1056
Histological Findings, Predictors of Severe Fibrosis, and Assessment of Factors with Effect on the Fibrosis Progression Rate in HIV-infected Patients with Chronic Hepatitis C in the Era of HAART
Ana Moreno*1, S Diz1, A Moreno2, L Moreno1, A Muriel3, J Zamora3, C Quereda1, M Perez-Elias1, R Barcena4, and S Moreno1
1Hosp Ramon y Cajal, Madrid, Spain; 2Hosp Ramon y Cajal, Madrid, Spain; 3Hosp Ramon y Cajal, Madrid, Spain; and 4Hosp Ramon y Cajal, Madrid, Spain
Background: Predictors of histological severity and the
role of HAART on the fibrosis progression rate (FPR) in HIV/hepatitis C virus (HCV)
co-infection are controversial.
Methods: From January 1998 to May 2007, 323 consecutive,
hepatitis B surface antigen (HBsAg)–, HCV-treatment-naïve HIV subjects
underwent liver biopsy. We assessed predictors of histological severity and
factors influencing fibrosis progression rate (FPR; cut-off FPR >0.1).
Results: Subjects' characteristics were: 75% male, prior intravenous
drug users (IDU) (87%), 40±5 years, genotype 1/4 (n = 254, 80%), prior
AIDS in 100 (31%). Median time of HCV-infection 20 years (3 to 31); 51% had
received both protease inhibitor (PI) and NNRTI (median 34 (1 to 108) and 18 (1
to 92) months). Median HAI 6; F0 (n = 29, 9%),
F1 (n = 121, 38%), F2 (n = 61, 19%), F3 (n = 69, 21%), F4
(n = 43, 13%). By univariate analysis, F3/F4 was associated with gamma
glutamyl transferase (GGT) ≥100 U/l (p = 0.007), nadir CD4 <200
cells/mL (p = 0.037), and, at liver biopsy, absolute CD4 counts (p
= 0.001), prothrombin activity (p = 0.0001), albumin (p = 0.0001),
bilirubin (p = 0.0001), aspartate aminotransferase (AST) (p = 0.0001),
alanine aminotransferase (ALT) (p = 0.03), GGT (p = 0.021), AP (p
= 0.0001), and platelet count (0.0001), but not time of HCV infection, exposure
to/time on PI (p = 0.1 and 0.074) or NNRTI (p = 0.8 and 0.47),
HCV-genotype, or HCV RNA levels. After multivariate analysis, F3/F4 was
associated to age (OR 1.075, 95%CI 1.022 to 1.131, p = 0.005), prior IDU
(OR 2.316, 95%CI 1.037 to 5.170, p = 0.04), GGT ≥100 U/L (OR
2.057, 95%CI 1.232 to 3.436, p = 0.006), and lower CD4 counts (OR 0.999,
95%CI 0.998 to 1, p = 0.004). Estimated median FPR was 0.09 units/year (IQR
0.05 to 0.15; >0.1 units/year in 128; 42%). By univariate analysis, exposure
to PI (p = 0.032) and, at liver biopsy, GGT ≥100 U/I (p = 0.02),
and lower CD4 counts (p = 0.03) were associated to PFR >0.1. Prior IDU,
exposure to/time on NNRTI, time on PI or being HAART-naïve were not. By
multivariate analysis, exposure to PI (OR 1.861, 95%CI 1.031 to 3.359, p
= 0.039) and GGT ≥100 U/l (OR 1.743, 95%CI 1.070 to 2.838, p = 0.026)
predicted FPR>0.1. Subjects ever exposed to PI were older (p = 0.033),
with higher incidence of prior AIDS (p = 0.001), lower nadir CD4 counts
(p = 0.001) or CD4 counts <200 cells/mL during follow-up (p = 0.001).
Conclusions: Liver biopsy showed F3/F4 in 34%. Older age, IDU,
GGT ≥100 U/l and lower CD4 counts at liver biopsy predicted F3/F4.
Neither exposure to/time on PI/NNRTI significantly affected histological
severity, but PI exposure and GGT ≥100 U/l at liver biopsy were
associated to a higher FPR. In patients with PI exposure, there was a
significantly higher frequency of factors predicting histological severity:
older age, severe immunosuppression, and AIDS.
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