Liver Transplantation For HCV-related Cirrhosis Research Articles

Recent controversies in liver transplantation

The chronicle backdrop of liver transplantation (LT) is an intricate story to reveal- it is an adventure of extraordinary achievement and catastrophic disappointments. Historically, controversies and LT seems to be synonymous.
 Despite the improvements in results, LT is still facing lots of challenges and controversies, whereby demand is high but the resources, primarily concerned to donor, are very limited.
 We have focused our perspective on LT for HCV-related cirrhosis and nutritional support for cachectic patients awaiting LT.

High sustained virological response to pegylated interferon and ribavirin for recurrent genotype 3 hepatitis C infection post-liver transplantation.

Treatment outcomes of recurrent HCV genotype 3 (GT-3) after liver transplantation (LT) are ill-defined. To determine efficacy, predictors, and long-term survival after treatment of recurrent HCV GT-3 infection, post-LT, with a combination of pegylated interferon (PEG) and ribavirin (RBV). We studied all LT recipients (LTR) in our program treated with PEG and RBV for recurrent HCV GT-3 between Jan 1st 2002 and Dec 31st 2013. Antiviral therapy (AVT) was started if histology showed recurrent HCV with ≥ stage 2 fibrosis. Treatment was intended for 24 or 36 weeks, depending on early virologic response, and/or 24 weeks consolidation. Primary endpoint was sustained virological response (SVR). We also studied predictors of SVR and long-term patient survival. Among 492 LT for HCV-related cirrhosis and/or hepatocellular carcinoma performed during the study period, 110 (22%) had HCV GT-3 infection. Fifty-two (10.5%) HCV GT-3 patients had indications for AVT. Six were unable to complete the AVT, three because of clinical decompensation and one each because of metastatic disease involving the brain, lung cancer, and ductopenic rejection. Forty-seven (90%) patients achieved early virological response (EVR) and 37 (71%) achieved SVR. Predictors of SVR were EVR (p < 0.001), stage ≤ 3 fibrosis (p = 0.008), and 36 weeks treatment duration (p < 0.001). Less advanced fibrosis ≤ 3 was independent predictor of SVR (OR 0.18, 95% CI 0.05-0.67). SVR patients had actuarial (Kaplan-Meier) 1, 3, and 10 year post-treatment survival of 100, 100, and 95%, compared with 87, 78, and 20% for non-SVR patients (p < 0.001, log rank test). Efficacy of AVT for recurrent HCV GT-3 post-LT is high, and comparable with that for non-transplant patients. Less advanced fibrosis is an independent predictor of SVR. SVR improves long-term survival.

CC Genotype at rs12979860 of IL28B Is Associated With Lower Risk of New-onset Diabetes After Transplantation in Adult Patients With Liver Transplantation for Hepatitis C Cirrhosis

IntroductionNew-onset diabetes mellitus after transplantation (NODAT) in patients undergoing liver transplantation (LT) for hepatitis C virus (HCV)-related cirrhosis is associated with more aggressive HCV recurrence on the graft, rapid progression of fibrosis, and lower rate of sustained viral response to antiviral therapy. The CC genotype at rs12979860 of the IL28B is associated with greater rates of spontaneous clearance of HCV and response to antiviral therapy. IL28B acts on the interferon-stimulated genes through the JAK-STAT pathway, which is related to the development of insulin resistance. The aim of this study was to investigate whether IL28B rs12979860 polymorphism is associated with the development of NODAT after LT for cirrhosis owing to HCV infection. MethodsWe analyzed 99 patients (age, 52.7 ± 9.4 years; 70% male) who underwent LT for HCV-related cirrhosis, with ≥1 year of follow-up and with available DNA sample. NODAT was defined starting from the sixth month after LT, according to the international consensus guidelines. Genotyping was carried out by real-time polymerase chain reaction and analysis of the melting temperature with the LightCycler 480 system. ResultsTwenty-eight patients (28.3%) developed NODAT. CC genotype at rs12979860 of IL28B was associated with a lesser incidence of NODAT versus non-CC genotypes (P = .05; odds ratio, 0.31; 95% CI, 0.11–0.92). We did not find any association between NODAT and age at transplantation, gender, pretransplant body mass index, presence of hepatocellular carcinoma, type of initial immunosuppression (cyclosporine, tacrolimus or corticosteroids) or acute rejection treated with steroids. ConclusionThe CC genotype at rs12979860 of IL28B is a protective factor for NODAT in patients with LT for HCV-related cirrhosis.

