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Session 162 Poster Abstracts
Impact of HBV or HCV on Disease Progression in HIV-Infected Persons
Session Day and Time: Tuesday, 1 - 4 pm
Poster Hall


926
Steatosis in HIV/HVC-co-infected Patients
A Mohsen1, D. O'Shea*2, B Portmann3, O Barry2, H Tuite2, C Donnelly2, C Bergin2, and S Norris2
1Chelsea and Westminster Hosp, London, UK; 2St James's Hosp, Dublin, Ireland; and 3Inst of Liver Studies, King's Coll Hosp, London, UK

Background:  Hepatitis C virus (HCV) -induced liver disease has become a significant problem in HIV-infected persons. However, data are limited on the relative effect of steatosis on HCV-induced fibrosis progression in HIV-1/HCV. Our aim was to assess the impact of steatosis on HCV progression in co-infected patients.

 

Methods:  We analyzed 134 HCV/HIV-co-infected patients. Detailed epidemiological data were collected, and liver biopsies were scored by a single observer (modified Ishak).  Univariate and multivariate analysis were done to investigate for association with steatosis.

Results:  The majority of co-infected persons were male (75%) but only a third had received HAART (32%) with a median CD4 count of 326 at biopsy. Risk factor for HCV acquisition was intravenous drug use in 75%. Univariate logistic regression analysis showed significant association between steatosis and  HCV genotype 3 (OR = 5.58, 95%CI 1.67 to 18.58, p = 0.005), severe fibrosis (OR = 4.07, 95%CI 1.61 to 10.26, p = 0.003) and inflammatory grade (OR = 2.74, 95%CI 1.10 to 6.81,  p = 0.03). There was no significant association with gender distribution, age at HCV infection, estimated duration of HCV, source of infection, body mass index, ART, CD4 cell count, HIV viral load or alcohol intake. Multivariable analysis confirmed the association between steatosis and severe disease (fibrosis stage 3 and 4) (OR = 7.65, 95%CI 1.67 to 35.07, p = 0.009), and HCV genotype 3 (OR = 8.18, 95%CI 1.91 to 34.99, p = 0.005). 

Conclusions:  Steatosis in HIV/HCV-co-infected patients was independently associated with advanced liver fibrosis and genotype 3 disease. Factors that modify steatosis should be given more attention in this group with accelerated HCV disease progression.