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Editorial [Antiviral treatment in liver cirrhosis due to hepatitis C virus] 2003
Martínez-Bauer E, Forns X. · Servicio de Hepatología. Institut de Malalties Digestives. Hospital Clínic. Barcelona. España. · Gastroenterol Hepatol. · Pubmed #12732104 No free full text.
This publication has no abstract.
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Article Antiviral therapy increases the risk of bacterial infections in HCV-infected cirrhotic patients awaiting liver transplantation: A retrospective study. 2009
Carrión JA, Martínez-Bauer E, Crespo G, Ramírez S, Pérez-del-Pulgar S, García-Valdecasas JC, Navasa M, Forns X. · Liver Unit, Institut de Malalties Digestives, Hospital Clinic, Ciberehd and IDIBAPS, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain. · J Hepatol. · Pubmed #19217183 No free full text.
Abstract: BACKGROUND/AIMS: Recurrence of hepatitis C after liver transplantation (LT) is universal and may cause premature graft loss. We evaluated the efficacy and safety of antiviral therapy in HCV-infected patients with decompensated cirrhosis awaiting LT. METHODS: Fifty-one patients underwent treatment with peginterferon-alfa-2a and ribavirin. A control group of 51 untreated individuals awaiting LT were matched by age, Child-Pugh and MELD scores and time on the waiting list. RESULTS: Case and control patients were comparable for all relevant variables. Fifteen treated patients (29%) had undetectable HCV-RNA at the time of transplantation and 10 (20%) achieved SVR. Early virological response and non-1 genotype were the strongest predictors of viral clearance. There was a higher incidence of bacterial infections in treated patients vs controls, particularly in Child-Pugh B-C individuals (17 vs 3 episodes) (log-rank=0.0016). Importantly, the incidence of spontaneous bacterial peritonitis (SBP) in patients who were not receiving norfloxacin prophylaxis (n=83) was significantly higher in the treated group than in controls (log-rank=0.01). CONCLUSIONS: Our data demonstrate that antiviral treatment prevents hepatitis C recurrence in 20% of HCV-infected patients. However, treatment should be recommended with caution in individuals with poor liver function who do not receive norfloxacin prophylaxis for SBP, since it increases the risk of bacterial infections.
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Article Hospital admission is a relevant source of hepatitis C virus acquisition in Spain. 2008
Martínez-Bauer E, Forns X, Armelles M, Planas R, Solà R, Vergara M, Fàbregas S, Vega R, Salmerón J, Diago M, Sánchez-Tapias JM, Bruguera M, Anonymous00002. · Liver Unit, Hospital Clínic de Barcelona, IDIBAPS, Ciber de Enfermedades Hepáticas y Digestivas, Ciberehd, Spain. · J Hepatol. · Pubmed #17998149 No free full text.
Abstract: BACKGROUND/AIMS: Isolated cases of acute hepatitis C, as well as hepatitis C outbreaks transmitted by health-care related procedures, have drawn attention to nosocomial transmission of HCV. The aim of this study was to investigate the current relevance of nosocomial HCV infection. METHODS: For this purpose, we performed a retrospective epidemiological analysis of all cases of acute hepatitis C diagnosed in 18 Spanish hospitals. Between 1998 and 2005, 109 cases were documented. RESULTS: The most relevant risk factors registered during the 6-month period preceding the diagnosis of acute hepatitis C were: hospital admission in 73 (67%) cases, intravenous drug use in 9 (8%), accidental needlestick injury in 7 (6%) and sexual contact in 6 (5%). Among the 73 patients in whom hospital admission was the only risk factor, 33 underwent surgery and 24 were admitted to a medical emergency unit or a medical ward; the remaining 16 patients underwent an invasive diagnostic or therapeutic procedure. Sixty two patients underwent antiviral therapy and 51 (82%) achieved a sustained virological response. In 47 patients treatment was not indicated (in 24 due to spontaneous resolution of HCV infection). CONCLUSIONS: In most patients with acute hepatitis C the only documented risk factor associated with the infection is hospital admission. These results stress the need for strict adherence to universal precaution measures. Fortunately, most cases of acute hepatitis C either resolve spontaneously or after antiviral therapy.
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Article Sensitivity to antiviral therapy may change after liver transplantation in patients with chronic hepatitis C virus infection. 2006
Feliu A, Carrión JA, Massaguer A, Martínez-Bauer E, García-Retortillo M, González P, Costa J, Sánchez-Tapias JM, Forns X. · Liver Unit, Institut de Malalties Digestives, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain. · J Viral Hepat. · Pubmed #16901285 No free full text.