Management of Hepatitis C Virus Infection in Liver Transplantation with Adacolumn Apheresis

Recurrent hepatitis C virus (HCV) is a major cause of liver transplant loss, hepatic failure, and retransplantation need. Posttransplantation antiviral therapy in patients with evidence of recurrent disease is the mainstay of management. Although HCV is a hepatocellular pathogen, there is increasing evidence that the virus can infect and persist in other cells. In particular, granulocytes and monocytes/macrophages are known to constitute extrahepatic sites for HCV replication and dissemination. The aim of this study was to apply Adacolumn apheresis as a possible therapeutic alternative to conventional drug therapy to manage HCV infections. Seven patients who underwent liver transplantation for HCV-related cirrhosis were eligible for the study. The patients underwent 5 1-hour sessions for 5 consecutive days. The first treatment was performed in the anhepatic phase of liver transplantation with the intent to early reduce infected granulocytes and monocytes/macrophages. The patients were evaluated over the 5 days after inclusion with 3- and 6-months follow-ups. Early apheresis treatments in the anhepatic phase and over the following 4 days after transplantation produced low viral loads in 4 patients, negative viral loads in 2 patients, and increased viremia in 1 patient. At follow-up, the viremia load was stable in 6 patients without increased transaminase levels. At the end of the treatment cycle, almost all immune cells of the 6 patients maintained CD4+/CD8+ T-cell ratios. The optimal timing of treatment initiation is unknown, but early preemptive therapy is recommended to decrease the risk for recurrent infection. Although this study investigated the responses among a small number of patients, it documented that the Adacolumn changed cellular immunity, promoting early virologic responses.

Characterization of the Cross-Neutralizing Antibody Response Against Hepatitis C Virus in the Liver Transplantation Setting

Neutralizing antibody (nAb) activity during the course of natural infection is believed to be crucial to combating virus propagation. The aim of this study was to measure the impact of nAb response on HCV early kinetics and genetic evolution in the liver transplantation (LT) setting. A cohort of 28 patients undergoing LT for HCV-related cirrhosis was included in the study. Viral load, nAb titers and hypervariable region 1 (HVR1) sequences were determined in serum samples obtained before and at different time points after LT. Serum nAb titers were assessed using HCV pseudoparticles (HCVpp). HVR1 sequences were obtained by direct sequencing. Patients were classified according to viral kinetic patterns (plateau or increasing), during the first week after LT. All patients demonstrated high titers of nAbs before LT, although this was not associated with early kinetic patterns or HVR1 evolution during the first week after LT. We found that in patients with plateau HCV early kinetics, the virus required adaptive mutations, while in those with increasing viral loads, the HVR1 region remained largely conserved (p = 0.015). These data suggest that HCV adaptation via selection of the best-fitted variants may account for early viral kinetics following LT.

S1004 Month 4 Post-OLT Liver Biopsy Accurately Predicts Subsequent Fibrosis in Those Undergoing Orthotopic Liver Transplantation for HCV-Related Cirrhosis

