Contributed by Anthony J. Demetris, M.D.
PATIENT HISTORY:
Per referral report, the patient is a 40 year-old female who was transplanted for fulminant hepatitis 3 years ago. The etiology of her original disease was never clarified. Review of outside material.

Final Diagnosis (Case 46)

PART 1: ALLOGRAFT LIVER, NEEDLE BIOPSY -
  1. MODERATE ACUTE CELLULAR REJECTION WITH PROMINENT CENTRAL VENULITIS (RAI 2+2+2=6/9).
  2. NO PREVIOUS BIOPSIES AVAILABLE FOR COMPARISON.
PART 2: ALLOGRAFT LIVER, NEEDLE BIOPSY -
  1. MILD ACUTE CELLULAR REJECTION WITH PROMINENT CENTRAL VENULITIS (RAI 2+1+2=5/9).
  2. SIMILAR OR SLIGHTLY IMPROVED IN COMPARISON TO PREVIOUS BIOPSY.
  3. FOCAL BILE DUCT LOSS IN FOUR OF FOURTEEN (4/14) PORTAL TRIADS.

Previous Biopsies on this Patient:
None

TPIS Related Resources:
Liver Allograft Rejection Grading
Liver Transplant Topics


Gross Description - Case 46


The specimen consists of four (4) consult slides,Part 1, and seven (7) consult slides,Part 2, from Emory University Hospital, 1364 Clifton Road, NE, Atlanta, Georgia 30322 with accompanying surgical pathology reports.


Microscopic Description - Case 46


(Part 1: 2 HE, 1 Trichrome, 1 PAS/D)
The normal lobular architecture is distorted by mild to moderate portal expansion because of fibrosis and a moderate mononuclear inflammatory cell infiltrate. Duct damage is clearly appreciated in half or more of the triads. Focal duct loss may be developing in approximately four of ten triads. There is also mild interface activity.

Throughout the lobules, there is Kupffer cell hypertrophy and occasional acidophilic bodies. Occasional foam cell clusters are also seen. However, the most striking change is the prominent central venulitis with perivenular hepatocellular dropout. No definite viral inclusions or ground glass cells are seen. The PAS/D stain nicely shows the bile duct infiltration and damage, with lymphocytes located inside the basement membrane.

(Part 2: 2 HE, 1 PAS, 1 PAS/D, 1 Iron, 1 Reticulin) The normal lobular architecture is slightly distorted secondary to mild to moderate portal expansion because of mild fibrosis and a mild, predominantly mononuclear inflammatory cell infiltrate. Focal bile duct infiltration and damage are easily seen.

Throughout the lobules, there is Kupffer cell hypertrophy and occasional acidophilic bodies. However, there is little evidence of disarray. The most striking lobular change is the presence of centrilobular hepatocellular inflammation, dropout and hemorrhage. This is associated with a perivenular mononuclear inflammatory cell infiltrate containing lymphocytes, plasma cells and pigmented macrophages. No definite viral inclusions or ground glass cells are seen.

Overall, the histopathologic changes in both biopsies are most consistent with an active cellular rejection with prominent central venulitis. Bile duct damage and focal bile duct loss are also easily seen.


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