Contributed by Randall G. Lee, M.D.
PATIENT HISTORY: Per referral letter, the patient is a 46-year-old male who was transplanted twice in the Fall of 1995. His primary liver disease was Hepatitis C. The patient has a high titer PCR for Hepatitis C. His transaminase are 7 x normal. Review of outside material.

Final Diagnosis (Case 18)

PART 1: ALLOGRAFT LIVER, NEEDLE BIOPSY (10/31/96) -
  1. CHRONIC HEPATITIS WITH MILD INFLAMMATORY ACTIVITY AND MILD PORTAL FIBROSIS.
  2. NO EVIDENCE OF ACUTE REJECTION.

PART 2: ALLOGRAFT LIVER, NEEDLE BIOPSY (1/21/97) -

  1. CHRONIC HEPATITIS WITH MILD INFLAMMATORY ACTIVITY AND PORTAL-PORTAL BRIDGING FIBROSIS.
  2. MILD CHRONIC BILE DUCT DAMAGE.
  3. NO EVIDENCE OF ACUTE REJECTION.

PART 3: ALLOGRAFT LIVER, WEDGE AND NEEDLE BIOPSY (2/6/97) -

  1. CHRONIC HEPATITIS WITH MILD INFLAMMATORY ACTIVITY AND PORTAL-PORTAL BRIDGING FIBROSIS.
  2. MILD TO MODERATE CHRONIC BILE DUCT DAMAGE.

COMMENT:
Although significant bile duct loss is not noted, the changes of chronic duct injury raise the possibility of early chronic rejection. In some instances, similar duct changes can be associated with chronic hepatitis C, but they are typically focally distributed in that setting. Correlation with liver enzymes (including the GGTP) is necessary.

Previous Biopsies on this Patient:
NONE

TPIS Related Resources:
Liver Allograft Rejection Grading
Liver Transplant Topics


Gross Description - Case 18

The specimen consists of seven (7) consult slides Part 1 (4), Part2 (2) and Part3 (1) with accompanying surgical pathology reports.


Microscopic Description - Case 18

The liver biopsy show progression of chronic hepatitis with the appearance of features suggestive of chronic hepatitis C. There is portal fibrosis and mild inflammatory activity in the initial biopsy together with minimal macrovesicular steatosis. These changes become more pronounced in the second biopsy where early portal to portal bridging fibrosis is identified. Here the inflammatory activity is mild but there is an occasional lymphoid aggregate and mild macrovesicular steatosis, features consistent with chronic hepatis C. In this biopsy occasional sporadic bile ducts appear atrophic and have enlarged darkly staining nuclei. These changes more evident in the final biopsy which demonstrates several angular and dysmorphic duct with densely staining cytoplasm. Because of there uniform distribution in the latter biopsy the possibility of chronic rejection needs to be considered in addition to chronic hepatitis C. Clinical correlation with the gamma glydanile transpeptidase levels would be helpful in further accessing the bile duct injury.


Please mail comments, corrections or suggestions to the TPIS administration at the UPMC.