The presence of intestinal bacteria in blood (bacterial translocation)
is associated with more severe liver disease in people who are co-infected
with HIV and hepatitis C virus, Spanish investigators report in the online
edition of the Journal of Acquired Immune
Deficiency Syndromes.
Large numbers of HIV-positive people are co-infected with hepatitis C
virus. Liver disease caused by hepatitis C is an important cause of serious
illness and death in these patients.
The pace of liver disease is faster in co-infected people than in
those who are hepatitis C-monoinfected. However, the reasons for this are
unclear.
Glossary
- enteric
-
Associated with the gut.
Bacterial translocation is the mechanism by which some enteric
conditions cause liver disease. Infection with HIV has also been associated
with bacterial translocation. This may cause the chronic immune activation that
contributes to the accelerated course of liver disease seen in co-infected
people.
Investigators in Madrid wanted to establish a clearer understanding of
bacterial translocation in co-infected people and the association between the
severity of bacterial translocation and the extent and pace of liver disease.
They therefore designed a study involving 255 co-infected people who had
undergone a liver biopsy between 2000 and 2007. In addition,100 HIV/hepatitis
C-uninfected people who had been blood donors were included as controls. All participants had tests to see if they had the DNA of intestinal bacteria in their blood. The
stage and pace of liver fibrosis was assessed in those with HIV and hepatitis
C.
The co-infected participants had a median age of 40, three-quarters were
men, and their median CD4 cell count was 483 cells/mm3. Most (85%)
were taking antiretroviral therapy and 71% had an undetectable viral load.
Baseline hepatitis C viral load was above 500,000 IU/ml in 73% of co-infected participants.
Significant fibrosis was present in 53% of patients and 27% had advanced
fibrosis.
Intestinal bacteria were detectable in the blood of 96% of co-infected
participants compared to 7% of controls (p < 0.001).
Moreover, co-infected participants with a CD4 cell count below 350 cells/mm3
had significantly higher levels of bacteria in their blood than those with CD4
cell counts above this level (157 vs 112 copies/ml, p = 0.03).
“HIV/hepatitis C virus-co-infected patients had higher plasma levels of
bacterial DNA than healthy controls,” write the investigators. “Patients with CD4 cell counts < 350 cells/mm3 had higher plasma bacterial DNA
than those with CD4 cell counts above 350 cells/mm3.”
People with more advanced fibrosis and faster progression of liver
disease had higher levels of intestinal bacteria in their blood than those
without these markers of liver disease (p < 0.05).
Each 100 copy/ml increase in bacterial load increased by 20% the chance
of having a higher fibrosis score (OR = 1.20; 95% CI, 1.00-1.44, p = 0.045).
Participants with a bacterial load above 175 copies/ml had the highest risk of
having more advanced liver fibrosis (OR = 3.04; 95% CI, 1.37-6.75, p = 0.006)
and faster progression of liver disease (OR = 2.97; 95% CI 1.24-7.09, p =
0.014).
“Our data show that bacterial translocation was associated with severe
liver disease among HIV infected patients with chronic hepatitis C,” conclude
the authors. “Future studies are needed to validate these results and to
evaluate whether plasma levels of bacterial DNA are a predictive and/or
surrogate marker of liver disease in HIV/hepatitis C-co-infected patients.”