Contributed by Randall G. Lee, M.D.
PATIENT HISTORY:
Per referral report, the patient is a 48-year-old male. S/P liver transplant, 1994. Rising liver function tests. AST 216; ALT 320; (+) HCV; TB 1.6; APHOS 141 (38-120). Review of outside material.

Final Diagnosis (Case 52)

ALLOGRAFT LIVER, NEEDLE BIOPSY-
  1. BILE DUCT CHANGES WITH DUCTULAR PROLIFERATION AND MIXED PORTAL INFLAMMATION (EXCLUDE BILE DUCT STRICTURE).
  2. CANALICULAR CHOLESTASIS, CHOLESTATIC ROSETTES, AND DIFFUSE HEPATOCYTE SWELLING (see diagnostic comment).
  3. MINIMAL MACROVESICULAR STEATOSIS.

Comment:
The changes in the bile ducts, including atrophy and focal damage, together with the other portal findings raise the possibility of a bile duct stricture or other form of biliary obstruction, and this should be excluded, if clinically indicated, by cholangiography or other means. Such changes may also be an early indication of evolving chronic rejection, although other features to support that diagnosis are not seen. The history of HCV in conjunction with the hepatocyte swelling also prompts consideration of a fibrosing cholestatic form of recurrent Hepatitis C.

Previous Biopsies on this Patient:
None

TPIS Related Resources:
Liver Allograft Rejection Grading
Liver Transplant Topics


Gross Description - Case 52


The specimen consists of five (5) consult slides with an accompanying surgical pathology report.


Microscopic Description - Case 52


The liver biopsy shows intact hepatic architecture with slight fibrosis and expansion of the portal tracts. The portal tracts demonstrate atrophic bile ducts with loss in a rare portal tract. There is a mixed inflammatory infiltrate including neutrophils, focal lymphocytes and rare eosinophils. Subendothelial infiltration is not seen, and lymphocytic duct damage is not a prominent feature. The hepatocytes are swollen and there is foci of canalicular cholestasis with cholestatic rosetting of liver cells. Lobular inflammation is minimal other than an occasional neutrophil and a rare focal necrosis. No viral inclusions are identified and no central venulitis is seen.

Overall, the changes suggest an ongoing cholestatic process. Given the portal alterations, a bile duct problem should initially be excluded and the possibility of early chronic rejection or an evolving fibrosing cholestatic hepatitis C can also be considered.


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