Dr. Mark Nelson made a very illustrative comparison with famous John Coffin’s definition of AIDS pathogenesis (from 1996), putting HCV as a train about to reach an edge, saying that development of ESLD (end-stage liver disease) has inflammation as determinant of speed (replacing HIV viral load in Coffin’s model) and fibrosis as the distance (replacing CD4 count), when were talking about HIV/HCV co-infected patients. Staging fibrosis is crucial to indicate who and when to treat concerning viral hepatitis. Liver biopsies are invasive and combining tests to ascertain liver fibrosis, like biomarkers and transient elastography could help that. In today`s session, a paper from Spain showed us a 30% HCV relapse after complete suppression at the end of treatment in HIV co-infected subjects from PRESCO study, most of them with genotypes 1-4, against a 25% relapse in HCV only patients. The UK group presented a meta analysis of 22 studies to determine Transient Elastography (FibroScan) cutoff values for the detection of significant hepatic fibrosis and cirrhosis in HIV-positive subjects. They proposed cut-off LSM values by TE (FibroScan) for =F2 be 8.44 kPa and 16.14 kPa for F4 to HCV patients. Those co-infected with HIV may have altered cut-off values. BMI, alcohol, smoking, gender and age were not significantly associated with LSM in their HIV-positive study population. Looking for Occult HBV or HCV viremia in women from the HER study, Lynn Taylor, US, found a 4.7% of OHBV among HIV-positive women and only 1 case of OHCV. OHBV was associated with a poorer control of HIV, and the authors suggested that OHBV may be parenterally transmitted. Roger Bedimo, US, presented a paper on HCV infection as a risk factor for cardiovascular disease in HIV-infected subjects. HCV co-infection was associated with a significantly increased risk of AMI and CVD in the pre-HAART era. This effect appears to decline in the HAART era for AMI, but not for CVD. The last presentation, from Spain, investigated the outcomes of HIV/HCV co-infected patients from 2 trials, by exposure to peg-IFN alfa-2a or alfa-2b. On-treatment analyses were made to estimate the intrinsic potency of pegIFNa-2a versus -2b after adjusting for other covariates. After analyzing HCV RNA levels at weeks 4, 12 and 24, they concluded that peg-IFN alfa-2a had a greater intrinsic antiviral effect, probably related to its longer half-life.

THAB0201 -- Introduction: liver fibrosis and its importance in prognosis and clinical decisions - Mark Nelson, United Kingdom

Staging fibrosis is crucial to indicate who and when to treat concerning viral hepatitis. Liver biopsies are invasive and combining tests to ascertain liver fibrosis, like biomarkers and transient elastography could help that. HIV/HCV patients should have their liver status staged, so they can be treated in order to avoid the evolution to cirrhosis. Dr. Nelson made a very illustrative comparison with John Coffin’s definition of AIDS in 1996 as a train about to reach an edge, saying that development of ESLD (end-stage liver disease) has inflammation as determinant of speed (replacing HIV viral load in Coffin’s model) and fibrosis as the distance (replacing CD4 count).


THAB0202 -- HCV relapses upon completion of peg-interferon plus Ribavirin in HIV-infected patients: rate, timing and predictors - Jose Medrano, Spain