Clinical outcome in a cohort of HIV/HCV co-infected patients: HCV RNA presence associated to higher GGT levels.

ALOISI N; MONZANI C; CORTI M; CANDELA M; PRIMIANI L; BASTON M; PÉREZ BIANCO R; DE TEZANOS PINTO; BRACCO MM; BARÉ P

Congreso; XXX International congress of the World Federation of Hemophilia; 2012

Clinical, immunological and virological markers were considered to evaluate clinical conditions in a group of 38 HIV/HCV coinfected hemophilic patients. Different parameters like age, HIV and HCV presence and viral loads, hepatic enzymes (AST, ALT, GGT, ALP), CD4, CD8 and platelet counts were evaluated as surrogate clinical progression markers. APRI and FORNS indexes were also calculated. In addition, IL28b polymorphisms were studied to look for an association with their clinical evolution. Student t test or Mann Whitney were used to compare quantitative results while Chi square or Fisher tests for qualitative analysis. We observed no statistically significant differences for markers between genotypes CC and CT+TT groups (p>0.05). Ten out of 38 patients (26%) showed values higher than 2X Normal GGT values with a median reaching 204 UI/l (mean: 198±72 UI/l). Among the group with non detectable (ND) HCV RNA in plasma (spontaneous or therapy-induced clearance) (n=9), higher platelet counts were observed (p=0.04) in parallel with lower GGT (p=0.03), lower FORNS index (p=0.008) and greater CD4+ cell counts (p=0.03). When considering the group with ND HIV viral load, CD4 were significantly increased (p=0.004) but also, higher GGT levels were observed (133 vs 66 UI/l; p=0.02). Analysis of the data inside this group showed that patients with detectable HCV viral loads had significantly higher GGT levels (175 vs 48 UI/l, p=0.01) and FORNS index was also increased but no statistically significant (5.85 vs 4.5, p=0.06), than patients with ND HCV loads. In the present report the GGT increase was significantly associated to the presence of the HCV RNA in plasma samples. The mechanisms for GGT increase are not yet well understood and the true meaning of the GGT alteration frequently observed in chronic HCV infected patients remains unclear. The pathological changes in the liver due to viral presence could result in an overflow of GGT into the bloodstream. This observation deserves further analysis on the mechanisms involved.