As
reported at the 8th Annual International Congress on Drug Therapy in HIV Infection
(HIV8), held last week in Glasgow, researchers from Hospital Carlos III in Madrid,
Spain, studied the impact of antiretroviral therapy and metabolic complications
on fibrosis in coinfected patients.
Advanced
liver fibrosis was defined by a FibroScan (elastometry) score higher than 9.5
kilopascals (Kpa). Total exposure to each antiretroviral drug was calculated from
a pharmacy database.
Results
•
A
total of 490 HIV-HCV coinfected patients were identified, of whom 38% had advanced
liver fibrosis.
•
The
total coinfected group and those with advanced fibrosis were similar in terms
of demographic characteristics (age 43 vs 41 years; 77% vs 67% male).
•
Mean
CD4 cell counts were 488 vs 553 cells/mm3, and peak HCV viral loads were 6.4 vs
6 log IU/mL, respectively.
•
Overall,
3.5% of patients were HAART-naive, while 34.7% had received nevirapine (Viramune),
48.7% had received efavirenz (Sustiva/Stocrin), and 74.1% had taken protease inhibitor
(PI)-based regimens.
•
By
univariate analysis, the following factors were significantly associated with
advanced fibrosis:
- blood glucose level (126 vs 112 mg/dL); - triglyceride
level (198 vs 161 mg/dL); - lack of interferon-based therapy (57 vs 44%).
•
HCV
genotype and hepatitis B virus infection (HBsAg positivity) were not significantly
associated with fibrosis.
•
There
were no significant differences in the mean exposure to nevirapine (0.83 vs 0.82
years) or efavirenz (1.1 vs 1 years), nor to different nucleoside/nucleotide reverse
transcriptase inhibitors (NRTIs), in patients with and without advanced fibrosis.
•
However,
patients with advanced fibrosis had a longer mean duration of PI use (3.7 vs 3.1
years; P < 0.05).
•
By
multivariate analysis, the following factors were significantly associated with
advanced fibrosis:
- age (OR 1.9; P = 0.002); - male sex (OR 1.8; P
= 0.01); - CD4 cell count (OR 0.9; P = 0.002); - blood glucose (OR 1.2;
P =0.001).
Conclusion
"CD4
T-cell depletion is associated with advanced liver fibrosis in HIV positive patients
with chronic hepatitis C," the researchers concluded. "Insulin resistance
and liver steatosis, as reflected by higher glucose and triglyceride levels in
subjects with advanced liver fibrosis, might contribute to faster progression
of liver fibrosis in HIV-HCV coinfected patients. The specific role of protease
inhibitors, which may cause hyperlipidemia and insulin resistance, on liver fibrosis,
warrants further investigation."
11/21/06
Reference P
Barreiro, P Labarga, A Ruiz-Sancho, and others. Factors associated with progression
of liver fibrosis in HIV/HCV co-infected patients: influence of antiretrovirals
and metabolic disturbances. 8th Annual International Congress on Drug Therapy
in HIV Infection (HIV8). Glasgow, UK. November 12-16, 2006. Abstract P313.
