Chronic active hepatitis (CAH) |
Piecemeal necrosis defined as the destruction of liver cells at the interface between parenchyma and connective tissue with a predominantly mononuclear inflammatory infiltrate. Aggregation of lymphocytes and macrophages surrounds the hepatocytes with a spreading wave of necrosis. As the liver parenchyma is destroyed, sheets of connective tissue are laid down, which initially contain an inflammatory infiltrate resulting in a “maple leaf” configuration to the portal tract. |
Chronic persistent hepatitis (CPH) |
CPH is characterized by chronic inflammatory infiltration of portal tracts with preserved lobular architecture and little or no portal fibrosis with expanded tracts. There is no significant piecemeal necrosis. CPH disease is mostly stationary and in many instances resolves spontaneously, far more frequently than CAH. |
Hepatomegaly |
Defined clinically as a palpable liver and usually, but not always, confirmed by ultrasound or CT scanning or at post mortem. |
Lipoid hepatitis |
A combination of CAH with LE cell phenomena. May be distinguished from SLE by the absence of antibodies to double stranded DNA. |
Nodular regenerative hyperplasia of the liver |
Characterized by diffuse nodularity of the liver with little or no fibrosis and has been found in association with autoimmune disease, drug treatment, and a variety of hematological disorders. |
Primary biliary cirrhosis |
PBC is an autoimmune inflammatory disorder associated with a high serum titer of anti-mitochondrial antibodies. Histological appearance is divided into four stages: |
(I) florid bile-duct lesions with lymphoid aggregates |
(II) ductular proliferation |
(III) scarring (septal fibrosis and bridging) |
(IV) cirrhosis |
Primary sclerosing cholangitis |
A chronic inflammatory disorder with fibrosis and obliteration of the bile ducts. It is strongly associated with inflammatory bowel. |