Sclerosing cholangitis following severe trauma: Description of a remarkable disease entity with emphasis on possible pathophysiologic mechanisms

Figure 1 A: Liver function tests of patient 3 in the first month showing the strong increase of cholestasis followed by a milder rise of aminotransferases; B: Long-time course of AP (red) and ALT (black) of all patients showing the initial strong increase of AP with a subsequent slow decrease and only a mild initial rise of ALT with nearly normal values in the long term.

Figure 2 MRT of patient 2 (T1-weighted after contrast medium) showing an area centrally in the liver with reduced signal intensity, a dilatation of the bile duct in segment 6, and splenomegaly.

Figure 3 ERCP of patient 3 showing a normal cystic and common bile duct, but multifocal short strictures and dilatations of the intrahepatic bile ducts (4 mo after occurrence of cholestasis).

Figure 4 Liver histology of patient 4 (13 mo after occurrence of cholestasis). A: Portal inflammation, severe cholestasis with bile thrombi, HE (20x); B: Lymphocytic infiltration of a small bile duct (arrow). Periodic acid Schiff’s reaction after treatment with diastase (100x); C: Immunostaining for cytokeratin 7. Regenerative bile duct proliferations show a strong expression of cytokeratin 7 (25x).