Recurrent and new hepatitis C virus infection after liver transplantation (original) (raw)
Related papers
Clinical significance of hepatitis C virus (HCV) infection in liver transplant recipients
1994
Hepatitis C virus (HCIO infection was studied in 60 liver transplant recipients. Antibodies to HCV were tested by both a second-generation ELISA test and a four-recombinant immunoblot assay (4-RIBA) just before the transplant and every three months thereafter. HCV RNA detection was performed by polymerase chain reaction (PCR) at least three times after the transplant in all the patients. Thirty-nine patients tested negative by ELISA before LT (group A), 14patients tested positive by both serological tests (group B), and seven tested positive only by ELISA (group C). Posttransplant hepatitis was diagnosed in 11/14 in group B in comparison with 3/39 in group A (P < 0.001) and 1/7 in group C (P < 0.05). HCV RNA was detected in the sera of 14/14 patients in group B but in only 1/7 in group C and 6/39 in group A. Only 2~15patients developed posttransplant hepatitis in the absence of HCV RATA detection. These data suggest that HCV is the major cause of hepatitis after LT. Patients HCV seropositive by RIBA test before the transplant formed a group of high-risk patients for developing viremia and hepatitis afterwards.
Prospective study of hepatitis C virus infection after orthotopic liver transplantation
Transplantation Proceedings, 1997
The aims of this study were to (i) evaluate the prevalence and the incidence of hepatitis C virus (HCV) infection in hemodialysis patients in two different centers in São Paulo (Brazil), (ii) determine the time required to detect HCV infection among these patients by serology or PCR, (iii) establish the importance of alanine aminotransferase determination as a marker of HCV infection, and (iv) identify the HCV genotypes in this population. Serum samples were collected monthly for 1 year from 281 patients admitted to hospital for hemodialysis. Out of 281 patients, 41 patients (14.6%) were HCV positive; six patients seroconverted during this study (incidence = 3.1/1000 person-month). In 1.8% (5/281) of cases, RNA was detected before the appearance of antibodies (up to 5 months), and in 1.1% (3/281) of cases, RNA was the unique marker of HCV infection. The genotypes found were 1a, 1b, 3a, and 4a. The presence of genotype 4a is noteworthy, since it is a rare genotype in Brazil. These data pointed out the high prevalence and incidence of HCV infection at hemodialysis centers in Brazil and showed that routine PCR is fundamental for improving the detection of HCV carriers among patients undergoing hemodialysis.
Liver Transplantation, 2006
The aim of this study was to evaluate how the immunohistochemical detection of liver hepatitis C virus (HCV) antigens (HCV-Ag) could support the histologic diagnosis and influence the clinical management of post-liver transplantation (LT) liver disease. A total of 215 liver specimens from 152 HCV-positive patients with post-LT liver disease were studied. Histologic coding was: hepatitis (126), rejection (34), undefined (24; coexisting rejection grade I and hepatitis), or other (31). The percentage of HCV-Ag infected hepatocytes were evaluated, on frozen sections, by an immunoperoxidase technique. HCV-Ag were detectable early in 57% of cases within 30 days post-LT, 92% of cases between 31 and 180 days, and 74% of cases after more than 180 days. Overall, HCV-Ag were detected more frequently in histologic hepatitis as compared to rejection (P Ͻ 0.0001) with a higher percentage of positive hepatocytes (P Ͻ 0.00001). In 16 patients with a high number of HCV-Ag-positive hepatocytes (65%; range 40-90%) a clinical diagnosis of recurrent hepatitis (RHC) was made despite inconclusive histopathologic diagnosis. Multivariate analysis identified the percentage of HCV-Ag-positive hepatocytes and the time post-LT as independent predictors for RHC (P ϭ 0.008 and P ϭ 0.041, respectively) and the number of HCV-Ag-positive hepatocytes Ն50% as the only independent predictor for nonresponse (P Ͻ 0.001) in 26 patients treated with ␣-interferon plus ribavirin. In conclusion, HCV reinfection occurs early post-LT, reaching its peak within 6 months. Immunohistochemical detection of post-LT HCV reinfection support the diagnosis of hepatitis when the histologic features are not conclusive. A high number of infected cells, independently from the genotype, represents a negative predictive factor of response to antiviral treatment.