Abstract: In hepatitis C virus (HCV)-infected patients, it is generally assumed that the pattern of response to antiviral therapy remains unaltered after liver transplantation (LT). However, changes in the circulating HCV quasispecies and in the gene expression profiles of the graft might influence response to treatment after LT. We evaluated 22 HCV-infected patients who received antiviral treatment while awaiting LT and in whom HCV infection recurred. Eleven of these patients underwent a new antiviral treatment course. Our study analyses the early virological response to both treatment courses to assess the influence of the changes in HCV on the response to therapy. Patients were considered early virological responders (EVR) if viral load declined > or = 2 log10 during the first 12 weeks of therapy. The remaining individuals were considered nonresponders (NR). HCV sequences from hypervariable region 1 and nonstructural 5A (NS5A) region before both treatment regimens were compared. Of 11 patients, 8 (73%) showed identical early response to both courses of therapy (group A: five EVR-EVR, three NR-NR). Interestingly, the response changed in three patients (27%) (group B): two NR became EVR after transplantation, whereas one EVR became NR. Fixation of mutations within the NS5A occurred preferentially in group B (100%) compared with group A (37%)(P = 0.12). However, the number of fixed mutations was not significantly different between groups, suggesting that the changes in sensitivity to therapy after LT are not exclusively dependent on variations in HCV strains. In conclusion, in HCV-infected patients undergoing LT, the pattern of response to antiviral treatment may change after transplantation, and this possibility needs to be incorporated in clinical practice.
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Article Peginterferon-alfa2a plus ribavirin for 48 versus 72 weeks in patients with detectable hepatitis C virus RNA at week 4 of treatment. 2006
Sánchez-Tapias JM, Diago M, Escartín P, Enríquez J, Romero-Gómez M, Bárcena R, Crespo J, Andrade R, Martínez-Bauer E, Pérez R, Testillano M, Planas R, Solá R, García-Bengoechea M, Garcia-Samaniego J, Muñoz-Sánchez M, Moreno-Otero R, Anonymous00009. · Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain. · Gastroenterology. · Pubmed #16890599 No free full text.
Abstract: BACKGROUND & AIMS: Patients with chronic hepatitis C who do not respond rapidly to therapy have a low chance of developing a sustained virologic response (SVR) when treated for 48 weeks. This study investigated whether treatment for 72 weeks increases the rate of SVR in patients with detectable hepatitis C virus (HCV)-RNA levels at week 4 of treatment. METHODS: A total of 510 treatment-naive patients were treated with peginterferon-alfa2a (180 microg/wk) plus ribavirin (800 mg/day). Patients with detectable HCV-RNA levels at week 4 (n = 326) were randomized to complete 48 (group A, n = 165) or 72 weeks (group B, n = 161) of treatment. Patients with undetectable HCV-RNA levels at week 4 (n = 184) were allocated into group C (n = 148) or group D (n = 36), according to HCV genotype and baseline viremia, and treated for 24 or 48 weeks, respectively. All patients were followed-up for 24 weeks after the end of treatment. RESULTS: The end-of-treatment response rate (61%) was similar in groups A and B, but the SVR rate was higher in group B (45% vs 32% in A; P = .01). In genotype 1-infected patients randomized to group A (n = 149) or B (n = 142), SVR rates were 28% and 44%, respectively (P = .003). The incidence of adverse events was similar in all groups. Treatment discontinuation was more frequent in group B (36%) than in group A (18%) (P = .0004). SVR rates in groups C and D were 79% and 64%, respectively. CONCLUSIONS: Extension of treatment with peginterferon-alfa2a plus ribavirin from 48 to 72 weeks significantly increases the rate of SVR in patients with detectable viremia at week 4 of treatment.
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Article Development and validation of two models for early prediction of response to therapy in genotype 1 chronic hepatitis C. 2006
Martínez-Bauer E, Crespo J, Romero-Gómez M, Moreno-Otero R, Solá R, Tesei N, Pons F, Forns X, Sánchez-Tapias JM. · Liver Unit, Hospital Clínic, IDIBAPS, Barcelona, Spain. · Hepatology. · Pubmed #16374857 No free full text.
