of cell swelling

Acidophil bodies or Councilman bodies

Eosinophilic globule or fragments of apoptotic hepatocytes where deposits of HBsAg are found (Leber Magen Darm 1982;12:146)

Granular or vacuolated cytoplasm might be present

Other features: cholestasis, Kupffer cell activation, endotheliitis, bile duct damage, ductular reaction and mild hepatocellular siderosis (Am J Clin Pathol 1984;81:162)

Chronic hepatitis B

Inflammatory cell infiltration

Mononuclear infiltration of portal tracts

Both interface hepatitis and lobular hepatitis can be seen

Hepatocellular changes

Hallmark of chronic hepatitis B virus infection

Ground glass appearance (of the central part of the cytoplasm) of hepatocytes when HBsAg is elevated or in active viral replication (Viruses 2019;11:386)

Active viral replication can also be demonstrated by hepatocyte nuclei or cytoplasmic stain of HBcAg

Nuclei of hepatocytes may contain large amounts of core protein and have a pale, homogenous appearance on H&E sections, described as sanded

Marked variation in size and appearance of hepatocyte nuclei and close contact between hepatocytes and lymphocytes might be seen

Enlargement of portal tracts due to infiltration of mononuclear cells (J R Soc Med 1985;78:391)

Lobular spotty necrosis (J R Soc Med 1985;78:391)

Hepatocyte death, atrophy, regeneration and fibrosis

• Hepatitis B vaccination is the main preventive measure (susceptible people)

• Birth-dose vaccination is especially important to prevent mother-to-child transmission

• Complete vaccination schedule provides very high protection

• Screening of pregnant women helps identify mothers who need measures to reduce vertical transmission

• Safe blood transfusion, screened blood products, and safe injection practices are essential

• Avoid sharing needles, razors, toothbrushes, and other blood-contaminated items

• Safer sexual practices reduce transmission risk

• Post-exposure prophylaxis with hepatitis B vaccine and, when indicated, hepatitis B immunoglobulin can reduce infection after exposure

• Testing and vaccination of household contacts, sexual contacts, and other high-risk persons are important

• Ultrasonography is the first-line imaging study for liver size, parenchymal pattern, splenomegaly, ascites, portal hypertension, and focal liver lesions

• Imaging may be normal or nonspecific in early acute or chronic hepatitis

• Long-standing disease may show chronic liver disease pattern, coarse echotexture, surface nodularity, splenomegaly, collateral vessels, and ascites

• FibroScan / elastography helps noninvasive assessment of fibrosis in chronic HBV

• CT or MRI is used when focal liver lesion, hepatocellular carcinoma, portal vein thrombosis, or other complication is suspected

• Regular ultrasound surveillance is important in chronic HBV patients at risk for hepatocellular carcinoma

Note

• Imaging does not diagnose HBV itself; it assesses liver involvement, fibrosis, portal hypertension, and complications such as HCC:

More info::

• FibroScan interpretation depends on disease context, fasting state, inflammation, cholestasis, congestion, and probe used

• Liver stiffness values below about 10 kPa make advanced chronic liver disease less likely in many settings

• Values around 10–15 kPa may suggest advanced chronic liver disease

• Values ≥15 kPa are strongly suggestive of compensated advanced chronic liver disease

• CAP is the steatosis parameter; higher CAP suggests greater hepatic fat content

Classical HBsAg serotypes:

• adr

• adw

• ayr

• ayw

and they can be further subdivided, but the four major serotypes are the main classic group

Genotype

• HBV genotypes A–J

• They have geographic distribution and may differ in disease course and treatment-related behavior.

These are not exactly “serotypes,” but they are clinically important and worth mentioning in the same section or a small subsection:

• Precore mutation — especially G1896A

• Basal core promoter mutations — especially A1762T / G1764A

• Polymerase mutations related to antiviral resistance such as YMDD motif mutations

• Surface antigen escape / diagnostic escape mutations in selected cases.

• The virus reaches the liver through the bloodstream and preferentially infects hepatocytes

• It may present as acute or chronic infection

• Chronic infection can lead to chronic hepatitis, fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma

• Transmission occurs through blood, sexual contact, and perinatal exposure

• Many patients remain asymptomatic for long periods, especially in chronic infection

• Vaccination is the main preventive measure