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Session 125-Poster Abstracts
Acute Hepatitis C Infection
Wednesday, 2-4 pm; Poster Hall
Paper # 642    
Liver Fibrosis Progression after Acute HCV Infection in HIV+ Individuals
Martin Vogel*1, E Page2, P Holmes2, J Wilkinson2, C Schwarze-Zander1, S Mauss3, A Baumgarten4, J-C Wasmuth1, M Nelson2, J Rockstroh1, and the NEAT Study Group
1Univ of Bonn, Germany; 2Chelsea and Westminster Hosp, London, UK; 3Practice Mauss/Schmutz/Hegener/Athmann, Düsseldorf, Germany; and 4Practice Dupke/Baumgarten/Carganico, Berlin, Germany

Background:  Recent data suggested high fibrosis progression rates after sexually acquired acute HCV infection (AHC). This may be due to the fact that in contrast to traditional risk populations in most cases of sexually transmitted HCV infections occur in already HIV-infected individuals. Here we investigate the impact of AHC on liver fibrosis progression.

Methods:  HIV+ patients with AHC were asked to participate in a prospective study on the evaluation of liver fibrosis progression after AHC by means of transient elastometry (FibroScan). A standardized questionnaire captured standard demographic factors, risk factors for liver fibrosis such as NASH, alcohol abuse and HAART exposure, and details of acute HCV infection. Stiffness values ≤ 6 kPa were assigned Metavir fibrosis score F1, 6.1 to 9.0 kPa F2, 9.1 to 12 kPa F3 and > 12 kPa F4. Prior AHC no fibrosis (F0) was assumed unless biopsy or FibroScan were available. Fibrosis progression rate (FPR) was calculated dividing the difference in fibrosis units by the time of follow-up. Only patients with a chronic course of AHC, or if FibroScan prior to anti-HCV therapy was available, were included for analysis.

Results:  In this study, 28 male patients (median age 39 years) were enrolled. Main transmission risk was MSM (89%). Symptomatic AHC was observed in 8 (29%) of patients, median maximal ALT was 487 IU/L. Most patients had acquired HCV genotype 1 infection (n = 23, 82%), followed by genotype 4 (n = 4, 14%) and genotype 2 (n = 1, 4%). Median HCV-RNA was 5.9 log. Risk factors associated with liver fibrosis were observed in 14 (50%) of patients (alcohol or past alcohol abuse n = 2, chronic HBV n = 1, drug-abuse n = 9, diabetes n = 1, lipodystrophy n = 3). Median HAART exposure was 43 months. Median follow-up was 0.4 years and the overall calculated fibrosis progression rate (FPR) was 3.8 Metavir fibrosis units per year. Plotting FPR over follow-up time revealed short observation times being strongly correlated with high fibrosis progression rates (figure 1). No interaction of risk factors for cirrhosis or HAART exposure with follow-up time was observed.

Figure 1:

Conclusions:  Calculated high fibrosis progression rates after acute HCV infection in HIV-positive individuals are probably influenced by short observation periods. A linear model for fibrosis progression, as is currently applied in the setting of chronic HCV infection, should be used with caution in the setting of acute HCV infection.