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.
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.
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.
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.
emergence of anti-HBe antibodies and loss of detectable HBeAg in a person who was previously HBeAg positive and anti-HBe antibody negative.
this phase may follow HBeAg seroconversion and is characterised by periodic HBV reactivation with ﬂuctuating serum HBV DNA levels, raised aminotransferases and hepatic inflammation.
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.
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.
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.
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.
antibody against the hepatitis B core antigen that is detectable for 4–6 months after contracting HBV and that indicates recent infection.
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).
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).
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.
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.
inflammation of a salivary gland.
a relatively common type of glomerulonephritis in adults.
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.
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.
reappearance of active hepatic inflammation in a patient known to have been in the inactive HBsAg carrier state or to have resolved hepatitis B.
1 log10 IU/mL increase in serum HBV DNA after stopping therapy (confirmed with at least two determinations >4 weeks apart).
HCV RNA undetectable (<50 IU/mL) at end of treatment but becoming detectable by 24-weeks after therapy was stopped.
detectable previous HBV infection without further virological, biochemical or histological evidence of active virus infection or hepatic inflammation.
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.