Hepatitis C Research

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  Durability of Sustained Virologic response in patients with Chronic Hepatitis c after treatment With Interferon 2b Alone or in Combination with Ribavirin
  Impact of Pegylated Interferon alfa-2b (Peg-Intron) and Ribavirin on Progression of Liver Fibrosis in patients with Chronic Hepatitis C
  Abstract 676. ACUTE HEPATITIS C: NATURAL COURSE AND RESPONSE TO ANTIVIRAL TREATMENT
  HALT-C Trial: 4-year study of Maintenance Therapy in 1350 patients
   

 

  Abstract 281. Durability of Sustained Virologic response in patients with Chronic Hepatitis c after treatment With Interferon 2b Alone or in Combination with Ribavirin

This study looked at 400 patients in 3 studies who achieved a sustained response. The key

findings were:
 
 

  1. late relapse (after achieving the sustained response) occurred only in 2.5% of patients
  2. the late relapsers occurred within the first 2 years. There were no relapsers after 2 years
  3. 2 relapsers had detectable HCV-RNA in the liver; 3 had detectable HCV-RNA in the liver and did not relapse
  4. the risk of relapse after achieving sustained response was 5%

The purpose of this study was to assess the durability of response in patients who were sustained responders 24 weeks after therapy. John McHutchison reported in an oral session on a analysis of 2089 patients from 3 large scale international studies comparing interferon alfa-2b alone to interferon alfa-2bplus ribavirin (Davis et al, NEJM 1998;339:1493, McHutchison et al NEJM 1998; 339:1485; Poynard et al, Lancet 1998;352:1426). Many of these patients have been followed for up to 4 years. This analysis looked at the 558 patients who achieved a sustained response to evaluate their rate of failure. Of the 558 SVRs 455 patients received IFN+RBV and 103 patients received IFN. 395 of the 558 agreed to participate in this long-term follow-up. All patients were treatment-naive or relapsers and received 24 or 48 weeks treatment. Of the 395 patients, 151 naive received IFN/RBV for 48 weeks, 112 naive patients received IFN/RBV for 24 weeks, 59 relapsers received IFN/RBV for 24 weeks, 61 received IFN alone for 48 weeks, and 12 received IFN alone for 24 weeks (4 naive 24 weeks, 61 naive 48 weeks, 8 relapse 24 weeks).
 
Serum HCV-RNA was measured by NGI LLQ 100 copies/ml. These patients are also assess yearly for disease progressionby physical exam and hemotological and biochemical (ALT/AST) testing. This analysis was completed as of February 2001 and the endpoint was viral relapse after achieving sustained response. About 2/3 of patients were male, 42-47 years of age, and about 74-79 kg. 37% were genotype 1, 26% genotype 2, 34% genotype 3, and 3% genotype 4/5. Although there is a low percentage of genotype 1 in this analysis McHutchison said that they found no difference in study outcomebetween genotyp 1 vs non-genotype 1. Baseline fibrosis Metavir Stage: 60-80% of patients had F0-F1. 12-29% had F3/F4. And 4-20% had missing information. Baseline viral load was 3.0-4.1 million copies/ml. ALT was 3.2 to 3.6 times the upper limit of normal.
 
RESULTS
 
· 59% of the 395 patients in the study have been followed for 4 years after the end of treatment, 3% for 5 years, 26% for 3 years, 8% for 2 years, and 3% for 1 year.
 
· Only 10 out of 395 patients (2.5%) who had a sustained response (24 weeks after ending treatment)--

 

  • 7 had received IFN/RBV
  • 5 of 7 were naive and relapsed in 3-24 weeks after stopping therapy
  • 2 were relapsers
  • 3 patients received IFN alone

· All 10 late relapsers reappearance of HCV-RNA within 2.5 years after stopping therapy or 2 years after the 24 week follow-up period.
 
· There have been no relapses after 2 years of follow-up.
 
