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A Bi-Monthly Publication of the Hepatitis Support Project

February 10, 2008
Volume 5, Issue 3

Liz Highleyman

To download pdf version click here

In This Issue:

• 14-week Treatment for Genotype 2/3

• Insulin Resistance in Genotype 2/3 Patients

• RVR Predicts SVR in Coinfected Patients

• Marijuana and Fibrosis Progression

• Risk of Lymphoma

14-week Treatment for Genotype 2/3
Hepatitis C virus (HCV) genotypes 2 and 3 are easier to treat than genotype 1, and the standard course of interferon-based therapy is 24 weeks. But shorter treatment may be adequate for selected patients, according to a report in the January 2008 issue of Hepatology.  In the Scandinavian North-C trial, O. Dalgard and colleagues studied 428 previously untreated genotype 2 (20%) or 3 (80%) chronic hepatitis C patients. All were started on pegylated interferon alfa-2b (PegIntron) plus 800-1400 mg/day weight-based ribavirin. About 70% achieved rapid virological response (RVR; undetectable HCV RNA at week 4) and were randomly assigned to continue therapy through 14 or 24 weeks. In an intent-to-treat analysis, 81% of patients in the 14-week group and 91% in the 24-week group achieved sustained virological response (SVR). While this did not meet the predefined criteria for “non-inferiority,” the researchers concluded that “the SVR rate after 14 weeks of treatment is high, and although longer treatment may give slightly better SVR [rates], we believe economical savings and fewer side effects make it rational to treat patients with genotype 2 or 3 and RVR for only 14 weeks.”

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Insulin Resistance in Genotype 2/3 Patients
Though HCV genotype 2 and 3 patients respond better to treatment than those with genotype 1, similar factors predict poor response. As reported in the January 2008 Journal of Hepatology, H. Poustchi and colleagues studied the relationship between insulin resistance and achievement of SVR in 141 genotype 2/3 patients treated with either conventional or pegylated interferon plus ribavirin. Overall, the SVR rate was 77%. Individuals who achieved SVR had a lower mean serum insulin level (10.7 vs 22.2 mcU/mL) and less insulin resistance (HOMA-IR score of 2.5 vs 6.1) compared with nonresponders. Higher body mass index (BMI) and more advanced fibrosis were both independently associated with greater insulin resistance. After adjusting for fibrosis stage, patients with a HOMA-IR score below 2 were 6.5 times more likely to achieve SVR than those higher scores. The researchers concluded that, “Even in treatment-responsive genotypes 2 and 3, high HOMA-IR is associated with a reduced response,” and suggested that, “Improving insulin sensitivity may be a useful adjunct to antiviral therapy in these individuals.”

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RVR Predicts SVR in Coinfected Patients
While HIV/HCV coinfected patients as a group tend to respond less well to interferon-based therapy than HIV negative individuals, studies increasingly show that HCV viral kinetics and predictors of treatment response are similar. As reported in the January 2, 2008 issue of AIDS, L. Martin-Carbonero and colleagues with the Spanish PRESCO trial studied 389 coinfected patients (49% genotype 1; 1% genotype 2; 38% genotype 3; 12% genotype 4) treated with pegylated interferon alpha-2a (Pegasys) plus 1000-1200 mg/day weight-based ribavirin. Genotype 1or 4 patients were treated for either 48 or 72 weeks, while those with genotype 2 or 3 were treated for either 24 or 48 weeks; those who did not achieve early virological response by Week 12 discontinued therapy. Overall SVR rates were 36% for patients with genotype 1, 72% for genotypes 2/3, and 33% for genotype 4. Regardless of genotype, RVR was the strongest predictor of SVR, with positive predictive values of 90% for genotype 3, 83% for genotype 4, and 69% for genotype 1. Low baseline HCV RNA (below 500,000 IU/mL) was associated with SVR only for the genotype 1 patients, and extending treatment did not improve sustained response rates. “Undetectable HCV RNA at week 4 is the best predictor of curing chronic hepatitis C in HCV/HIV coinfected patients,” the authors concluded. They added that “HIV patients with HCV [genotype] 3 and RVR may permit shortening therapy duration to only 24 weeks.” International coinfection treatment guidelines have recommended 48 weeks of anti-HCV therapy for all HIV positive patients regardless of genotype, but the latest revision (published in the May 31, 2007 issue of AIDS) agrees that 24-week treatment “could be advised” for genotype 2/3 patients with RVR, low HCV viral load, absence of advanced fibrosis, good adherence, and adequate doses of weight-based ribavirin.

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Marijuana and Fibrosis Progression
Patients with chronic hepatitis C may use medical marijuana to help manage side effects of interferon-based treatment, but a recent study showed that long-term daily cannabis use may contribute to more rapid liver fibrosis progression. As reported in the January 2008 issue of Clinical Gastroenterology & Hepatology, J.H. Ishida and colleagues interviewed 204 chronic hepatitis C patients between 2001 and 2004, assessing demographic characteristics, risk factors, and cannabis and alcohol use. About 14% of respondents reported daily cannabis use within the past 12 months, 45% reported occasional use, and 41% reported no use. Compared with occasional or no use, daily marijuana use was strongly associated with moderate-to-severe fibrosis (Ishak stages F3-F6) relative to mild or absent fibrosis (stages F0-F2). However, frequent cannabis use was not strongly linked to mild fibrosis (stages F1-F2) compared with absent fibrosis (stage F0). Moderate-to-heavy alcohol consumption and higher HCV RNA viral load also predicted worse fibrosis. Based on these findings, the researchers recommended that, “HCV-infected individuals should be counseled to reduce or abstain from cannabis use.”

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Risk of Lymphoma
Several studies have shown that people with chronic hepatitis C may be at greater risk for malignant lymphoma (Hodgkin’s disease and non-Hodgkin’s lymphoma). But this higher risk may be reversed with successful anti-HCV treatment, according to a study in the December 2007 American Journal of Medicine. Y Kawamura and colleagues conducted a retrospective analysis of the incidence of malignant lymphoma in 501 untreated chronic hepatitis C patients in Japan and 2,708 individuals who had received interferon-based therapy. They found that treated non-responder patients with persistent HCV RNA had lower cumulative lymphoma incidence rates compared with untreated patients at Year 5 (0.4% vs 0.6%) and Year 10 (1.5% vs 2.3%), though rates were the same at Year 15 (2.6%). But among patients who achieved SVR, none developed malignant lymphoma through Year 15. The researchers concluded that, “[S]ustained virologic response induced by interferon therapy protects against the development of malignant lymphoma in patients with chronic HCV.”

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