Abstract: Early prediction of response to therapy in genotype 1 chronic hepatitis C is difficult. Two predictive models, a pretreatment scoring model (PreT-SM) and a fourth week of therapy scoring model (4w-SM) were constructed in a cohort of 104 patients from a single center (estimation cohort) and validated in a cohort of 141 patients from four independent centers (validation cohort). Individual scores were calculated using variables independently associated with sustained virological response (SVR). Baseline viral load, aspartate aminotransferase/alanine aminotransferase ratio, serum cholesterol, and a numerical score for noninvasive estimation of liver fibrosis were included in the PreT-SM; HCV RNA clearance and PreT-SM scores were included in the 4w-SM. Receiver operating characteristic analysis revealed the area under the curve in the estimation cohort and in the validation cohort to be, respectively, 0.856 and 0.847 for the PreT-SM and 0.908 and 0.907 for the 4w-SM. Low scores were associated with SVR, high scores with non-SVR. The best cutoff scores from the PreT-SM (7 and 9.70) identified, respectively, 36% of patients with SVR and 41% of those with non-SVR from the validation cohort, with high accuracy (> or =90% positive predictive value [PPV] and specificity). Similarly, cutoff scores of 3.20 and 5.60 from the 4w-SM identified, respectively, 71% of patients with SVR and 53% of those with non-SVR from the same cohort with high accuracy (PPV and specificity >92%). In conclusion, these models predicted response to therapy before or after 4 weeks of treatment in approximately 60% of genotype 1 patients and may be valuable for the management of this condition.
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Article Nosocomial transmission of HCV in the liver unit of a tertiary care center. 2005
Forns X, Martínez-Bauer E, Feliu A, García-Retortillo M, Martín M, Gay E, Navasa M, Sánchez-Tapias JM, Bruguera M, Rodés J. · Liver Unit, Institut de Malalties Digestives, Hospital Clinic, IDIBAPS, Barcelona, Spain. · Hepatology. · Pubmed #15619236 No free full text.
Abstract: Despite its medical and legal implications, there are no prospective studies analyzing the incidence and mechanisms involved in the nosocomial transmission of hepatitis C virus (HCV) in liver units. This study prospectively investigates the nosocomial transmission of HCV in the liver unit of a tertiary care center from August 2000 to October 2002. The median prevalence of HCV infection among hospitalized patients was 50%. Anti-HCV-negative patients admitted to the liver unit during the study period were prospectively followed, and serum markers of HCV infection were repeated 6 months after discharge. All known risk factors for HCV transmission (including the physical allocation of HCV-infected and noninfected patients during hospitalization) were recorded. Complete follow-up data were available in 1301 (84.5%) of 1540 patients. Six patients (0.46%) acquired HCV infection (annual incidence: 0.27/100 admissions). Phylogenetic analyses of recovered HCV sequences identified the source of infection as an HCV-infected roommate (3 cases) and a patient receiving care by the same nurse team (1 case). The most relevant risk factors associated with HCV acquisition were duration of hospitalization (>10 days; OR, 35; 95% CI, 1.96-622) and hospitalization with an HCV-infected roommate (>5 days; OR, 12; 95% CI, 1.39-103). In fact, HCV infection occurred in 1.7% of the 357 patients hospitalized longer than 10 days. In conclusion, HCV nosocomial infection appears to occur via patient-to-patient transmission in liver units, particularly in individuals who require long hospitalizations. Continuous reinforcement of universal prevention measures and, when possible, isolation of patients at higher risk might further reduce nosocomial HCV transmission.
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Article Identification of chronic hepatitis C patients without hepatic fibrosis by a simple predictive model. 2002
Forns X, Ampurdanès S, Llovet JM, Aponte J, Quintó L, Martínez-Bauer E, Bruguera M, Sánchez-Tapias JM, Rodés J. · Liver Unit, Institut de Malalties Digestives, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Catalonia, Spain. · Hepatology. · Pubmed #12297848 No free full text.
Abstract: Liver biopsy is required for staging hepatic fibrosis in patients with chronic hepatitis C, but it is an expensive procedure with occasional complications and poor patient acceptance. This cohort study was designed to assess the accuracy of a noninvasive method aimed to discriminate between patients with and without significant liver fibrosis (stages 2-4 versus 0-1). Clinically relevant variables were analyzed in a cohort of 476 consecutive untreated patients (estimation group, 351 patients; validation group, 125 patients) with chronic hepatitis C who underwent a liver biopsy. Multivariate analysis identified age, gamma glutamyl transpeptidase (GGT), cholesterol, platelet count, and prothrombin time as independent predictors of fibrosis. We constructed a model and a score system combining age, GGT, cholesterol, and platelet count that proved useful to identify patients without significant hepatic fibrosis. The area under the ROC curve was 0.86 for the estimation group and 0.81 for the validation group. Using the best cutoff score (less than 4.2), presence of significant fibrosis (F2 to F4) could be excluded with high accuracy (negative predictive value of 96%) in 125 (36%) of 351 patients. Similarly, it could be excluded with the same certainty in 49 (39%) of the 125 patients of the validation group. Only 2 patients with liver fibrosis stage 2 were incorrectly classified. In conclusion, a combination of easily accessible variables accurately predicts the absence of significant fibrosis and might render liver biopsy unnecessary in more than one third of patients with chronic hepatitis C.
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