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A Bi-Monthly Publication of the Hepatitis Support Project

January 25, 2007
Volume 4, Issue 2

Liz Highleyman

To download pdf version click here

In This Issue:

Hepatitis C

• HCV Treatment for Injection Drug Users on Naltrexone

• Impact of Steatosis on HCV Treatment

• Steatosis in African Americans

• HCV Linked with Lymphoma

• CD4 Count Linked with Immune Response to HCV

• Higher Cardiovascular Risk in Coinfected Patients

• HCV Reduced Antiretroviral Lipid Elevations

HCV Treatment for Injection Drug Users on Naltrexone

Some physicians are reluctant to treat hepatitis C in active or recent injection drug users, but recent studies have shown that drug users can achieve sustained responses to interferon-based therapy if they can maintain good adherence. In the January 2007 issue of Hepatology, G.P. Jeffrey and colleagues reported on a study of anti-HCV treatment of IDUs maintained on subcutaneous implants of the opiate antagonist naltrexone (not yet approved by the U.S. FDA). Among the first 50 subjects who completed treatment with interferon plus ribavirin, 34 (68%) experienced an end-of-treatment response, and 31 (62%) achieved sustained virological response (SVR). About 20% stopped treatment early due to side effects or poor adherence, and about half received antidepressants or antipsychotic medications during treatment. Among the patients who achieved SVR, 42% reported occasional injection drug use during and after treatment. The researchers noted that the results observed in this study were comparable to those previously reported for non-IDU patients, leading them to recommend that “HCV antiviral therapy should be offered to this large and currently under-treated group.”

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Impact of Steatosis on HCV Treatment

Liver steatosis (fat accumulation) has been associated with accelerated liver fibrosis progression and poorer response to antiviral therapy. As described in the January 2007 Journal of Viral Hepatitis, J. Westin and colleagues monitored steatosis in liver biopsy samples from 231 patients with chronic hepatitis C treated with pegylated interferon plus ribavirin in the international DITTO trial. The researchers found that steatosis impaired early virological response during treatment in patients infected with both genotype 3 and non-3 HCV, but negatively affected final treatment outcomes mainly in individuals with non-3 genotypes. They concluded that “interventions aiming at reducing hepatic steatosis prior to the onset of antiviral therapy may be of benefit to patients infected with HCV of the non-3 genotypes,” but that “[p]atients infected with genotype 3, on the other hand, should be offered early antiviral treatment.”

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Steatosis in African Americans

It is well established that African Americans respond more poorly to interferon-based therapy compared with Caucasians. In the January 2007 issue of Hepatology, H.S. Conjeevaram and colleagues reported on a study comparing rates of liver steatosis in African-American and Caucasian patients with chronic genotype 1 hepatitis C who participated in a clinical trial of pegylated interferon plus ribavirin. Liver biopsy results, available for 194 African-American and 205 Caucasian patients, showed that 61% of the African Americans and 65% of the Caucasians had steatosis. In a univariate analysis, steatosis was associated with insulin resistance, higher body mass index, larger waist circumference, higher serum triglyceride levels, higher ALT and AST levels, and histological scores for liver inflammation and fibrosis. After adjusting for these factors, African Americans had a lower risk of steatosis than Caucasians. Insulin resistance – but not steatosis – was associated with a lower rate of sustained virological response.

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HCV Linked with Lymphoma

In the December 2006 issue of Gastroenterology, A. Nieters and colleagues from Germany described a large, multicenter, case-control study to assess the association between chronic hepatitis C and lymphoma. The analysis included 1807 case patients with newly diagnosed lymphoma and 1788 matched control subjects without lymphoma. HCV infection was detected in 53 patients with lymphoma (2.9%) and 41 control subjects (2.3%). When the analysis was restricted to individuals with detectable HCV RNA (indicating active viral replication), the increase in lymphoma risk was even greater. More specifically, HCV infection was associated with diffuse large B-cell lymphoma, but not with chronic lymphocytic leukemia or follicular, Hodgkin’s, or T-cell lymphoma. The researches concluded that, “These results support a model that chronic HCV replication contributes to lymphomagenesis and establish a specific role of HCV infection in the pathogenesis of diffuse large B-cell lymphoma.”

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CD4 Count Linked with Immune Response to HCV

HCV infection is more likely to become chronic and liver disease tends to progress more rapidly in individuals coinfected with HIV, which may be related to diminished HCV-specific T-cell responses. In the December 12, 2006 issue of PLoS Medicine, A.Y. Kim and colleagues reported on a study examining the association between HIV disease and an individual’s ability to maintain spontaneous control of HCV without treatment. The study included 60 HIV/HCV coinfected patients and 34 HCV monoinfected individuals, half of whom demonstrated spontaneous control of HCV. Among the coinfected participants, T-cell lymphoproliferative responses were more frequent among those who spontaneously controlled HCV. However, lymphoproliferative responses were less frequent among coinfected patients with spontaneous HCV clearance compared with HIV negative individuals. Preservation of HCV-specific lymphoproliferative responses in coinfected individuals was associated with a higher nadir (lowest-ever) CD4 cell count. During the follow-up period, among those who had previously spontaneously controlled HCV, HCV recurrence occurred in 24% of coinfected patients but in none of the HIV negative individuals. Further, HCV-specific T-cell responses were not observed in any patients with nadir CD4 counts below 300 cells/mm3, despite immune reconstitution after starting antiretroviral therapy for HIV. The researchers concluded that maintaining higher CD4 T-cell counts – either through long-term non-progression of HIV disease or through early antiretroviral therapy – played a crucial role in spontaneous control of HCV in coinfected individuals.

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Higher Cardiovascular Risk in Coinfected Patients

Given the aging population and the metabolic side effects associated with some antiretroviral drugs, cardiovascular disease is a growing concern for HIV positive people. In the January 11, 2007 issue of AIDS, M. Freiberg and colleagues reported on a cross-sectional study to examine the association between hepatitis C and cardiovascular disease in 395 individuals in the HIV-LIVE cohort of HIV-infected patients with current or past alcohol problems; half were coinfected with HCV. The researchers found that cardiovascular disease was more common among HIV/HCV coinfected participants compared to those with HIV alone (11% vs 3%). The association between HCV infection and cardiovascular disease persisted after adjusting for age and other sociodemographic characteristics, substance use, and known cardiovascular risk factors.

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HCV Reduced Antiretroviral Lipid Elevations

While the Freiberg study suggests that HCV infection may increase the risk of cardiovascular disease in people with HIV, another recent study indicated that HCV may have a protective effect. It is well known that certain anti-HIV drugs – in particular protease inhibitors – can raise total cholesterol and triglyceride levels in the blood, thereby increasing the risk of heart disease. As reported in the January 2, 2007 issue of AIDS, C.L. Cooper and colleagues evaluated blood fat levels in 357 HIV monoinfected and 115 HIV/HCV coinfected patients receiving antiretroviral therapy between January 1996 and June 2005. After a year on therapy, mean changes in total cholesterol were 1.24 mmol/L in HIV monoinfected patients compared with 0.01 mmol/L in coinfected patients. Further, 8% of HIV monoinfected individuals, but fewer than 1% of coinfected patients, stopped antiretroviral drugs due to metabolic complications. Likewise 8% of HIV monoinfected patients, but no coinfected patients, started lipid-lowering drugs. Among coinfected patients who achieved a sustained virological response to interferon-based therapy for hepatitis C, total cholesterol increased by 0.85 mmol/L, but cholesterol did not increase in nonresponders/relapsers. The authors concluded that, “HCV coinfection appears to confer a degree of protection from HAART-related lipid complications.”

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