Consult Report - Case 30
Contributed by Anthony
Demetris, M.D.
PATIENT HISTORY:
Per referral letter, the patient is a 57-year-old Saudi male with
end stage liver disease due to Hepatitis B who was transplanted
on 12/2/96. He has had good liver functions until quite
recently. He developed a persistent fever which has defied every
work up. He has been cultured from every site, scanned from head
to toe, surgically explored, and biopsied in multiple locations.
An excisional biopsy of a supraclavicular lymph node turned out
to be a localized area of necrosis within the subcutaneous
tissue. There is no real granuloma formation or evidence of a
pre-existing lymph node. All cultures have been negative. No
evidence of PTLD. He has been imperically treated with numerous
antibiotics, anti-fungal agents, and anti-tuberculous agents--all
without result. Currently, his serum chemistries are TB 15.9; AP
255; GGT 345; AST 340; ALT 276, ALB 2.9; PT 13.8. His
immunosuppression has been discontinued. Review of outside
material for followup.
Final Diagnosis (Case 30) [D982-97]
ALLOGRAFT LIVER, NEEDLE BIOPSY -
- TREATED ACUTE (CELLULAR) REJECTION, CURRENTLY, NO
SIGNIFICANT ACTIVITY.
- LESS INFLAMMATION AND NECROSIS IN COMPARISON TO MOST
RECENT PREVIOUS BIOPSY (OSSL#D808-97).
- BILE DUCT LOSS IN TWO OF FOUR (2/4) SMALL PORTAL TRIADS AND
BILIARY EPITHELIAL ATROPHY, SUGGESTIVE, BUT NOT DIAGNOSTIC
OF THE EARLIEST PHASES OF CHRONIC REJECTION (see microscopic
description).
Previous Biopsies on this Patient:
]D808-97]
TPIS Related Resources:
Liver Allograft Rejection Grading
Liver Transplant Topics
Gross Description - Case 30 [D982-97]
The specimen consists of two (2) consult slides labeled D982-97. No surgical pathology
report is received with the specimen.
Microscopic Description - Case 30 [D982-97]
The normal lobular architecture is intact, but the biopsy is
small and fragmented. Four small and one large portal tract are
identified. Approximately three of the portal triads are either
devoid of bile ducts or contain very small atrophic biliary
epithelial cells. There is no significant portal inflammatory
cell infiltrate, but the portal tract connective tissue appears
slightly collagenized.
Throughout the lobules, there is Kupffer cell hypertrophy,
thickening of the plates, regenerative change, mild perivenular
sclerosis and perivenular hepatocellular swelling. No definite
viral inclusions or ground glass cells are seen.
Compared to the most recent previous biopsy (OSSL# D808-97),
there has been a decrease in the portal and perivenular
inflammation and there is less hepatocellular necrosis and
dropout.
Overall, the histopathological changes are most consistent with a
treated acute rejection, which has improved since the previous
sampling. Even though the number of portal triads sampled is
small, the loss of bile ducts in two and atrophic changes into
others are suggestive, but not diagnostic of the earliest
features of chronic rejection. If duct damage and loss is a
widespread process it should be clinically manifest by
disproportionate elevations of the gamma glutamyltranspeptidase
and alkaline phosphatase. Rebiopsy to examine more portal triads
would help to substantiate the presence of ductopenia.
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TPIS administration at the UPMC.
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