· Researchers looked at naive vs relapser, 24 vs 48 weeks treatment, genotype 1 vs non-genotype 1, low vs high viral load, low vs higher fibrosis, and found no factor predicted relapse
 
· The overall risk for late relapse looking out to 4 years was <5%, when using Kaplan-Meier curve, except for the 12 patients who received IFN alone for 24 weeks who had a high risk for late relapse --The corresponding actuarial likelihood (Kaplan-Meier) of maintaining response after 4 years in patients who initially achieved SR is: IFN/RBV 24 weeks therapy naive 97%, IFN/RBV 48 weeks therapy naive 99%, and IFN/RBV 24 weeks therapy relapsers 96%
 
· There were 5 patients who had HCV-RNA detected in their liver (not blood) in the 24 week post-treatment liver biopsy. These 5 patients were sustained responders so they had PCR negative in the blood. Two of the 5 subsequently relapsed
 
· 95% had normal ALT during the long-term follow-up of this study
 
· One patient developed liver cancer (hepatocellular carcinoma). He had pre-existing cirrhosis, was a sustained responder (I think he was a previous relapser IFN alone) who has not relapsed. HCC developed 39 months after treatment. Other than this 1 patient there was no evidence of hepatic decompensation as documented by physical exam
 
 

Impact of Pegylated Interferon alfa-2b (Peg-Intron) and Ribavirin on Progression

of Liver Fibrosis in patients with Chronic Hepatitis C
 
Reported by Jules Levin

Based on 2 biopsies 20 months apart, this study reported:
 
 

  • Sustained responders improved activity grade, were less likely to have worsened activity, and less likely to see worsened fibrosis
     
  • On average non-responders with fibrosis (F2, F3, and F4) could stop fibrosis progression
     
  • On average sustained responders with fibrosis (f2, F3, and F4) show regression of fibrosis
     
  • 49% with cirrhosis showed some degree of reversal of cirrhosis from F4 stage to either F3, F2 or F1; achieving a sustained response was a significant factor
     

Thierry Poynard first commented on aims of therapy: (1) to achieve a sustained virologic response which permits fibrosis regression, disappearance of extrahepatic manifestations, disappearance of contamination risks; (2) to block fibrosis progression in patients without a sustained virologic response (perhaps also using a suppressive maintenance therapy).
 
Editorial note from Jules Levin: Blocking fibrosis progression in nonresponders remains controversial. A number of studies have found fibrosis can be slowed or stopped in transient responders and nonresponders. Some studies have found nonresponders are not able to block fibrosis progression. And it also depends how you define a nonresponder. Mitch Shiffman reported in his study in Gastroenterology (1999; 117: 1164-1172) that patients with some early viral load reduction (1.4 log) and some early fibrosis improvement during therapy are able to sustain viral load reduction and improved histology (liver condition) with ongoing maintenance interferon therapy for the two years of this study. What about patients who are unable to reduce viral load at all and who don't show early fibrosis improvement? I think this remains a question. Two large multiple-year studies HALT-C by the NIH & Roche and CO-PILOT from Schering are exploring this question now. The findings Poynard presented here and earlier at EASL in the Spring of 2001 have been controversial. The question of whether nonresponders can reverse, slow or stop fibrosis progression is perhaps the most controvesial question currently. Poynard first presented this data at EASL but the presentation here at AASLD had several additional new pieces of information. Several observers and researchers I spoke with at AASLD do not buy his findings (the controversy). One doctor told me he does not see these kinds of benefits in his practice. I think other researchers do feel these data have merit.
 
Poynard pooled data on 3,010 HCV treatment naive, HIV negative patients with paired biopsies from 4,493 patients in 4 trials receiving 10 different regimens (Poynard et al, McHutchison et al, Lindsay et al, and Mannes et al.)
 
The ten regimens included IFN 24 weeks, IFN 48 weeks, PegIntron 0.5 ug/kg, PegIntron 1.0 ug/kg, PegIntron 1.5 ug/kg, IFN/RBV 24 weeks, IFN/RBV 48 weeks, PegIntron 0.5 ug/kg+RBV, PegIntron 1.5 ug/kg/RBV.
 
Some characteristics of the 3,010 patients: 66% male, 43 years age, 80 kg weight, 53% IVDUs, genotype 1 70%, genotype 2 28%, genotype 4,5,6 3%, viral load 4 million.
 
