Post renal transplant/HCV induced Fibrosing Cholestatic Hepatitis A series of three cases Authors :Sheefa Khan1 , Puja Sakhuja1, Ranjana Gondal1,Shiv K Sarin2 Institution : 1 - G.B..Pant, Delhi, 2 - ILBS, Delhi. Fibrosing cholestatic hepatitis (FCH) has recently been described after solid organ transplantation in patients with hepatitis C virus (HCV) infection. Fibrosing cholestatic hepatitis (FCH) is a severe and progressive form of liver dysfunction seen in organ transplant recipients infected with hepatitis B virus or hepatitis C virus (HCV) and has been attributed to cytopathic liver injury. Clinicians should remain vigilant for FCH in this clinical setting and consider antiviral treatment. We present a series of three cases of post renal transplant/HCV induced fibrosing cholestatic hepatitis . Background Aims Three patients underwent cadaveric renal transplantation for end-stage renal disease. The time intervals between transplant and the biopsy diagnosis of FCH for the three patients were 7 months, 1 year and 5 years. All 3 patients presented with jaundice, hyperbilirubinemia, and mild to moderate elevations in AST/ALT and alkaline phosphatase. All 3 patients were detected HCV positive. Biopsy was performed and a diagnosis of FCH was made on histopathological findings Case report Case1 Case 2 Case 3 Age (yrs)/Sex 49/M 34/M 56/M Bilirubin (mg/dl) 25.8 8.2 15.8 6.4 8 17.6 AST/ALT (IU/l) 97/ 77 88/ 56 44/ 42 33/ 17 162/ 115 302/ 197 Alk.Phosphatase (IU(/l) 545 207 641 576 200 221 HBsAg -ve Anti-HCV +ve HCV RNA (IU/ml) 1.86×108 High >107 Architectural distortion Portal tracts – Moderate to marked expansion Cholestasis associated changes: Bile ductular proliferation, biliary pigment, ballooning degeneration, feathery degeneration Minimal to mild inflammatory infiltrate consisting of lymphocytes and neutrophils, On Masson's Trichrome stain marked fibrosis: Portal, periportal, perisinusoidal, diffuse. Case 1A.20x.HE Case 1B.10x.MT Case 1C.10x.MT Microscopy Case report Case 2A.20x.HE Case 2B.10x.MT Case 2C.10x.MT Case 3A.10x.HE Case 3B.10x.MT Case 3C.10x.MT HCV infection is an important cause of liver disease after renal transplant, but its influence on long-term graft and patient survival is still unclear. Currently, it is accepted that patients with HCV infection develop biochemical liver abnormalities more frequently than HCV(-) patients (1). FCH has only been described in immunosupressed patients (with HIV, bone marrow and solid organ transplants) with chronic hepatitis C or B.FCH has been postulated to result from unimpeded viral replication within hepatocytes culminating in direct cytopathic effect in the setting of immunosupression.2 FCH has a very poor prognosis with rapid progression to hepatic failure and death within months of diagnosis. 1. Medical literature regarding the most optimal theraeutic approach in FCH is still limited. The viral cytopathic effect offers a rationale for the use of anti viral agents to treat this condition, however the role of antiviral treatment still remains unclear.3 Discussion When cholestatic and/or hepatic deterioration develops in an HCV-infected organ allograft recipient, the diagnosis of FCH should be considered in order to institute prompt and appropriate therapy. Liver biopsy has an important role in diagnosis of FCH. Conclusion 1.Fibrosing Cholestatic hepatitis in hepatitis C virus-infected renal transplant recipients. Bustillo EM, Ibarrola C, COLINA F, Castellano G, Fuertes A, Andres A, Aguado JM, Rodicio JL, and Morales JM. Departments of Nephrology, Pathology, Gastroenterology, Microbiology and ‘Infectious Diseases, ial Transplant lO[Suppl I 1: 58-67, 1995. 2. Hepatitis C infection and post-transplantation liver disease. Transplant Unit, Hospital 12 de Octubre, Madrid, Spain. Pereira BIG: Nephrol . 3.Fatal hepatitis C associated fibrosing cholestatic hepatitis as a complication of cyclophosphamide and corticosteroid treatment of active glomerulonephritis. Saleh F, Ko HH, Davis JE, Apiratpracha W, Powell JJ, Erb SR, Yoshida EM. Annals of Hepatology 2007;6(3):July-September:186-189. References