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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.
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