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Hepatitis – Glossary


Acute exacerbation or flare of hepatitis B

intermittent ALT/AST elevations to >10 times the upper limit of normal and more than twice the baseline value in a patient with hepatitis B.

Anti-HBcAg antibody

antibody against the hepatitis B core antigen that emerges during acute infection but does not protect against reinfection. It may be used as a marker of previous HBV infection.

Anti-HBsAg antibody

the protective antibody against the hepatitis B surface antigen that develops after resolution of acute HBV infection and after vaccination.


presence of abnormal proteins (cryoglobulins) in the blood. Cryoglobulins become insoluble at low temperatures. This produces a characteristic rash, and can lead to obstruction of small blood vessels in the fingers and toes in cold weather.

Direct-acting antiviral agent (DAA)

in HCV, a drug such as telaprevir or boceprevir, that directly targets the virus,  as apposed to treatmentslike pegylated interferon (peginterferon) alfa and ribavirin (RBV) that act on the host immune response rather than the virus itself.


a kidney disease involving inflammation of the glomeruli, it may present with haematuria and/or proteinuria or as acute renal failure.

HBeAg seroconversion

emergence of anti-HBe antibodies and loss of detectable HBeAg in a person who was previously HBeAg positive and anti-HBe antibody negative.

HBeAg-negative chronic hepatitis B

this phase may follow HBeAg seroconversion and is characterised by periodic HBV reactivation with fluctuating serum HBV DNA levels, raised aminotransferases and hepatic inflammation.

HBsAg-negative phase

a state characterised by loss of detectable HBsAg or HBV DNA in the blood but presence of detectable HBV DNA in the liver. Loss of HBsAg is associated with reduced risk of cirrhosis, decompensation and hepatocellular carcinoma, but immunosuppression may lead to reactivation.

Hepatitis B core antigen (HBcAg)

an HBV core protein antigen present inside complete virions and infected cells. HBcAg is not detectable in the blood of HBV-infected people, but anti-HBcAg antibodies appear during acute infection.

Hepatitis B e antigen (HBeAg)

a product of HBV infection that usually disappears from the blood after acute infection, but that can sometimes persist in chronic hepatitis B. Patients can be defined as having HBeAg-positive or -negative HBV infection.

Hepatitis B surface antigen (HBsAg)

the surface coat lipoprotein of HBV, which can be present in serum in hepatitis B. Tests for serum HBsAg are used to diagnose HBV infection.

IgM anti-HBcAg antibody

antibody against the hepatitis B core antigen that is detectable for 4–6 months after contracting HBV and that indicates recent infection.

Immune reactive phase

an HBeAg-positive state with lower serum HBV DNA levels than are seen in the immune tolerant phase of HBV infection, with moderate or severe hepatic inflammation (increased or fluctuating aminotransferase levels and more rapid fibrosis progression).

Immune tolerant phase

an early phase of HBV infection characterised by HBeAg positivity, high serum HBV DNA and mild or no hepatic inflammation (normal or low levels of aminotransferases and no or slow progression of fibrosis).

Inactive HBsAg carrier state

persistent HBV infection but with very low or undetectable serum HBV DNA and without significant ongoing hepatic inflammation (normal aminotransferases). May indicate a favourable long-term outcome with low risk of cirrhosis or hepatocellular carcinoma.

Lichen planus

an extremely itchy skin disease of unknown aetiology characterised by the presence of shiny, flat-topped mauve spots on the skin, often occurring on the insides of the wrist.

Lymphocytic sialoadenitis

inflammation of a salivary gland.

Membranous glomerulonephritis

a relatively common type of glomerulonephritis in adults.

Polyarteritis nodosa

a connective tissue disease characterised by the presence of patchy inflammation of arterial walls, or vasculitis. Common manifestations include arthritis, neuritis, asthma, skin rashes, hypertension, kidney failure and fever.

Porphyria cutanea tarda

a condition in which deficiency of an enzyme involved in haem biosynthesis results in enzyme substrate accumulation. This manifests clinically as blistering of light-exposed areas of skin.

Reactivation of hepatitis B

reappearance of active hepatic inflammation in a patient known to have been in the inactive HBsAg carrier state or to have resolved hepatitis B.

Relapse (HBV)

1 log10 IU/mL increase in serum HBV DNA after stopping therapy (confirmed with at least two determinations >4 weeks apart).

Relapse (HCV)

HCV RNA undetectable (<50 IU/mL) at end of treatment but becoming detectable by 24-weeks after therapy was stopped.

Resolved hepatitis B

detectable previous HBV infection without further virological, biochemical or histological evidence of active virus infection or hepatic inflammation.

Sustained virological response (SVR)

HCV RNA undetectable (<50 IU/mL) at 24 weeks after stopping treatment. SVR is generally thought to be equivalent to a ‘cure’ in HCV infection.