{"title":"Risk factors of accelerated liver fibrosis in HIV-HCV coinfection: a matched analysis: original","authors":"Ayman B. Ibrahim, A. Shpaner, J. Nieto, S. Saab","doi":"10.4314/SAGR.V2I3.30718","DOIUrl":null,"url":null,"abstract":"Introduction: Chronic liver diseases have become a significant cause of mortality in HIV patients. Few reports have assessed risk factors for HCV disease progression in HIV infected patients. \nObjectives: The aim of our study was to compare the progression rate of liver fibrosis in HIV-HCV coinfected patients with that of HCV-only infected patients. We sought to identify the risk factors associated with accelerated progression rates and higher fibrosis stage. \nMethods: Eighteen HCV/HIV coinfected patients were matched to fifty-four HCV patients in a 1 to 3 ratio. The matching variables included duration of HCV, alcohol use, age, gender and race. Both unmatched and matched analyses were performed on estimated fibrosis progression rate and fibrosis stage separately. An ordinal logistic regression analysis was used to identify risk factors. \nResults: Using Metavir unit system, the mean (+ standard deviation [SD]) estimated fibrosis rates were 0.26 (+ 0.17) and 0.11 (+ 0.09) for HIV-HCV coinfected and HCV-only patients respectively (unmatched analysis p=0.001). The mean (+ SD) duration of HCV infection was 22.05 (+ 1.10) and 15.50 (+ 2.20) for coinfected and HCV-only patients, respectively. There was a statistically significant difference in the proportion of patients with stage 4 liver fibrosis between both groups (HIV-HCV 33 %, HCV 9%, P =0.004). Ordinal Logistic Regression model (unmatched analysis) suggested that duration of HCV (Odds Ratio [OR]= 1.11, 95 % confidence interval [CI] 1.03 to 1.20, P = 0.01), HIV status (OR =9.49, CI 2.39 to 37.75, P = 0.001) (overall model R2= 0.16, F = 0.0002) and age (OR=1.14, CI 1.01 to 1.28, P = 0.03) are statistically significant independent predictors of accelerated progression rate and higher fibrosis stage. \nConclusions: Duration of HCV infection, age, and HIV status are significant independent predictors of accelerated fibrosis in HIV-HCV coinfected patient population. HIV-HCV coinfected patients should be counseled and their providers informed regarding the risk factors for accelerated progression of liver fibrosis. Further studies are needed to investigate the underlying biological and immunological mechanisms of accelerated liver fibrosis in HCV patients coinfected with HIV. South African Gastroenterology Review Vol.2(3) 2004: 14-17","PeriodicalId":39144,"journal":{"name":"South African Gastroenterology Review","volume":"2 1","pages":"14-17"},"PeriodicalIF":0.0000,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"South African Gastroenterology Review","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4314/SAGR.V2I3.30718","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 3
Abstract
Introduction: Chronic liver diseases have become a significant cause of mortality in HIV patients. Few reports have assessed risk factors for HCV disease progression in HIV infected patients.
Objectives: The aim of our study was to compare the progression rate of liver fibrosis in HIV-HCV coinfected patients with that of HCV-only infected patients. We sought to identify the risk factors associated with accelerated progression rates and higher fibrosis stage.
Methods: Eighteen HCV/HIV coinfected patients were matched to fifty-four HCV patients in a 1 to 3 ratio. The matching variables included duration of HCV, alcohol use, age, gender and race. Both unmatched and matched analyses were performed on estimated fibrosis progression rate and fibrosis stage separately. An ordinal logistic regression analysis was used to identify risk factors.
Results: Using Metavir unit system, the mean (+ standard deviation [SD]) estimated fibrosis rates were 0.26 (+ 0.17) and 0.11 (+ 0.09) for HIV-HCV coinfected and HCV-only patients respectively (unmatched analysis p=0.001). The mean (+ SD) duration of HCV infection was 22.05 (+ 1.10) and 15.50 (+ 2.20) for coinfected and HCV-only patients, respectively. There was a statistically significant difference in the proportion of patients with stage 4 liver fibrosis between both groups (HIV-HCV 33 %, HCV 9%, P =0.004). Ordinal Logistic Regression model (unmatched analysis) suggested that duration of HCV (Odds Ratio [OR]= 1.11, 95 % confidence interval [CI] 1.03 to 1.20, P = 0.01), HIV status (OR =9.49, CI 2.39 to 37.75, P = 0.001) (overall model R2= 0.16, F = 0.0002) and age (OR=1.14, CI 1.01 to 1.28, P = 0.03) are statistically significant independent predictors of accelerated progression rate and higher fibrosis stage.
Conclusions: Duration of HCV infection, age, and HIV status are significant independent predictors of accelerated fibrosis in HIV-HCV coinfected patient population. HIV-HCV coinfected patients should be counseled and their providers informed regarding the risk factors for accelerated progression of liver fibrosis. Further studies are needed to investigate the underlying biological and immunological mechanisms of accelerated liver fibrosis in HCV patients coinfected with HIV. South African Gastroenterology Review Vol.2(3) 2004: 14-17