HCVrelated end stage liver disease is the most common indication for OLT in the US. There is evidence that HCV-related fibrosis is accelerated post OLT leading to poorer survival compared to other etiologies. Our AIM was to identify factors in hepatitis C patients undergoing OLT that predict accelerated fibrosis 1 year post OLT. METHODS: Retrospective single center review of patients undergoing OLT due to HCVrelated cirrhosis from 2001 to 2008. Donor variables included age,gender,BMI,race,ETOH use,positive toxicology screen,presence of anti-HCV or anti-HBV, graft steatosis/fibrosis,CMV status,perfusion solution,organ procurement location, cold and warm ischemia time,sodium,creatinine,total bilirubin,aminotransferase levels. Recipient variables included age,race,gender,BMI,post OLT ICU duration,MELD score,prior ETOH abuse, presence of HCC,immunosuppression regimen,HCV genotype/viral load,lack of SVR,CMV status,pre-OLT TIPS,pre-OLT encephalopathy stage III-IV, pre-OLT ascites, post-OLT prolonged mechanical ventilation, post-OLT hypotension requiring pressors,ALT,Alk Phos,TB, ERCP post OLT,hyperglycemia post OLT,creatinine post OLT, rejection episodes, tacrolimus levels, and liver biopsy fibrosis stage scored by Metavir at month 4,and years 1-4 post OLT. Data were analyzed using Chi Square test, Fisher's Exact test and t-tests. The probit-normal model for correlated data and ordinal outcome was used to analyze repeated measures of fibrosis stage as the dependent variable with patient as a random effect. In both sets of analyses, adjustment for year 1 through 4 was also performed and year effect was evaluated.RESULTS: 114 HCV patients (mean ± SEM) age 52 ± 0.3 yrs, BMI 28 ± 0.5, MELD 16 ± 1, 77% male, 87% Caucasian underwent OLT with follow up liver biopsies available for review. Immunosuppression: ATG induction and tacrolimus monotherapy. Only the presence of month 4 fibrosis predicted fibrosis progression during years 1-4 post OLT by probit-normal (estimate 0.911 fibrosis units; p=0.004) and cumulative ordinal logistic regression (estimate 0.864 fibrosis units; p= 0.002). Specific year post OLT was not a predictor of later fibrosis. The interaction between month 4 fibrosis and year fibrosis was not significant. Conclusions:In HCV patients undergoing OLT, month 4 liver biopsy fibrosis level accurately predicts subsequent fibrosis. Those with stage 1-2 fibrosis at month 4 may be candidates for treatment of HCV to prevent further fibrosis progression.

Antiviral treatment in patients with hepatitis C virus-related cirrhosis awaiting liver transplantation

End stage liver disease due to hepatitis C virus (HCV) infection is the most common indication for liver transplantation (LT) worldwide. Regretfully, infection of the graft by HCV occurs almost universally after LT, causing chronic hepatitis and early progression to cirrhosis in a significant proportion of recipients. Moreover, graft and patient survival are significantly worse in patients undergoing LT for HCV-related cirrhosis than in those transplanted for other indications. Therefore, many LT centers consider antiviral treatment with interferon and ribavirin the mainstay of managing recurrent HCV disease in LT recipients. The optimal time to start treatment is unclear. In most instances, treatment is initiated when histological evidence of disease recurrence, either at protocol or on-demand liver biopsies, is observed after LT. However, antiviral treatment initiated before LT is a potential option for some patients for two reasons: first, clearing or suppressing HCV before LT may reduce or eliminate the risk of recurrent hepatitis C in the transplanted liver and thereby improve survival; second, clearing HCV in cirrhotic patient may halt disease progression and avoid the need for transplantation. In this article, the results obtained by pre-transplant antiviral regimens administered to HCV-positive cirrhotic patients awaiting LT are discussed.

Ferroportin-1 in the recurrence of hepatic iron overload after liver transplantation

Hepatic siderosis is frequent in patients with Hepatitis C virus (HCV) chronic hepatitis and considered secondary to advanced liver disease when detected in the explanted liver of cirrhotic patients submitted to transplantation. Here, we document the early recurrence of hepatic iron overload starting from host Kupffer cells and later involving hepatocytes in an Italian male submitted to liver transplantation for HCV-related cirrhosis, whose hemosiderosis was interpreted as related to a primary defect of iron handling by monocytic cells due to decreased Ferroportin-1 expression. He was negative for HFE mutations, had normal liver function, did not drink alcohol and had no erythropoietic defect. He was positive for the (CGG)(8/9) and the IVS1 -24 G>C Ferroportin-1 polymorphisms, associated with non-parenchymal iron overload, and had decreased Ferroportin-1 expression in monocytes. In conclusion, this case report documents the recurrence of progressive liver siderosis, which recalls Ferroportin disease, associated with decreased Ferroportin-1 expression in host monocytes repopulating the donor liver.

