L. Baiocchi et al., HEPATIC STEATOSIS - A SPECIFIC SIGN OF HEPATITIS-C REINFECTION AFTER LIVER-TRANSPLANTATION, Liver transplantation and surgery, 4(6), 1998, pp. 441-447
Hepatitis C virus (HCV) infection is one of the major causes leading t
o orthotopic liver transplantation (OLT) worldwide, Although viral inf
ection persists in almost all patients, the pathology of recurrent HCV
infection after OLT is not well characterized. To address this issue,
we compared the pathological findings of 28 patients who underwent tr
ansplantation for HCV-related cirrhosis (group A, aged 47 +/- 15 years
; 23 men, 5 women) with those of 21 patients who underwent transplanta
tion for nonviral indications (group B, aged 45 +/- 21 years; 13 men;
8 women) during the first year after transplantation, Patients from gr
oup A were assessed for serum HCV RNA by 5' untranslated region nested
polymerase chain reaction before and 1 year after OLT. Patients under
went protocol liver biopsies 3 months and 1 year after transplantation
. Group A patients more frequently had histological evidence of hepati
c steatosis than group B patients, both at 3 months (P = .003) and 1 y
ear (P = .003) after OLT. Fibrosis and portal inflammation were statis
tically more frequent in group A 1 year after transplantation. The sen
sitivity of steatosis in detecting histological disease recurrence was
100% at 3 months and 94% at 1 year; the specificity was 40% and 60%,
respectively. Conversely, steatosis was 100% specific in detecting vir
al recurrence, with a sensitivity of 89%, The 1-year actuarial inciden
ce of abnormal transaminase levels was 52% in group A and 13% in group
B (P = .05). No biochemical or histological differences between patie
nts infected with genotype 1b and patients with other HCV genotypes we
re found. Hepatic steatosis is a specific sign of viral recurrence aft
er liver transplantation and a less specific sign of disease recurrenc
e. HCV-infected liver transplant recipients often develop abnormal tra
nsaminase levels and liver fibrosis 1 year after OLT; these features a
re unrelated to HCV genotypes, (C) 1998 by the American Association fo
r the Study of Liver Diseases.