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P.400 Hepatitis C recurrence after liver transplantation agauE. Abdala
$184
Journal of Clinical Virology 2006, Vol 36 (suppl 2)
1-4 yrs. 5 of them underwent antiviral therapy after the chronic HCV was proven by biopsy within 1-3 yrs post OLT. Two pts genotype 1 are treated with low dose regimen of interferon alpha 1.5 MU 3. weekly and 6 0 0 4 0 0 m g RBV without side effects for 25 weeks till now. Biochemical but not virological response is achieved. 1 pt genotype 1 is treated with interferon alpha 3.3MU/weekly, RBV 800mg daily for 30 weeks also with biochemical response. 1 female genotype 3 had severe neutropenia 4 months after the same combined therapy and required cessation but in spite of therapy she has progressed in cholestatic hepatitis and is listed for retransplantation. The fifth patient who is genotype 1 refused the therapy after 2 months because of losing weight but has also progressed to cholestatic hepatitis and is still alive. Conclusion: 79% of post OLT HCV reinfected liver recipients in our hospital are surviving from one to four years in good condition. 20% HCV reinfected pts died within 6 months because of cholestatic disease, sepsis or CMV infection. Patients with post OLT HCV+ established infection are difficult to treat, with uncertain outcome.
~
Hepatitis C recurrence after liver transplantation
E. Abdala 1 *, A.C. Tonacio 1, P.R. Bonazzi 1, D.R.M. Gotardo 1, E.R.R. Figueira 1, M.R Freire 1, I.R Mendes Neto 1, R. Schuler 2, E.S. Mello 2, T. Bacchella 1, M.C.C. Machado 1. 1Liver Transplantation
Division, 2pathology Division, University of S#o Paulo Medical School, S#o Paulo, Brazil Background and Objectives: Recurrence of hepatitis C virus (HCV) infection after liver transplantation (LT) is virtually universal, and its severity has increased in recent years. Some factors have been described as predictors of recurrence severity, but they are not completely understood. The objective of the study is to describe the recurrence of hepatitis C after LT in 42 patients, and to analyze some possible risk factors. Methods: Retrospective analysis of 42 patients who underwent LT for cirrhosis secondary to chronic HCV infection and had at least one liver biopsy after 6 months. Recurrence of hepatitis was defined as histological chronic hepatitis in patients with positive serum HCVRNA, without evidence for rejection. Liver biopsy specimens were reviewed by a liver pathologist and scored for fibrosis according to Ishak et al. criteria. The endpoints for analysis were: recurrence in 1 year and cirrhosis. For the evaluation of cirrhosis only the patients who had a biopsy in the last 6 months were included. Factors related to the donor, the host, the virus and the LT procedures were analyzed. Categorical data were compared using %2 test or Fisher's Exact Test. Continuous variables were compared by MannWhitney test. The variables with a p less than 0.1 were submitted to a multivariate analysis. Results: The mean follow-up of the 42 patients was 5.2 years (SD 2.9), median 4.7 years. Thirty-two patients were men; the mean age was 50.55 years (SD 7.39). Thirty-eight (90.5%) had diagnosis of hepatitis recurrence, in a mean period of 28.58 months (SD 26.97), median 17.85 months. Recurrence in 1 year was detected in 10 (23.8%) cases. Cirrhosis was diagnosed in 4 of 32 evaluated patients (12.5%), 2 before 5 years (6.25%). The following factors were significant for one year recurrence in univariate analysis: Child-Pugh score pre-LT, genotype 1, preservation injury, receptor age, steroid bolus and acute rejection. For cirrhosis, the significant factors in univariate analysis were: genotype 1, history of alcohol consumption, preservation injury, receptor age, immunosuppression with tacrolimus versus cyclosporine, steroid bolus and acute rejection. No factor was significant in multivariate analysis. Conclusion: Most of the patients had histological diagnosis of hepatitis C recurrence, predominantly in the second year post-LT. Progression to cirrhosis after 5 years was less frequent than in other series. We could not detect a risk factor associated with one year recurrence or with cirrhosis development in a multivariate analysis.