Hepatitis C Virus-Infected Donors in Liver Transplantation

Preliminary findings suggest that hepatitis C virus (HCV)-infected liver transplant recipients receiving livers from HCV-infected donors may have a slower rate of fibrosis progression at 1 year. According to a case-control study presented May 20, 2007 at Digestive Disease Week 2007 in Washington, DC, a trend was seen in survival advantage for those receiving HCV-positive donor grafts compared with standard donor controls. “The use of HCV positive donors may be considered as a first line therapy to increase the available donor pool of organs in those undergoing orthoptic liver transplantation for HCV-related cirrhosis,” say researchers led by Paul Y. Kwo, Associate Professor of Medicine in the Division of Digestive Diseases at Indiana University School of Medicine in Indianapolis. This study utilized a case-control design to compare transplant outcomes for 38 recipients of livers from HCV-infected donors with those for 76 standard, nonextended criteria (ECD) donors (1 case/2 controls). Data were extracted from the transplant center registry, UNOS data, and the original on-site donor data chart. Thirty percent of all donors met non-ECD criteria (standard donors) and were included as potential matches for the case-control study. Each HCV-positive liver donor recipient was matched with 2 standard donor recipients as matched standard donor controls (MSDC) by (1) recipient age ± 10 years; (2) primary diagnosis; (3) cancer stage for those with hepatocellular carcinoma; (4) recipient Model for End-Stage Liver Disease score ± 5; and (5) donor age ± 10 years. Outcomes included graft and patient survival at 3 months, 1 year, and 2 years; perioperative death; and HCV recurrence by 4-month and 1-year fibrosis (F0–F4). The HCV donor and MSDC groups did not differ for recipient or donor demographics or in cold and warm ischemia times. Survival results and fibrosis progression are shown in Table 1. Median follow-up time was 36 months. Kaplan–Meier actuarial survival demonstrated improved graft survival for HCV-infected donors with a trend toward significance (P = .10).Tabled 1Hepatitis C-infected donorMatched standard donor controls (MSDC)n-value*TOTALn = 38n = 7690-day survival Graft37/38 (97.4%)72/76 (94.7%)NS Patient37/38 (97.4%)72/76 (94.7%)NS1-year survival Graft30/31 (96.8%)62/72 (86.1%)NS Patient31/31 (96.8%)63/72 (87.5%)NS2-year survival Graft16/19 (84.2%)49/62 (79.0%)NS Patient17/19 (84.2%)52/62 (83.9%)NSGraft loss within 7 days1/38 (2.6%)1/76 (1.3%)NSMean fibrosis at 4 months (F0–F4)0.680.330.08Mean fibrosis at 12 months (F0–F4).0861.05NSPercent change in fibrosis26%69% Open table in a new tab

Mild donor liver steatosis has no impact on hepatitis C virus fibrosis progression following liver transplantation

This study examines the impact of donor liver macrovesicular steatosis on recurrence of hepatitis C virus (HCV) disease after liver transplantation. Between 1998 and 2004, 113 patients underwent liver transplantation for HCV-related cirrhosis. Time to histologic recurrence (fibrosis score >or=2) was the primary endpoint of the study. Recurrence was graded according to the system of Ludwig and Batts. A Cox's proportional hazard regression model was used to analyse the association between donor liver steatosis and HCV recurrence. Recurrence-free survival for patients who received steatotic grafts was 82% and 47% at 1 and 4 years, respectively, and 81% and 52% for patients who received a non-steatotic liver. Donor macrovesicular steatosis (5-45%) was found to have no impact on HCV recurrence (P=0.47). Donor age (P=0.02) and cold ischaemia time (P=0.01) were found to increase the relative risk of HCV recurrence. The estimated risk of HCV recurrence increased by 23% for every 10-year increase in donor age. Similarly the risk of recurrence increased by 13% for every 1-h increase in cold ischaemia time. Mild-moderate donor liver macrovesicular steatosis has no impact on HCV recurrence after liver transplantation for HCV-related cirrhosis. Cold ischaemia time and donor age increased the likelihood of HCV recurrence.

Efficacy of Antiviral Therapy on Hepatitis C Recurrence After Liver Transplantation: A Randomized Controlled Study

