By Michael Carter

Anti-HIV treatment may mean that the rate of liver fibrosis is significantly slowed in patients with HIV and hepatitis C coinfection, according to a German study presented to the Fourth International Conference on HIV and Hepatitis C Coinfection in Madrid. The investigators found that there was no difference in degree of liver damage between HIV/hepatitis C coinfected patients who received antiretroviral therapy and that seen in individuals who were only infected with hepatitis C.

This finding adds weight to the recommendation in the recently revised British HIV treatment guidelines that early initiation of HIV therapy is especially important in HIV/hepatitis C-coinfected patients.

It is now well established that HIV/hepatitis C coinfected patients experience faster hepatitis C disease progression than patients who are only infected with hepatitis C. It is thought that this is because of the damage to the immune system that HIV causes. There is some evidence that the use of anti-HIV treatment can help slow the rate of liver disease in coinfected patients, but this is still a controversial area.

To gain a better understanding of the capacity for HIV therapy to prevent hepatitis C-related liver damage, investigators at the University of Bonn designed a study involving 141 patients. A total of 84 of these patients were only infected with hepatitis C virus, the remaining 57 were coinfected. The investigators used FibroScan investigations to assess the degree of liver stiffness in these two groups of patients. Demographic, and hepatitis/HIV-related disease data were analysed by the investigators to see if they could identify any factors associated with an increased risk of liver stiffness.

The two groups of patients were broadly similar, although the coinfected individuals were more likely to be infected with the hard to treat hepatitis C genotype 1 (82% vs. 70%), and were significantly more likely to have acquired hepatitis C after receiving infected blood products (44% vs. 0%).

Of the coinfected patients, 82% were taking HIV therapy, and the median CD4 cell count was 430 cells/mm3.

FibroScan investigations showed that both groups of patients had comparable, but nevertheless severe, liver stiffness (14.4 kPa in the monoinfected patients vs. 12.4 kPa in the coinfected individuals). This degree of liver stiffness is indicative of cirrhosis.

Although the investigators were unable to present data on the duration of hepatitis C infection in their patients, they believe that the large number of coinfected patients who were infected with hepatitis C after receiving infected blood products suggests that a significant number of patients had been infected over 25 years ago.

Most of the coinfected patients were taking HIV therapy or had high CD4 cell counts, but the CD4 cell count was below 200 cells/mm3 in 14% of coinfected patients. Average liver stiffness scores were 18.4 kPA amongst these patients with a low CD4 cell count compared to 11.5 kPA for patients with better immune function. This difference did not reach statistical significance, but this was because of small numbers and suggested to the investigators that a higher CD4 cell count was protective against hepatitits C-related liver damage.

The investigators concluded that their study confirms earlier research showing that coinfected patients taking antiretroviral therapy have their rate of liver disease slowed. They added, “our findings…may be a hint that fibrosis progression in well-treated HIV-positive patients will no longer be different from that in hepatitis C virus-monoinfected patients.”


Reference
Grunhage F. et al. No difference in liver fibrosis in a cohort of HIV/HCV-coinfected patients on HAART compared to HIV-negative HCV-patients assessed by transient elastography. Fourth International Workshop on HIV and Hepatitis Coinfection, Madrid, abstract 8, 2008.