Duration of HCV infection for patients was 18 years. Duration between the 2 biopsies was 20 months. The size of the biopsy in mm was 16.
 
25% had fibrosis (F2 13%, F3 7%, F4 5%-cirrhosis), and 73% had F1 (minimal fibrosis) and 2% had F0 (no fibrosis). About about 1/3 of patients had each of severe, moderate or mild activity (A1, A2, or A3).
 
The histological impact of each regimen was estimated by the percentage of patients with at least one grade improvement in the necrosis and inflammation (METAVIR score), the percentage of patients with at least one stage worsening in fibrosis METAVIR score and by the fibrosis progression rate per year.
 
Activity Grade Improvement (at least one grade improvement Metavir score)

                                        Improved                       Stabilized               Worsened

Sustained Responders         86%                                12%                        2%

Relapsers                             43%                                36%                        21%

Non-responders                   36%                                43%                        21%

 

This was new information presented for the first time at AASLD and not earlier at EASL. Being able to achieve a sustained virologic response is an important factor in being able to achieve a significant improvement in activity. Obviously, choosing the most effective regimen (its potency and tolerability) is important in being able to achieve a sustained response significantly and in turn improved activity and fibrosis. So, you want to use the most potent (antiviral activity) and tolerable regimen. Tolerabiliy is important because with more side effects and adverse events adherence may be more challenging.
 
Poynard reported an analysis of the change in activity grade by each of the ten regimens including PegIntron 1.5 ug/kg+RBV using the optimized weight based dose of RBV.
 
 

  • IFN alone 24 weeks: 39% of patients improved, 39% stabilized, 24% worsened
     
  • IFN alone 48 weeks: 41% improved, 40% stabilized,19% worsened
     
  • Peg-Intron 0.5 ug/kg: 48% improved, 35% stabilized, 20% worsened
     
  • Peg-Intron 1.0 ug/kg: 49% improved, 33% stabilized, 18% worsened
     
  • Peg-Intron 1.5 ug/kg: 49% improved, 33% stabilized, 18% worsened
     
  • IFN+RBV 24 weeks: 51% improved, 34% stabilized, 15% worsened
     
  • IFN+RBV 48 weeks: 64% improved, 24% stabilized, 12% worsened
     
  • Peg 0.5+RBV: 70% improved, 24% stabilized, 6% worsened
     
  • Peg 1.5+RBV: 65% improved, 23% stabilized, 12% worsened
     
  • Peg 1.5+RBV*: 73% improved, 21% stabilized, 6% worsened
     

*RBV optimized weight based dosing
 
I think its important to note that no data was presented by Poynard on the statistical significance of the differences between the regimens, either on the slides or verbally in his talk. So, you don't know if for example there is a real difference between the 41% of patients receiving IFN for 48 weeks who showed improvement and the 49% who showed improvement using PegInron 1.5 ug/kg. Or for that matter, you don't know for sure if there is a significant difference between standard IFN+RBV taken for 48 weeks (64% improved), PegIntron 0.5 ug/kg+RBV (70%), PegIntron 1.5 ug/kg+RBV (65% improved), and PegIntron 1.5 ug/kg+ optimzed dose of RBV based on weight (73%). In fact, Poynard's data shows little difference if any between the 70% of patients who saw improvement using the low dose of Pegintron 0.5+RBV compared to the patients receiving PegIntron 1.5 ug/kg+ optimized weight based dose of RBV who Poynard reported 73% of these patients experienced improved activity grade. There may not be any significant difference between 70% and 73%.
 
Fibrosis Stage Variation
 
(the percentage of patients with at least one stage change in fibrosis METAVIR score). The biopsies were performed 20 months apart so Poynard suggested that given more time fibrosis ought to continue to improve further for some patients. In particular, you might expect if any will continue to improve it would be sustained responders and perhaps some patients continuing on maintenance therapy.

