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A Bi-Monthly Publication of the Hepatitis Support Project

May 25 , 2007
Volume 4, Issue 10

Liz Highleyman

To download pdf version click here

In This Issue:

Hepatitis C

• HCV and Lymphoma

• FibroScan Predicts Portal Hypertension

• Racial Disparities in Portal Hypertension Treatment

• New HIV/HCV Coinfection Guidelines

• Treatment of Coinfected Patients

• HAART and Liver Disease Progression

HCV and Lymphoma HCV
infection may increase the risk of certain types of lymphoma (cancers of the lymphatic system), according to a study in the May 8, 2007 Journal of the American Medical Association. T.P. Giordano and colleagues conducted a retrospective analysis of 146,394 HCV positive and 572,293 HCV negative patients at U.S. Veterans Affairs medical facilities between 1997 and 2004; HIV positive individuals were excluded. Over more than 5 years of follow-up, 1,359 patients were diagnosed with non-Hodgkin’s lymphoma (NHL), 165 with Waldenström macroglobulinemia (a rare form of lymphoma), and 551 with cryoglobulinemia. Individuals with HCV had a 28% greater chance of developing NHL, nearly triple the risk for Waldenström macroglobulinemia, and about four times the risk for cryoglobulinemia. However, HCV positive patients were not at significantly increased risk for other hematological malignancies or thyroid cancer. The researchers concluded that, “Hepatitis C virus infection confers a 20% to 30% increased risk of non-Hodgkin lymphoma,” but emphasized that the overall lymphoma rate remained low; they also suggested that effective anti-HCV therapy could potentially reduce the risk of lymphoma. For more information on this study, see the June 2007 HCV Advocate (after June 1, 2007).

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FibroScan Predicts Portal Hypertension
Noninvasive liver stiffness measurement using transient elastography (FibroScan) can predict portal hypertension in patients with HCV-related cirrhosis, according to a study in the May 2007 issue of Hepatology. Portal hypertension, or increased pressure in the portal vein carrying blood to the liver, can cause life-threatening complications including variceal bleeding, ascites, and hepatic encephalopathy. Hepatic venous pressure gradient (HVPG) is the standard measure for assessing portal vein pressure, but this procedure is invasive and expensive. In a study by F. Vizzutti and colleagues, 61 chronic hepatitis C patients with diagnosed or suspected cirrhosis underwent transient elastography, HVPG measurement, and liver biopsy. Overall, there was a significant positive correlation between HVPG and transient elastography results. However, while the correlation was excellent for HVPG values less than 10-12 mmHg, it was not as good for higher values. There was also a correlation between liver stiffness and esophageal varices, but the negative and positive predictive values were only 66% and 77%, respectively. “We suggest that measurement of liver stiffness by transient elastography may represent a reliable noninvasive methodology for the prediction of clinically significant and severe portal hypertension, although not good enough to replace endoscopy for the detection of varices,” the investigators concluded.

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Racial Disparities in Portal Hypertension Treatment
In a related article in same issue,G.C. Nguyen and colleagues reported that African-American and Hispanic patients were less likely than whites to receive palliative and life-saving treatment for complications of portal hypertension. Based on the Nationwide Inpatient Sample, they identified 63,696 patients with cirrhosis who were hospitalized due to complications of portal hypertension between 1998 and 2003. They found that African-Americans and Hispanics were significantly less likely than whites to receive portosystemic shunts, prompt (within 24 hours of admission) endoscopy and treatment of bleeding varices, or liver transplantation. Compared with white patients, African-Americans were more likely – but Hispanics were less likely – to die in the hospital. Patients on Medicare or Medicaid, and those who were uninsured, were less likely to receive shunts, more likely to receive delayed endoscopy, and much less likely to receive liver transplants than those with private insurance. However, the researchers noted that the racial differences in treatment were independent of health insurance. “Further primary studies are warranted to confirm and elucidate the mechanisms of racial disparities in order to enact interventions to rectify them,” they concluded.

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New HIV/HCV Coinfection Guidelines
In the May 31, 2007 issue of AIDS, V. Soriano and an international panel of experts published updated guidelines for the management of hepatitis C in HIV positive individuals. The updated recommendations cover 11 areas, including management of patients with persistently normal ALT, noninvasive assessment of liver fibrosis, predictors of response to anti-HCV therapy, retreatment of coinfected nonresponders and relapsers, care of coinfected patients with end-stage liver disease, treatment of acute hepatitis C in HIV positive individuals, and management of patients with more than one hepatitis virus. In terms of optimal doses and duration of anti-HCV therapy, the authors recommended standard doses of pegylated interferon plus 1000-1200 mg/day weight-based ribavirin for 48 weeks for patients with all HCV genotypes, although they acknowledged that 24 weeks may be adequate for those with genotypes 2 or 3, while slow responders with genotypes 1 or 4 may benefit from longer therapy. The panelists also reviewed the latest data concerning interactions between anti-HCV medications and antiretroviral drugs, as well as hepatotoxicity due to antiretroviral agents. For further details, see the June 2007 HCV Advocate (after June 1, 2007).

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Treatment of Coinfected Patients
In the April 2007 Journal of Viral Hepatitis, M. Crespo and colleagues reported data from a study of 121 HIV/HCV coinfected patients randomly assigned to receive either conventional interferon or pegylated interferon alpha-2b (PegIntron; 1.5 mcg/kg/week) plus 800 mg/day fixed-dose ribavirin; subjects with genotypes 2 or 3 were treated for 24 weeks, while those with genotypes 1 or 4 were treated for 48 weeks. In an intention-to-treat analysis, the overall sustained virological response (SVR) rate was higher in the pegylated interferon compared with the conventional interferon arm (55% vs 26%). By genotype, SVR rates using pegylated interferon were 45% for genotype 1, 50% for genotype 4, and 71% for genotypes 2 or 3, which compare favorably with rates observed in prior coinfection studies. Virological response at weeks 4, 8, and 12 was highly predictive of SVR. However, 18% of patients developed hyperlactatemia (elevated blood lactate), a symptom of mitochondrial toxicity. This was clinically significant in six patients, two of whom died; in these individuals, mitochondrial DNA decreased significantly after starting anti-HCV treatment. While ribavirin itself can cause mitochondrial toxicity, this is more of a concern for coinfected patients who may also be taking antiretroviral drugs that can cause this side effect, and treatment should be tailored accordingly.

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HAART and Liver Disease Progression
In a related study reported in the April 1, 2007 issue of AIDS, H. Al-Mohri and colleagues used the noninvasive AST-to-platelet ratio index (APRI) biomarker test to assess fibrosis progression in 133 HIV/HCV coinfected patients and 540 HIV monoinfected individuals who did not have liver complications at baseline. According to the authors, there was “clearly a complex relationship” between antiretroviral therapy and fibrosis. While coinfected patients with higher CD4 cell counts and better HIV control had lower rates of fibrosis progression, HAART use was associated with increasing APRI scores in both coinfected and HIV monoinfected individuals. Overall, 4.5% of coinfected patients developed liver complications, compared with 1.1% of HIV monoinfected subjects, and the coinfected patients developed such complications sooner (2.85 vs 3.96 years). Despite prolonged HAART, coinfected patients “remain at increased risk of progression to end-stage liver disease,” the authors concluded. “Our findings highlight the need to treat HCV infection specifically, because immune restoration from HAART alone cannot be relied on to improve outcomes in HCV coinfection.”

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