Saturday 18 February 2012
The bile duct epithelium shows variable cytologic atypia, consisting of cytoplasmic eosinophilia, increased nuclear:cytoplasmic ratio, nuclear hyperchromasia, uneven nuclear spacing, and in some instances reactive epithelial hyperplasia.
In many of the listed diseases in this table, depletion of ducts may eventually result and is often, but not always, associated with a biliary fibrosis or even biliary cirrhosis.
Nonsuppurative cholangitis may be diffuse, involving the majority of portal tracts (e.g., severe acute cellular rejection), or focal (e.g., early stages of primary biliary cirrhosis).
As in duct paucity, the mechanism is multi-factorial, and relates to host immune responses against infectious agents, auto-antigens, and alloantigens.
Acute viral hepatitis, HCV
Acute viral hepatitis, HEV
Allograft, acute (cellular) rejection
Autoimmune hepatitis (autoimmune cholangitis)
Caroli disease (biliary cyst walls)
Chronic viral hepatitis, HCV
Drug-induced (see Table 5-11)
Graft versus host disease
Human immunodeficiency virus (HIV) (HIV-associated cholangiopathy)
Idiopathic adulthood ductopenia
Paucity of ducts syndrome, syndromatic (Alagille syndrome)
Primary biliary cirrhosis
Primary sclerosing cholangitis (also large ducts)
Recurrent pyogenic cholangiohepatitis (large ducts only)
- acute cholangitis