                                            Improved                  Stabilized                  Worsened

Sustained Responders                25%                         68%                           7%

Relapsers                                    16%                         67%                           17%

Non-responders                         17%                        62%                            21%

 

Again, Poynard did not present data on the statistical significance between any of the differences between the groups. But, he did comment orally in his presentation that the differences in the worsening category (7% vs 17% vs 21%) were statistically significant. I think its fair to conclude that a sustained responder has a better chance for improved fibrosis than a relapser and moreso than a non-responder. The difference in the worsening category between sustained responders and non-responders and relapsers (21% vs 7% and 17%) strikes my attention.
 
Fibrosis Progression Rate Per Year
 
Poynard reported the fibrosis progression rate per year in 1900 patients with F0-F1 (no or minimal fibrosis) with paired biopsies and known duration of infection.

                                         Rate Before Therapy           After

Non-responders                      0.053                              0

Sustained Responders           0.063                              0

p<0.001

 

Poynard is reporting here that in patients with HCV alone and little or no fibrosis their fibrosis progression rate per year stopped whether they were a non-responder or sustained responder. Since the biopsies were performed 20 months apart, you don't know what might occur regarding the fibrosis progression rate in 2-3 years or longer for non-responders. Non-responders may start progressing after being off therapy for a while. How long off therapy does it take for progression to get going or to get back to baseline? I don't know of any data on this. But some doctors tell me they think the benefit can last for a little while. Follow-up biopsies should be helpful in evaluating this.
 
Poynard reported on an analysis of fibrosis progression rate per year in 679 patients with extensive fibrosis (F2, F3, F4) with paired biopsies and known duration of therapy. Poynard commented that the progression rates in this group were very high before therapy.

                                            Rate Before Therapy                After

Non-responders                           0.135                                 0

Sustained Responders                0.139                               -0.591

p<0.001

Poynard said the sustained responders experienced a dramatic decrease or regression in fibrosis rate.
 
Fibrosis Stage Variation By Regimen
 
The percentage of patients with at least one stage change in fibrosis METAVIR score. Again, the biopsies were 20 months apart.
 
 

  • IFN 24 weeks: 12% of patients receiving this regimen experienced improved fibrosis, 65% stabilized, and 23% worsened
  • IFN 48 weeks: 16% of patients improved fibrosis, 66% stabilized, and 18% worsened
     
     
  • Peg 0.5 ug/kg: 22% improved, 62% stabilized, 17% worsened
     
  • Peg 1.0 ug/kg: 21% improved, 62% stabilized, 16% worsened
     
  • Peg 1.5 ug/kg: 17% improved, 65% stabilized, 18% worsened
     
  • IFN/R 24 wks: 20% improved, 66% stabilized, 14% worsened
     
  • IFN/R 48 wks: 20% improved, 66% stabilized, 14% worsened
     
  • Peg 0.5/RBV: 23% improved, 67% stabilized, 10% worsened
     
  • Peg 1.5/RBV: 23% improved, 57% stabilized, 20% worsened
     
  • Peg 1.5/R*: 24% improved, 68% stabilized, 8% worsened
     

*With Optimized weight based dosing
 
So far there does not appear to be any difference between the percent of patients showing improved or stabilized fibrosis stage between most of the regimens. In particular, there is no difference between Peg 1.5 with optimized weight based RBV dosing, Peg 1.5 with RBV but without weight based RBV dosing, and standard IFN + RBV for 48 weeks.
 
Again, Poynard did not present any data on the statistical significance of differences between groups in his slides. But he pointed out orally that there was a significant difference between the 8% worsening in the Peg 1.5+ optimized RBV arm compared to the 14% experienced by IFN/RBV 48 weeks arm. But, he did not comment on the point that the Peg 0.5/RBV arm was 10% compared to 8% with optimized RBV dose & higher PegIntron dose. Although, the biopsies were only 20 months apart and so some patients, as Poynard points out, may continue to improve further.
 