Recurrence of hepatitis C virus (HCV) infection is a relevant problem of liver transplantation programs. We evaluated the effect of antiviral therapy on disease progression in 81 HCV-infected liver transplantation recipients. Patients with mild hepatitis C recurrence (fibrosis stage F0 to F2, n = 54) were randomized to no treatment (group A, n = 27) or peginterferon alfa-2b/ribavirin for 48 weeks (group B, n = 27). Patients with severe recurrence (F3 to F4, cholestatic hepatitis) were treated (group C, n = 27). All patients (n = 81) underwent a liver biopsy at baseline and after follow-up; paired hepatic venous pressure gradient (HVPG) measurements were available in 51 patients. Thirteen (48%) patients of group B and 5 (18.5%) of group C achieved sustained virological response. Liver fibrosis progressed > or =1 stage in 40 (49%) of 81 patients: 19 (70%) of group A versus 7 (26%) of group B (P = .001) and in 14 (54%) of group C. HVPG increased (6.5 to 13 mm Hg, P < .01) in patients in whom fibrosis worsened, whereas it decreased (5 to 3.5 mm Hg, P = .017) or remained unchanged in those with fibrosis improvement or stabilization, respectively. The only variable independently associated with fibrosis improvement/stabilization was treatment (odds ratio [OR] =3.7, 95% confidence interval [CI] 1.3 to 10, P = .009). Among treated patients, alanine aminotransferase (ALT) normalization and viral clearance were independently associated with histological or hemodynamic improvement/stabilization (OR 5.3, 95% CI 1.5 to 18, P < .01; OR 7.4, 95% CI 1.4 to 38, P = .01; respectively). Our data demonstrate that in liver transplantation recipients, antiviral therapy slows disease progression (particularly in sustained virological responders), as shown by its effects on liver histology and on HVPG.

Liver transplantation for HCV‐related cirrhosis in a patient with gastric mucosa‐associated lymphoma (MALToma) pretreated with rituximab

End-stage liver disease due to chronic hepatitis C virus (HCV) infection is now the most frequent indication for liver transplantation. HCV infection is associated with extrahepatic disease including cryoglobulinemia and lymphoma. The number of patients requiring liver transplantation (LT) for cirrhosis secondary to HCV infection has increased over the past 10 years; consequently, associated extrahepatic manifestations (in particular hematological malignancies) will be more commonly observed in this patient group. The management of patients with both end-stage liver disease and significant HCV-related extrahepatic disease is undefined. We report a 59-year-old man in whom extranodal marginal-zone B-cell lymphoma arising in gastric mucosa-associated lymphoid tissue (MALToma) was successfully eradicated by rituximab administration and gastrectomy at LT for HCV-related cirrhosis. Our experience with rituximab in this patient suggests that it can be used safely in the setting of severe liver disease due to HCV infection. Rituximab may be useful in preventing progression of NHL until surgical extirpation is possible.

Prevention and treatment of HCV recurrence after liver transplantation

Prevention and treatment of HCV recurrence after liver transplantation

129 CMV infection and biliary tract complications are related with a poor outcome of liver transplantation for HCV-related cirrhosis

129 CMV infection and biliary tract complications are related with a poor outcome of liver transplantation for HCV-related cirrhosis

Hepatitis C virus kinetics during and immediately after liver transplantation

The study of hepatitis C virus (HCV) kinetics after liver transplantation (LT) might be important to design strategies to prevent HCV infection of the graft. We analyzed HCV kinetics during and immediately after LT in 20 consecutive patients undergoing LT for HCV-related cirrhosis. HCV RNA was quantified in blood samples obtained at regular intervals before, during, and after transplantation. HCV-RNA concentrations decreased in 18 of 20 patients during the anhepatic phase (mean decay slope −0.92, mean HCV elimination half-life 2.2 hours). We found a significant correlation between the HCV viral load decay and the blood loss during the anhepatic phase, indicating that the observed HCV clearance rates are maximum estimates. In fact, in 1 patient with an unusually long anhepatic phase of 20 hours and with minimum blood loss, the HCV elimination half-life was 10.3 hours. Eight to 24 hours after graft reperfusion a sharp decrease in HCV viral load occurred in 19 patients (mean decay slope −0.34, mean HCV elimination half-life 3.44 hours). HCV RNA became undetectable in only 1 patient. During the following days, HCV-RNA concentrations increased rapidly in 10 patients (mean HCV doubling time 13.8 hours), remained at similar levels in 4, and continued to decrease in 6. The only variable associated with a second-phase viral load decay was the absence of corticosteroids as part of the immunosuppressive regimen. In conclusion, a sharp decrease in HCV viral load occurs during the anhepatic phase and immediately after graft reperfusion, most likely owing to a lack of virion production and hepatic viral clearance. HCV infection of the graft, however, is an extremely dynamic process and viral replication begins a few hours after LT. (HEPATOLOGY 2002;35:680-687.)