Abstracts, 12th ISHVLD
11. Coinfection [-~-~
Hepatic steatosis in HIV and hepatitis C virus coinfected patients receiving antiretroviral therapy
V. Martinez 1 *, T. Ta 1, Z. Mokhtari 1, M. Guiguet 2, M. Valantin 1, E Charlotte 3, Y. Benhamou 4, E. Caumes 1, E Bricaire 1, C. Katlama 1.
1Department of Infectious Diseases, 21NSERM U720, 3Department of Anatomopathology, 4Department of Hepatology, HSpital Piti6-Salp~triere, Paris, France Objectives: To evaluate prevalence and severity of hepatic steatosis, and to assess risk factors influencing hepatic steatosis in HIV/HCV patients taking antiretroviral therapy (ART). Methods: A retrospective study was conducted on HIV/HCV patients treated by ART, who underwent liver biopsies from January 1995 to June 2005. All patients were negative for HBV testing and never been treated for HCV. All liver biopsies were read by the same pathologist. Hepatic steatosis was graded according to the percentage of hepatocytes affected: 0, none; 1, steatosis involving <33%; 2, 33-66%; and 3, >66%. Demographics and laboratory parameters were recorded at time of hepatic biopsy. Results: 127 HIV/HCV coinfected patients were included. Median age was 39 years (35-43), 82% were male, 89% were Caucasian, 78% had a past history of IV drug abuse. At the time of biopsy, HIV viral load was suppressed (<400 copies/ml) in 60% of patients and the median HIV viral load was 8589 copies/ml (IQR 1860-62,389) in patients remaining, CD4 cell count was 320/ram 3 (IQR 196-448). Median duration exposure to NRTI was 53 months, NNRTI 13 and 22 for PI. HCV genotype was: 62 (58%) genotype 1; 5% genotype 2; 27% genotype 3 and 10% genotype not determined. HCV-RNA was 3.161og10kUI/ml (IQR 2.92-3.54). Hepatic steatosis was observed in 79 of 127 patients (62%): 56 (44%) with steatosis grade 1; 7 (5%) grade 2 and 16 (13%) grade 3. In univariate analysis, hepatic steatosis was associated with age and AST levels, and negatively associated with serum total cholesterol levels. Moreover, hepatic steatosis was associated with higher HCV RNA load than in patients without steatosis. In multivariate analysis, independent determinants of hepatic steatosis were age >45 years, genotype 3 and abacavir use remained associated with decreased risk of hepatic steatosis. Conclusion: Hepatic steatosis was present in 62% of HIV-HCV coinfected patients receiving ART. In multivariate analysis, independent determinants of hepatic steatosis were age >45 years, genotype 3 and abacavir use remained associated with decreased risk of hepatic steatosis. Protective effect of abacavir, a non-thymidinic drug group with less mitochondrial damage, underlines the possible key role of DNA mitochondrial toxicity in the genesis of steatosis and suggests opportunity to prevent hepatic steatosis in HIV and HCV coinfected patients. Nevertheless, the role of drug classes and drugs within classes should be investigated in prospective studies.