Factors Associated With Absence of Extensive Fibrosis at 24 Months
 
n=2861, (20 months between biopsies), multivariate analysis
 
 

  • The baseline fibrosis stage (F0, F1) had the most impact. Patients with little or minimal fibrosis (stage F0, F1) had an 88% reduced risk for having extensive fibrosis in the second biopsy 20 months after the first biopsy and after therapy (Odds Ratio 0.12, p<0.001)
     
  • Achieving a sustained virologic response had the second most impact reducing risk for extensive fibrosis on the 2nd biopsy by 64% (OR 0.36, p<0.001)
     
  • Age lower than 49 had the third most impact reducing risk by 49% (OR 0.51, p<0.001)
     
  • Interestingly, Body Mass Index (<27) had the fourth most impact by reducing risk by 35% (OR 0.65, p<0.001)
     
  • Baseline activity (A0, A1: patients with little or no activity) had the fifth most impact by reducing risk by 30% (OR 0.70, p<0.02)
     
  • Viral Load <3.5 million reduced risk by 21% (OR 0.79, p=0.03)
     

I think the most interesting from the above data is that body mass index had an effect on outcome, Having more body mass increased risk. Expectedly, low viral load and achieving a sustained response were significant factors in reducing risk for having significant fibrosis in the 2nd biopsy.
 
Predictability of SVR After 12 week PCR Response
 
Poynard reported data similar to found with Pegasys+RBV on the predictability of sustained response based on the viral load response at 12 weeks. The analysis included 174 patients from the database who received PegIntron 1.5+RBV. 90% (n=120) who were PCR negative at week 12 achieved a sustained response. 26% who had a 2 log or greater reduction in PCR (n=23) achieved a sustained response. And 0 patients with <2 log reduction in viral load (n=31) at week 12 achieved a sustained response. The Pegasys analysis on using 12-week PCR response to predict outcome was more extensive and can be read in the NATAP AASLS report on this topic.
 
Can Cirrhosis Be Reversed?
 
153 patients with cirrhosis were included in this analysis. Poynard called these results surprising-- 49% (n=75) reversed cirrhosis. In the first biopsy 153 patients had F4 stage fibrosis (cirrhosis). In the second biopsy 23 patients had regressed to stage 3 (f3), 26 patients regressed to stage 2 (F2), 23 patients regressed to stage 1 (F1). And 78 patients still had stage 4. Poynard did comment on the sample size of liver taken in biopsy alluding to the limitations this presents.
 
Using a univariate analysis Poynard found the following significant factors in reversing cirrhosis:
 
 

  • using a reinforced regimen which I think he defined as IFN for greater then 24 weeks which I assume means or includes 48 weeks IFN/RBV and PegIntron/RBV regimens translates into a greater likelihood of reversing cirrhosis
     
  • achieving a sustained response (33% vs 15%) increases chance of reversing cirrhosis
     
  • reduction of activity grade in the second biopsy after therapy was a factor. 45% of patients with activity grade of A0/A1 in second biopsy reversed cirrhosis compared to 23% who did not have activity grade of A0/A1

     
    Another study using Pegasys monotherapy presented by Jenny Heathcote showed patients with cirrhosis could improve their histology (a histologic response in this study was defined as a decrease of at least 2 points on the 22-point Histological Activity Index). 30% using Pegasys montherapy achieved a sustained response vs 8% using standard interferon.
     
    www.natap.org/2001/sep/can_cirrhotics090401.htm
  • Please visit the above website for more information.
  •      We would like to thank Jules Levin

     

     

      Abstract 676. ACUTE HEPATITIS C: NATURAL COURSE AND RESPONSE TO ANTIVIRAL TREATMENT
      Tilman J Gerlach, Reinhart Zachoval, Norbert Gruener, Maria-Christina Jung, Klinikum Grosshadern Med Dept II, Muenchen Germany; Axel Ulsenheimer, Winfried Schraut, Inst fuer Immunologie, Muenchen Germany; Albrecht Schirren, Klinikum Grosshadern Med Dept II, Muenchen Germany; Martin Waechtler, Markus Backmund, Gen Hosp MŸnchen Schwabing, Muenchen Germany; Helmut Diepolder, Gerd Pape, Klinikum Grosshadern Med Dept II, Muenchen Germany
     
    Below is the program book abstract, which I think portrays the essence of the oral presentation at the AASLD meeting. Another report on this presentation is being prepared. As you may know, German researchers first reported on treating acute HCV at DDW in the Spring 2001. A published article followed by much attention occurred in the Fall 2001. Identifying persons with acute HCV is very difficult just as it is in identifying acutely infected persons with HIV. But, if such a person can be identified treatment consideration may be crucial. Identification & treatment of acutely infected persons can be an important public policy position. This may have particular application to health care workers.
     
