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News Review

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HEPATITIS JOURNAL REVIEW:
A Bi-Monthly Publication of the Hepatitis Support Project

January 15, 2006
Volume 3, Issue 1


Liz Highleyman

To download pdf version click here


In This Issue: Hepatitis C


HCV-Related Healthcare Utilization

HCV Viral Load and Risk of Death

HIV/HCV Coinfection News


HCV-Related Healthcare Utilization

While the rate of new HCV infections has declined dramatically in recent years, hepatitis C is placing increased demands on the healthcare system as people infected years or decades ago develop progressive liver damage. Despite attempts to increase public awareness about the disease, many patients still are not diagnosed until they develop advanced liver disease.

To gain a better understanding of the use of healthcare resources related to hepatitis C, William Grant, MD, and colleagues from Duke University analyzed inpatient data from the Healthcare Cost and Utilization Project, outpatient data from the National Ambulatory Medical Care Survey, and medication use data from the Verispan Source Prescription Audit; results were reported in the December 2005 issue of Hepatology. The researchers found that the number of HCV-related hospital admissions, number of days spent in a hospital, hospital financial charges, and number of physician visits increased by 25-30% annually from 1994 to 2001. The increased healthcare burden was seen primarily among individuals 40-60 years old, reflecting aging and associated disease progression in individuals infected in the past. While patients from racial/ethnic minority groups comprised about half of all HCV-related hospital admissions, they accounted for only 20% of physicians visits, suggesting they are receiving delayed diagnoses and later treatment. Increased healthcare usage was especially pronounced among HIV/HCV coinfected patients: in 1994, more than seven times as many hospitalizations as individuals with HCV alone. “Our findings highlight the urgency concerning HCV outcomes,” the authors concluded. “As patients continue to age and disease burden progresses, suboptimal decisions regarding HCV treatments will bring increasing opportunity costs for the health care system and society.”

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HCV Viral Load and Risk of Death

Unlike HIV disease, where higher viral load is clearly associated with worse disease progression, most past research has not found a link between HCV viral load and liver disease severity or mortality. But a new study, reported in the December 2005 issue of Hepatology, yielded contradictory results. Michie Hisada, MD, from the National Cancer Institute and colleagues analyzed data from 6,570 HCV-positive injection drug users enrolled between 1987 and 1991, some of whom were coinfected with HIV and/or human T-lymphotropic virus type II (HTLV-II). Comparing 84 patients who died of end-stage liver disease (ESLD) and 305 surviving subjects, the researchers found that the risk of death from ESLD increased as HCV viral load rose. However, the risk of AIDS-related death and mortality due to other causes was not associated with HCV RNA level. Interestingly, non-black patients had a higher rate of death due to ESLD, despite evidence from other studies that African-Americans experience more rapid HCV disease progression and poorer response to hepatitis C treatment. ESLD risk did not differ by HIV status after adjusting for HCV viral load, which conflicts with past research suggesting coinfected patients have more rapid liver disease progression. Although the authors concluded that “HCV RNA level is a predictor of [ESLD],” further research is needed to explain why these results differ so much from those seen in other studies.

In an accompanying editorial, Theo Heller, MD, and Leonard Seeff, MD, from the National Institute of Diabetes and Digestive and Kidney Diseases pondered possible reasons for the divergent findings, including methodological errors, noncomparable study populations (e.g., differing rates of injection drug use or coinfection), or use of different assays. Trying to tease out cause and effect, they raised the possibility that both higher HCV RNA and worse liver disease progression may be due to compromised immunityrather than higher HCV viral load somehow promoting ESLD. But if Hisada’s findings are confirmed, Heller and Seeff wrote, this suggests that reducing HCV viral load with effective therapy may thereby decrease the risk of death due to ESLD, even if HCV is not completely suppressed or eradicated.

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HIV/HCV Coinfection News

Grant’s findings of higher HCV-related hospitalization rates among HIV/HCV coinfected patients in 1994 (before the advent of effective combination anti-HIV treatment), as well as Heller and Seeff’s suggestion that immunosuppression may worsen HCV disease progression, raise to the question: Can controlling HIV with effective combination antiretroviral therapy (HAART) reduce the risk – or at least the speed – of liver disease progression?

Two recent studies suggest this is the case. In the January 2006 Journal of Hepatology, Norbert Bräu, MD, and colleagues reported on a retrospective analysis of data from 656 hepatitis patients; 42% also had HIV and most of these were on HAART. Among the 51% of coinfected patients who achieved undetectable HIV viral loads, liver fibrosis progression was slower than that seen in coinfected individuals with detectable HIV RNA. In fact, the fibrosis progression rate in coinfected patients with fully suppressed HIV was similar to that seen in HIV negative individuals with hepatitis C.

In the January 15, 2006 Clinical Infectious Diseases, Sumita Verma, MD, and colleagues also reported that effective anti-HIV treatment appears to slow fibrosis progression. They conducted a retrospective analysis of data from 85 HIV/HCV coinfected patients and 296 with HCV alone. Coinfected individuals on HAART had liver disease progression rates and necroinflammatory scores similar to those observed in patients with HCV alone. However, patients who received suboptimal anti-HIV therapy (e.g., treatment with less potent nucleoside reverse transcriptase inhibitor [NRTI] drugs, even if they added more potent drugs later) had more advanced liver disease and faster fibrosis progression. According to the authors, their results suggest that “it is not just the presence or absence of HAART, but the promptness with which it is initiated after HIV diagnosis that favorably impacts [sic] hepatic fibrosis.” In an accompanying editorial, Jade Ghosn, MD, discussed how these findings may influence decisions about whether HIV or hepatitis C should be treated first. Coinfected individuals with CD4 T-cell counts above 350 cells/mm3, she recommended, “should first be assigned to receive anti-HCV treatment, because tolerance of this treatment would be optimal in the absence of HAART.” Those who are unwilling or unable to initiate pegylated interferon plus ribavirin, however, “may benefit from early HAART.”

HIV viral load is not a direct marker of immune status, but is correlated with lower CD4 cell counts – an indication of compromised immunity. In Bräu’s study, only coinfected patients with CD4 counts below 500 cells/mm3 experienced accelerated fibrosis progression (although CD4 cell count was not independently associated with fibrosis progression rate in a multivariate analysis controlling for other factors). Paula Braitstein, PhD, and colleagues from British Columbia, in the January 15, 2006 Journal of Infectious Diseases reported further evidence confirming that coinfection with HCV appears to impair CD4 cell response in coinfected patients starting HAART. In their study of 606 coinfected patients and 580 with HIV alone, coinfected individuals took longer to achieve a CD4 count increase of 75 cells or more; during the first 48 weeks on HAART, coinfected patients gained an average of 20 cells/mm3, compared with 75 cells/mm3 for HIV monoinfected subjects.

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