Contributed by Anthony J. Demetris, M.D.
PATIENT HISTORY:
Per referral report, the patient is a middle aged Black female. S/P orthotopic liver transplant. Has normal bilirubin, transaminases in the 400s. Caped T-tube for the last 2 weeks and normal angiography. R/O rejection, infection and cholangitis. A recently conducted cholangiogram shows dysparity between the donor and recipient ducts and perhaps some delayed emptying. The patient is being treated with Cyclosporin immunosuppression and it has been difficult to maintain adequate levels. Review of outside material.

Final Diagnosis (Case 82)

ALLOGRAFT LIVER, NEEDLE BIOPSY -
  1. MILD ACUTE CELLULAR REJECTION WITH PROMINENT BILE DUCT DAMAGE AND CENTRAL VENULITIS (RAI 4/9).
  2. DUCTULAR AND CHOLANGIOLAR PROLIFERATION WITH BILIARY EPITHELIAL CELL ATROPHY AND PYKNOSIS, SUGGESTIVE OF BILIARY TRACT OBSTRUCTION OR STRICTURING; BILIARY SLUDGE AND ISCHEMIC CHOLANGITIS SHOULD BE EXCLUDED.
  3. INCREASED DUCTAL DAMAGE AND CENTRILOBULAR HEPATOCELLULAR INFLAMMATION AND DROPOUT IN COMPARISON TO PREVIOUS BIOPSY (BY REPORT).

Previous Biopsies on this Patient:
None

TPIS Related Resources:
Liver Transplant Topics

Gross Description - Case 82

The specimen consists of one (1) consult slide with an accompanying surgical pathology report.

Microscopic Description - Case 82

(1 HE)
The normal lobular architecture is distorted by mild to moderate portal expansion because of fibrosis, and a mild to moderate mixed inflammatory cell infiltrate containing numerous eosinophils, focal ductular and cholangiolar proliferation. No definite portal venulitis is seen, but duct infiltration and damage are easily appreciated. In addition, there is portal edema and two or three of approximately twelve to fourteen portal tracts are devoid of small bile ducts. In addition, ductal atrophy and apoptosis are easily appreciated.

Throughout the lobule, there is mild Kupffer cell hypertrophy and an increased number of acidophilic bodies, but little evidence of lobular disarray. However, there is also zonal centrilobular hepatocellular necrosis and dropout with perivenular mononuclear inflammation. No definite viral inclusions or ground glass cells are seen.

Overall, the histopathological changes suggest that more than one insult is contributing to allograft dysfunction. The portal tract edema and duct and cholangiolar proliferation, along with an increase in acute inflammatory cells is suggestive of biliary tract obstruction or stricturing, as previously suggested. In addition, the marked bile duct damage, increased portal eosinophilia, focal bile duct loss and zonal centrilobular hepatocellular dropout with inflammation and hemorrhage are suggestive of a superimposed acute rejection reaction, which is a new process since the previous biopsy.

Although, I cannot absolutely exclude the possibility of a co- existent hepatitis, rejection and biliary tract pathology appear to be the primary processes at this time.

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