    Background: Although screening of blood products for hepatitis C virus (HCV) has virtually eliminated post-transfusion hepatitis C, HCV still causes about 20% of cases of acute hepatitis today. These patients frequently present with acute symptomatic hepatitis C, which differs in many aspects from patients with post-transfusion hepatitis C. Little is known, however, about the natural course and the optimal treatment strategy for acute hepatitis C as it presents today.
     
    Methods: The diagnosis of a HCV in fifty-six consecutive patients was based on seroconversion to anti-HCV antibodies or clinical and biochemical criteria (acute onset of hepatitis with elevation of ALT at least 10x the upper limit of normal, exclusion of other liver diseases) and on the presence of HCV-RNA by RT-PCR in the first serum sample.
     
    Results: Fifty-six consecutive patients with acute hepatitis C were diagnosed in two large referral centers for infectious diseases and hepatology. 47/56 patients presented with symptomatic disease (fatigue (24%), abdominal pain (14%), jaundice (24%), nausea (19%)) while 9/56 were clinically asymptomatic. The major risk factors for acute HCV infection were IV-drug abuse (n=14), recent medical procedures (n=17), HCV-positive sexual partner (n=5), and needle-stick injury in medical employees (n=5), in 15 patients (27%) no risk factor or possible source of infection could be identified. Six patients received immediate antiviral therapy (IFN-a alone or in combination with ribavirin), 10 patients refused to therapy or were not eligable for IFN-a therapy. In 50 patients, not being treated immediately, the natural course of acute HCV was further studied: 34/50 (68%) patients initially cleared the virus spontaneously within a median of 11,9 weeks (range 2 to 24 weeks), but only twenty-three (47%) persistently remained HCV-RNA negative until the end of follow-up (median 23months, range 6 to 55 months) and were classified as self-limited hepatitis C. In eleven patients (22%) HCV RNA relapsed after a median of 23 weeks (range 8-86 weeks) and 16/50 (32%) patients did not clear HCV infection spontaneously and developed chronic hepatitis C. Patients with self-limited hepatitis C (n=22) and those developing chronic hepatitis C (n=28) did not differ with regard to age, risk factors for HCV infection, HCV-genotype, or initial viral load. However, symptomatic disease, female sex, and a high peak bilirubin level were strong predictors of spontaneous HCV clearance. While 49% of patients with symptomatic acute HCV cleared infection spontaneously, none of the patients with asymptomatic acute HCV (n=9) cleared HCV infection without treatment.
     
    Since the majority (86%) of patients with spontaneous viral clearance lost HCV RNA within twelve weeks after onset of symptoms, antiviral therapy was recommended to patients who did not loose HCV RNA by week 12 after onset of symptoms. Of 34 patients with chronic hepatitis C, 24 patients started either interferon-alpha alone or in combination with ribavirin. So far, twenty-one patients responded with loss of HCV-RNA and normalization of aminotransferases; 15 of 16 IFN-responders who have completed follow-up (>6 months after end of treatment) are sustained responders and one patient relapsed. Five responders are still under follow-up (end-of-follow-up sustained response rate 82%) and three patients did not respond to antiviral therapy. Although not mentioned in the results but discussed in the oral presentation was the 6 patients who were treated immediately upon identification. And I recall 4 or 5 of them had a virologic response.
     