Clinical Infectious Diseases, 1998
We designed a prospective study to assess the time course and evolution of hepatitis C virus (HCV) infection in 152 patients who underwent a liver transplantation (LT) in our institution. Forty-four recipients (29%) were infected by HCV after transplantation: 40 who developed recurrent infection after LT and four who acquired infection during or after LT. No differences were found in survival actuarial rates at 1, 2, and 4 years after transplantation for patients infected by HCV vs. noninfected ones. Graft hepatitis occurred in 66% of HCV-infected recipients: 18 developed chronic active hepatitis (10 of them with intense fibrosis) and 2 developed cirrhosis during the follow-up. Infection by the HCV-1b genotype was found in 79% of the infected recipients and in 100% of those in whom histologic evolution was worst. Fourteen grafts were lost in 44 HCV-infected recipients, in comparison with 12 in 108 HCV-negative patients (P Å .007), mostly because of chronic rejection. HCV infection did not affect life expectancy in the midterm follow-up for LT patients. However, it was often associated with the occurrence of early and severe graft hepatitis and with a higher incidence of graft loss due to chronic rejection.
Liver International, 2008
Introduction: The mechanisms by which severe cholestatic hepatitis develops after liver transplantation are not fully understood. Reports on immunohistochemical distribution of hepatitis C virus (HCV) antigens are still scarce, but recently, HCV immunostaining was suggested for early diagnosis of cholestatic forms of recurrent hepatitis C in liver grafts. After purification, Rb246 pab anticore (aa1-68) yielded specific, granular cytoplasmic staining in hepatocytes. Signal amplification through the Envision-Alkaline Phosphatase System avoided endogenous biotin and peroxidase. Aims/Methods: Rb246 was applied to liver samples of explants of 12 transplant recipients, six with the most severe form of post-transplantation recurrence, severe cholestatic hepatitis (group 1) and six with mild recurrence (group 2). We also assessed immuno-reactivity at two time-points post-transplantation (median 4 and 22 months) in both groups. HCV-core Ag was semiquantified from 0 to 31 in each time point. Serum HCV-RNA was also measured on the different time points by branched DNA. Results: In the early post-transplant time point, one patient had a mild staining (11), two patients had a moderate staining (21) and the other three had no staining in group 1, compared with five patients with no staining (0) and one patient with mild staining (11) in group 2. Late post-transplant liver samples were available in nine patients, and two out of four samples in group 1 showed a mild staining, compared with no staining patients in five patients in group 2. Strikingly, on the explant samples, HCV immunostaining was strongly positive in group 1, and mildly positive in group 2. Two out of five samples showed 31 staining, and three samples showed 21 staining in group 1; two out of five samples showed no staining, two samples showed 11 staining and one sample showed 21 staining in group 2. Serum HCV-RNA was significantly higher in group 1, on both time-points posttransplantation. HCV-core Ag was not directly associated with serum HCV-RNA on the different time points. Conclusion: These preliminary results suggest that strong HCV immunostaining in the explant is predictive of more severe disease recurrence. Chronic hepatitis C virus (HCV) infection is the leading indication for liver transplantation, estimated at 35-45% (1). In that population, recurrent infection post-transplantation is almost universal, with a 10-to 20-fold increase in levels of viraemia (2). The majority of transplant recipients will develop histological evidence of disease as a result of recurrent HCV infection, if followed for up to 5 years, with a significant proportion progressing to chronic hepatitis and cirrhosis (3-7). The natural history of HCV infection post-transplantation is now beginning to be delineated, and we have limited understanding of the factors that influence disease progression. After transplantation, the majority of patients evolve to a slowly
Liver transplantation for hepatitis C virus (HCV) non-viremic recipients with HCV viremic donors
American Journal of Transplantation, 2018
The demand for liver transplantation continues to outpace the supply of donor organs in the United States. 1 In the context of this organ shortage, it is essential to make the best use of all transplantable organs. Previously, donor livers infected with hepatitis C virus (HCV) typically have been either discarded or used in patients already infected with HCV. 2-4 Donor livers infected with HCV are still not widely accepted for non-viremic recipients, due to concerns regarding HCV transmission, the natural history of untreated HCV infection after liver transplantation, and limited evidence in this specific population. 5 Highly effective and well-tolerated direct-acting antiviral (DAA) therapies are now available for the treatment of HCV infection and can eliminate HCV in the allograft in greater than 95% of cases. 6 In the setting of the ongoing organ shortage, the opioid epidemic, and the advent of DAA therapy, more HCV-infected donor organs are being utilized to expand the donor pool, and non-viremic patients are being given the option to accept these grafts in some centers, including ours. 4,7,8 The aim of our study was to summarize the posttransplant outcomes after donor-derived HCV infection in non-viremic liver transplant recipients at our institution.