192 Case reports experienced a histopathologically typical acute rejection episode with marked bile duct injury prior to HCV recurrence, and it is therefore possible that the bile duct injury had, in some way, interfered with the pattern of HCV damage. Third, the use of immunosuppressive agents could have interfered with the immune mediatedor direct cytopathic HCV related injury. This granulomatous bile duct destruction was comparable to the florid duct lesion described as a characteristic feature of PBC and whose presence has recently been used as evidence of PBC recurrence liver grafts6. Because we have shown that such a lesion may also develop as a result of HCV infection in the liver graft of a patient not transplanted for PBC, we believe it should not be considered as the hallmark of PBC. References 1. Lekowitch JH. Sch8 ER, Davis GL et uJ. Pathological diagnosis of chronic hepatitis C: a multicenter comparative study with chronic hepatitis B. Gastroenterology 1993: 104: 595-603. 2. Scheuer PJ. Ashrafzadeh P. Serlock S el aJ. The pathology of hepatitis C. Hepatology 1992: 15: 567-571. 3. Bach N. Thung SN. Schaffner F. The histological features ofchronic hepatitis C and autoimmune chronic hepatitis: a comparative analysis. Hepatology 1992: IS: 572-577. 4. Czaja AJ. Carpenter HA. Sensitivity. specificity, and predictability of biopsy interpretations in chronic hepatitis. Gusrroeritmlogy 199 3: 5. Emile JF, Sebagh M. Feray C et al. The presence of epithelioid granulomas in hepatitis C virus-related cirrhosis. Hum. Pathof. 6. Balan V, Batts KP. Poraykho MK et al. Histological evidencc for recurrence of Primary Biliary Cirrhosis after liver transplantation.