    Conclusions: In the management of acute HCV infection a high spontaneous viral clearance rate within the first twelve weeks after onset of symptoms has to be considered. The strategy to treat symptomatic patients who remained HCV-RNA positive beyond three months after onset of disease led to an overall sustained viral clearance in 90% of patients, while unnecessary treatment was avoided in those with spontaneous viral clearance. In contrast patients with asymptomatic acute HCV infection are unlikely to clear the virus spontaneously and antiviral therapy should be commenced as early as possible.
       HALT-C Trial: 4-year study of Maintenance Therapy in 1350 patients
     
      Written for NATAP by Mark Sulkowski, MD, Johns Hopkins University School of Medicine

    Abstract 279. Retreatment of Interferon And Interferon-Ribavirin Non-Responders with Peginterferon-alpha-2a (Pegasys) And Ribavirin: Initial Results from the Lead-In Phase of the Halt-C Trial

    The HALT-C trial was designed to determine if long term maintenance interferon therapy, administered over 4 years, could prevent histologic progression, reduce the development of hepatocellular carcinoma and the need for hepatic transplantation in patients with chronic HCV and advanced fibrosis or cirrhosis who remain HCV-RNA (+) despite therapy. Since peginterferon plus ribavirin is more effective than standard interferon/ribavirin for treatment of chronic HCV all patients enrolled in the HALT-C trial were first treated with peginterferon plus ribavirin during the lead-in phase of this trial.

    This study is enrolling 1350 patients with advanced liver disease (bridging fibrosis/cirrhosis, Ishak Fibrosis stage > 3) and no evidence of hepatic decompensation. All patients had previously failed to respond to interferon-based therapy administered for at least 12 weeks. After screening, all patients received pegylated interferon alfa-2a (180 mcg weekly) plus ribavirin (1 - 1.2 grams/day). Patients who are HCV-RNA (-) at week 20 continue therapy for 48 weeks total. Patients who are HCV-RNA (+) either stop treatment or receive a maintenance dose of Pegasys 90ug/week for 3.5 years.

    Dr. Adrian Di Bisceglie presented on-treatment virologic response data on the first 268 patients who completed at least 20 weeks of therapy within this ongoing study. For the purpose of this presentation, viral response was defined as an undetectable HCV-RNA level at treatment week 20. 15 (5.6%) patients discontinued therapy prior to week 20. At week 20, 107 of 268 patients (42%) (based on an intention-to-treat analysis) had an undetectable HCV RNA level. These patients will continue therapy for an additional 28 weeks and, per protocol, will not enter the "maintenance" phase of the study. There were several important "sub-group" analysis presented. Persons who had only failed prior interferon monotherapy were much more likely to achieve a response than those who failed prior interferon/ribavirin combination therapy (53% > 31%) and African-Americans were significantly less likely to respond than others (10% < 43%).

    In addition, a large number of patients had dose reductions of the PEG-interferon (53%), ribavirin (44%) or both (47%). Thus, while the discontinuation rate was quite low (~5%), it remains uncertain if such dose reductions will impair the overall effectiveness of the therapy. Nonetheless, these results are encouraging and suggest that persons with advanced liver disease who failed to respond virologically to prior therapy may benefit from a course of pegylated interferon/ribavirin.

    Editorial note: Baseline data for 268 patients-- 41% of patients in study had cirrhosis at baseline. 84% were genotype 1. Mean ALT was 124. 88% were Caucasian. 63% had received IFN+RBV. Mean HCV-RNA was 3.5 million IU/mL. Mean age 50. The degree of fibrosis was associated with response (44% Ishak 3-4 [bridgng fibrosis] vs 31% Ishak 5-6 [cirrhosis], p=0.03). Gender was not associated with response (40 vs male vs 36% female, NS). Genotype was a factor in response Genotype 2b: 88%; genotype 3a: 93%, genotype 1a: 30%; genotype 1b: 39%; genotype 2a: 35%. Baseline HCV-RNA did not appear to influence response. Mean reduction in HCV-RNA was 3.7 log; 45% had a 3+ log reduction, while 15% had a 2-log reduction, 21% had a 1-log reduction, and 18% had <1-log reduction. It will be interesting to see if the patients with little viral load reduction demonstrate improved, stopped, or slowed fibrosis.
    The long-term goals or outcomes from HALT-C will take several years to achieve. These interim results are similar to those seen in several other smaller studies reported at the conference.
     
    Reviewed Feb 2004
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