11a. Hepatitis virus coinfections
:•[-•-•
Occult hepatitis B virus infection in French patients with chronic hepatitis C
S. Mrani 1 *, I. Chemin 1, R Pradat 2, R Chevalier3, E Zoulim 1, C. Tr6po 1. 1Hepatology, INSERM U271, 2Hepatology, HStel Dieu
Hospital, 3Microbiology, La Croix Rousse Hospital, Lyon, France Background
and Objectives: Occult hepatitis B virus (HBV) infection (HBV-DNA in serum without hepatitis B surface antigen [HBsAg]) is common in chronic hepatitis C patients. However, its prevalence and consequences are still a matter of controversy. The aim of this study was to evaluate the frequency of occult HBV among HCV. Methods: HBV and HCV was detected by serological assays. Quantification of serum HCV RNA was performed with the COBAS
Journal of Clinical Virology 2006, Vol 36 (suppl 2)
1-4 yrs. 5 of them underwent antiviral therapy after the chronic HCV was proven by biopsy within 1-3 yrs post OLT. Two pts genotype 1 are treated with low dose regimen of interferon alpha 1.5 MU 3. weekly and 6 0 0 4 0 0 m g RBV without side effects for 25 weeks till now. Biochemical but not virological response is achieved. 1 pt genotype 1 is treated with interferon alpha 3.3MU/weekly, RBV 800mg daily for 30 weeks also with biochemical response. 1 female genotype 3 had severe neutropenia 4 months after the same combined therapy and required cessation but in spite of therapy she has progressed in cholestatic hepatitis and is listed for retransplantation. The fifth patient who is genotype 1 refused the therapy after 2 months because of losing weight but has also progressed to cholestatic hepatitis and is still alive. Conclusion: 79% of post OLT HCV reinfected liver recipients in our hospital are surviving from one to four years in good condition. 20% HCV reinfected pts died within 6 months because of cholestatic disease, sepsis or CMV infection. Patients with post OLT HCV+ established infection are difficult to treat, with uncertain outcome.
~
Hepatitis C recurrence after liver transplantation
E. Abdala 1 *, A.C. Tonacio 1, P.R. Bonazzi 1, D.R.M. Gotardo 1, E.R.R. Figueira 1, M.R Freire 1, I.R Mendes Neto 1, R. Schuler 2, E.S. Mello 2, T. Bacchella 1, M.C.C. Machado 1. 1Liver Transplantation
Division, 2pathology Division, University of S#o Paulo Medical School, S#o Paulo, Brazil Background and Objectives: Recurrence of hepatitis C virus (HCV) infection after liver transplantation (LT) is virtually universal, and its severity has increased in recent years. Some factors have been described as predictors of recurrence severity, but they are not completely understood. The objective of the study is to describe the recurrence of hepatitis C after LT in 42 patients, and to analyze some possible risk factors. Methods: Retrospective analysis of 42 patients who underwent LT for cirrhosis secondary to chronic HCV infection and had at least one liver biopsy after 6 months. Recurrence of hepatitis was defined as histological chronic hepatitis in patients with positive serum HCVRNA, without evidence for rejection. Liver biopsy specimens were reviewed by a liver pathologist and scored for fibrosis according to Ishak et al. criteria. The endpoints for analysis were: recurrence in 1 year and cirrhosis. For the evaluation of cirrhosis only the patients who had a biopsy in the last 6 months were included. Factors related to the donor, the host, the virus and the LT procedures were analyzed. Categorical data were compared using %2 test or Fisher's Exact Test. Continuous variables were compared by MannWhitney test. The variables with a p less than 0.1 were submitted to a multivariate analysis. Results: The mean follow-up of the 42 patients was 5.2 years (SD 2.9), median 4.7 years. Thirty-two patients were men; the mean age was 50.55 years (SD 7.39). Thirty-eight (90.5%) had diagnosis of hepatitis recurrence, in a mean period of 28.58 months (SD 26.97), median 17.85 months. Recurrence in 1 year was detected in 10 (23.8%) cases. Cirrhosis was diagnosed in 4 of 32 evaluated patients (12.5%), 2 before 5 years (6.25%). The following factors were significant for one year recurrence in univariate analysis: Child-Pugh score pre-LT, genotype 1, preservation injury, receptor age, steroid bolus and acute rejection. For cirrhosis, the significant factors in univariate analysis were: genotype 1, history of alcohol consumption, preservation injury, receptor age, immunosuppression with tacrolimus versus cyclosporine, steroid bolus and acute rejection. No factor was significant in multivariate analysis. Conclusion: Most of the patients had histological diagnosis of hepatitis C recurrence, predominantly in the second year post-LT. Progression to cirrhosis after 5 years was less frequent than in other series. We could not detect a risk factor associated with one year recurrence or with cirrhosis development in a multivariate analysis.
