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Influence of ARTs in the Progression of Liver Fibrosis in HCV/HIV Coinfected Patients: effect of hepatoxicity and metabolic abnormalities
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....Factors independently associated with advanced liver fibrosis were alcohol abuse, low CD4 counts, and elevated glucose.....The influence of HAART on the progression of liver fibrosis in HIV/HCV coinfected patients may be a "double-edged sword". While liver fibrosis progression could be delayed by enhancing CD4 counts, causing episodes of ALT elevations and higher glucose and triglyceride levels HAART might accelerate liver damage.....
Reported by Jules Levin
EASL, Barcelona, Spain
P. Barreiro 1, L. Martin-Carbonero 1, F. Blanco 1, P. Labraga 1, J.
Gonzalez-Lahoz 1, V. Soriano 1
1 Department Of Infectious Diseases, Hospital Carlos III, Madrid, Spain
Background: Chronic hepatitis C is a frequent source of complications in HIV+ patients under effective HAART. Other unidentified factors, apart from immune suppression, might be involved in the acceleration of liver fibrosis in HIV/HCV coinfected patients.
Methods: All consecutive HIV+ patients with chronic HCV infection (HCV-RNA pos) on regular follow-up at our institution were examined. Advanced liver fibrosis (ALF) was defined as liver stiffness >9.5 Kpa using transient elastometry (FibroScan). Total exposure to antiretroviral (ARV) drugs was estimated using the pharmacy-computerized database.
Results:
A total of 489 HIV/HCV coinfected patients were identified, of whom 37% had ALF.
In the univariate analysis, older age (44 vs 42 years), male gender (76% vs 67%), current or past elevated alcohol consumption (55% vs 34%), higher mean CD4 counts (486 vs 553 cells/uL), greater peak HCV-RNA (6.4 vs 6 log IU/mL), ALT (88 vs 64 IU/L), glucose (102 vs 98 mg/dL) and triglycerides (167 vs 148 mg/dL) were all significantly associated with ALF compared to patients without ALF (p<0.05).
A total of 3,291 coinfected patients-years of ARV exposure were further analysed. Only 3.5% were HAART-naive, while 34.7%, 48.7% and 74.1% had received NVP, EFV or PI in the past.
There was a significant association between liver fibrosis measurements and duration of PI exposure (rho:0.11; p=0.01), even more pronounced for ritonavir-boosted PI (rho:0.18; p<0.001).
No such correlation was found for any nucleoside analog, nor for NVP or EFV. Mean biochemical parameters during NNRTI vs PI/r regimens were as follows: ALT 85.6 vs 81.0 IU/L (p=0.4); glucose 99.6 vs 99.9 mg/dL (p=0.8); triglycerides
162 vs 179 (p=0.1).
In the multivariate analysis, factors (OR [95% CI]) independently associated with ALF were alcohol abuse (2.1 [1.2-3.5]), low CD4 counts (0.8 [0.8-0.9] per 100 cells/uL) and elevated ALT (1.2 [1.1-1.3] per 10 IU/L) and elevated glucose (1.5 [1.1-1.9] per 10 mg/dL).
Conclusions:
The influence of HAART on the progression of liver fibrosis in HIV/HCV coinfected patients may be a "double-edged sword". While liver fibrosis progression could be delayed by enhancing CD4 counts, causing episodes of ALT elevations and higher glucose and triglyceride levels HAART might accelerate liver damage.
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