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Hepatic Steatosis in HIV/HCV-co-infected Patients Receiving ART
Valerie Martinez*, N Ta, Z Mokhtari, M A Valantin, F Charlotte, R Agher, Y Benhamou, E Caumes, C Katlama, and F Bricaire
Hosp Pitié-Salpétrière, Paris, France
Background:
We wanted to evaluate prevalence and severity of
hepatic steatosis and to assess risk factors
influencing liver steatosis in HIV/hepatitis C virus
(HCV)-co-infected patients taking ART.
Methods: A retrospective study was conducted on HIV/HCV-co-infected
patients treated by ART, who underwent liver biopsies from 1995 to 2005. All
patients were negative for HBV testing. All liver biopsies were read by the
same pathologist. Hepatic steatosis was graded
according to the percentage of hepatocytes affected:
0 = none; 1 = steatosis involving <33%; 2 = steatosis involving 33 to 66%; and 3 = steatosis
involving >66%. Demographics and laboratory parameters were recorded at time
of liver biopsy. Cumulative exposure to ART was reported from the initiation of
ART to liver biopsy date. Statistical analysis was perfomed
using SPSS version 13.0.
Results: We included 118 HIV/HCV-co-infected patients.
Median age was 40 years (28 to 67), 81.4% were male, 89% were Caucasian, 80% had
a past history of injecting drug abuse. At the time of biopsy, median duration
of HIV infection was 10 years (1 to 22), HIV viral load was not detected
(<200 copies/mL) in 50% of patients and the median
HIV viral load was 2524 copies/mL (204 to 439,091) in
patients remaining, CD4 cell count was 336/mm3 (6 to 1009). Median
cumulative exposure to nucleoside reverse transcriptase inhibitors (NRTI) was
14 years, non-NRTI (NNRTI) 2.75, and protease inhibitors (PI) 7.35. HCV
genotype was determined in 103 patients: 60 (58.3%) genotype 1; 5 (4.9%) genotype 2; 26
(25.2%) genotype 3, and 12 (17.7%) genotype 4. HCV RNA was 3850 KUI/mL (0.5 to 76,640). Steatosis was
observed in 73 of 118 patients (62%): 51
(43.2%) with steatosis grade 1, 8 (6.8%) grade 2, and 14 (12 %) grade 3. Steatosis
was significantly correlated with hepatic fibrosis (p = 0.001), negatively correlated with total cholesterol (p = 0.001) but not with triglyceride. Liver
steatosis was more frequent in HCV genotype 3 (80.8%
compared to 55% in genotype 1, 40% in 2, 33.3% in 4) and more severe (46.2%
compared to 1.7% in genotype 1, 20% in 2, 0% in 4) (p <0.0001). By univariate analysis, exposure
to abacavir and nevirapine were
associated with a decreased risk (0R = 3.19; 95%CI 1.07 to 9.5 and 2.55; 95%CI
1.1 to 5.9, respectively) of liver steatosis (p = 0.05 and p = 0.032 respectively for abacavir and nevirapine).
Conclusions:
Liver steatosis appears
in 62% of HIV/HCV-co-infected patients receiving ART. Steatosis
was associated with genotype 3, hepatic fibrosis and cholesterolemia.
The role of drug classes and drugs within classes should be investigated in
prospective studies.
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