Abstracts, 12th ISHVLD
11. Coinfection [-~-~
Hepatic steatosis in HIV and hepatitis C virus coinfected patients receiving antiretroviral therapy
V. Martinez 1 *, T. Ta 1, Z. Mokhtari 1, M. Guiguet 2, M. Valantin 1, E Charlotte 3, Y. Benhamou 4, E. Caumes 1, E Bricaire 1, C. Katlama 1.
1Department of Infectious Diseases, 21NSERM U720, 3Department of Anatomopathology, 4Department of Hepatology, HSpital Piti6-Salp~triere, Paris, France Objectives: To evaluate prevalence and severity of hepatic steatosis, and to assess risk factors influencing hepatic steatosis in HIV/HCV patients taking antiretroviral therapy (ART). Methods: A retrospective study was conducted on HIV/HCV patients treated by ART, who underwent liver biopsies from January 1995 to June 2005. All patients were negative for HBV testing and never been treated for HCV. All liver biopsies were read by the same pathologist. Hepatic steatosis was graded according to the percentage of hepatocytes affected: 0, none; 1, steatosis involving <33%; 2, 33-66%; and 3, >66%. Demographics and laboratory parameters were recorded at time of hepatic biopsy. Results: 127 HIV/HCV coinfected patients were included. Median age was 39 years (35-43), 82% were male, 89% were Caucasian, 78% had a past history of IV drug abuse. At the time of biopsy, HIV viral load was suppressed (<400 copies/ml) in 60% of patients and the median HIV viral load was 8589 copies/ml (IQR 1860-62,389) in patients remaining, CD4 cell count was 320/ram 3 (IQR 196-448). Median duration exposure to NRTI was 53 months, NNRTI 13 and 22 for PI. HCV genotype was: 62 (58%) genotype 1; 5% genotype 2; 27% genotype 3 and 10% genotype not determined. HCV-RNA was 3.161og10kUI/ml (IQR 2.92-3.54). Hepatic steatosis was observed in 79 of 127 patients (62%): 56 (44%) with steatosis grade 1; 7 (5%) grade 2 and 16 (13%) grade 3. In univariate analysis, hepatic steatosis was associated with age and AST levels, and negatively associated with serum total cholesterol levels. Moreover, hepatic steatosis was associated with higher HCV RNA load than in patients without steatosis. In multivariate analysis, independent determinants of hepatic steatosis were age >45 years, genotype 3 and abacavir use remained associated with decreased risk of hepatic steatosis. Conclusion: Hepatic steatosis was present in 62% of HIV-HCV coinfected patients receiving ART. In multivariate analysis, independent determinants of hepatic steatosis were age >45 years, genotype 3 and abacavir use remained associated with decreased risk of hepatic steatosis. Protective effect of abacavir, a non-thymidinic drug group with less mitochondrial damage, underlines the possible key role of DNA mitochondrial toxicity in the genesis of steatosis and suggests opportunity to prevent hepatic steatosis in HIV and HCV coinfected patients. Nevertheless, the role of drug classes and drugs within classes should be investigated in prospective studies.
11a. Hepatitis virus coinfections
:•[-•-•
Occult hepatitis B virus infection in French patients with chronic hepatitis C
S. Mrani 1 *, I. Chemin 1, R Pradat 2, R Chevalier3, E Zoulim 1, C. Tr6po 1. 1Hepatology, INSERM U271, 2Hepatology, HStel Dieu
Hospital, 3Microbiology, La Croix Rousse Hospital, Lyon, France Background
and Objectives: Occult hepatitis B virus (HBV) infection (HBV-DNA in serum without hepatitis B surface antigen [HBsAg]) is common in chronic hepatitis C patients. However, its prevalence and consequences are still a matter of controversy. The aim of this study was to evaluate the frequency of occult HBV among HCV. Methods: HBV and HCV was detected by serological assays. Quantification of serum HCV RNA was performed with the COBAS