Hepatitis C Virus Genomic Variability in Untreated and Immunosuppressed Patients

To investigate whether immune pressure enhances the genetic diversity of the hepatitis C virus (HCV) hypervariable region 1, nucleotide sequences were compared in multiple sera, collected longitudinally, from three untreated patients and four patients undergoing liver transplantation for HCV-related cirrhosis. A minor variant became dominant in three of three patients following transplantation and persisted unchanged for months. Compared with untreated HCV carriers, transplant recipients had fewer quasispecies, fewer nucleotide changes (1.61 and 2.58/month), fewer amino acid sequence changes (0.40 and 1.94/month), as well as higher ratio of transitional to transversional mutations (2.57 and 0.98,P< 0.02) and lower replacement to silent mutations (1.33 and 8.21,P< 0.01). The two patients with the least genomic variation died of HCV graft infection. The data suggest that HCV variants which infect the graft are selected by recipient immune pressure at the time of transplant and that preferential replication in the graft is enhanced by routine immunosuppression.

Long-term outcome of hepatitis C infection after liver transplantation.

End-stage cirrhosis related to hepatitic C virus (HCV) is a common reason for liver transplantation, although viremia ia known to persist in most cases. We investigated the impact of persistent HCV infection after liver transplantation on patient and graft survival and the effects of the HCV genotype and the degree of HLA matching between donor and recipient on the severity of recurrent hepatitis. A group of 149 patients with HCV infection who received liver transplants between January 1982 and April 1994 were followed for a median of 36 months; 623 patients without HCV infection who underwent liver transplantation for end-stage chronic liver disease were used as a control group. A total of 528 liver-biopsy specimens from the HCV-infected recipients were reviewed, including 82 obtained one year after transplantation as scheduled and 39 obtained at five years as scheduled. In addition, biopsy specimens were obtained from 91 of the HCV-negative patients five years after transplantation. Cumulative survival rates for the 149 patients with HCV infection were 79 percent after one year, 74 percent after three years, and 70 percent after five years, as compared with rates of 75 percent, 71 percent, and 69 percent, respectively, in the HCV-negative transplant recipients (P=0.12). Of the 130 patients with hepatitis C infection who survived more than 6 months after transplantation, 15 (12 percent) had no evidence of chronic hepatitis on their most recent liver biopsy (median followup, 20 months), 70 (54 percent) had mild chronic hepatitis (median, 35 months), 35 (27 percent) had moderate chronic hepatitis (median, 35 months), and 10 (8 percent) had cirrhosis (median, 51 months). Graft loss occurred after a median of 303 days in 27 of the 149 patients, including 5 with HCV-related cirrhosis and 3 with HCV-related cholestatic hepatitis. Infection with HCV genotype 1b was associated with more severe graft injury, whereas the primary immunosuppressive regimen used and the extent of HLA mismatching between donors and recipients had no significant effect on this variable. After liver transplantation for HCV-related cirrhosis, persistent HCV infection can cause severe graft damage, and such damage is more frequent in patients infected with HCV genotype 1b than with other genotypes. After five years, the rates of graft and overall survival are similar between patients with and those without HCV infection.

Influence of the genotypes of hepatitis C virus on the severity of recurrent liver disease after liver transplantation

Background/Aims: Several genotypes of hepatitis C virus (HCV) have been identified by phylogenetic analysis, but their clinical relevance remains elusive. Liver transplantation for HCV-related cirrhosis offers a unique opportunity for prospective studies of this issue. Methods: Sixty anti-HCV-positive liver recipients with precise virological and histological assessments were included. HCV genotype was determined with both typespecific capsid primers and a line probe genotyping assay. Results: HCV genotype 1b was the predominant type before transplantation (40 of 60 patients); after liver transplantation, acute and chronic active hepatitis developed more frequently in these patients than in patients infected by other genotypes (31 of 40 and 24 of 40 vs. 8 of 20 and 4 of 20 patients). Actuarial rates of acute hepatitis and chronic active hepatitis were 77% and 59%, respectively, 3 years after transplantation in patients infected by type 1b and 40% ( P = 0.008) and 22% ( P = 0.004) in those infected by other types. There was no statistical relation between the level of HCV viremia and HCV genotypes both before and after transplantation. In contrast, after transplantation, serum HCV RNA values were significantly increased in patients who developed hepatitis after transplantation. Conclusions: This study provides direct evidence that HCV 1b is associated with more aggressive recurrent liver disease than other genotypes.

Value of HCV RNA quantitation in diagnosis of acute graft dysfunction after liver transplantation for HCV-related cirrhosis

Value of HCV RNA quantitation in diagnosis of acute graft dysfunction after liver transplantation for HCV-related cirrhosis