There is no difference in hepatic fibrosis rates of patients infected with hepatitis C virus and those co-infected with HIV

Souza, Andrea Ribeiro de; Tovo, Cristiane Valle; Mattos, Ângelo Alves de; Chaves, Silvia Clelia

doi:10.1590/s0100-879x2006005000200

Cited by 11 publications

(20 citation statements)

References 35 publications

(40 reference statements)

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“…Random-effects estimation generated a stage-constant FPR of 0.117 and stage-specific FPRs of 0.128 (F0→F1), 0.059 (F1→F2), 0.078 (F2→F3), and 0.116 (F3→F4). The stage-constant rate (0.117) is within the range (and near the midpoint) of other stage-constant estimates from samples of HIV-negative patients with HCV infection due to other exposures (range 0.07, 0.151) (Mathurin, Moussall, Cadranel, Thibault, Charlotte, Dumouchel, Cazier, Huraux, Devergie, Vidaud, Opolon, & Poynard, 1998; Bonacini, Groshen, Yu, Govindarajan, & Lindsay, 2001; Mohsen, Easterbrook, Taylor, Portmann, Kulasegaram, Murad, Wiselka, & Norris, 2003; Rodríguez-Torres, Ríos-Bedoya, Rodríguez-Orengo, Fernández-Carbia, Marxuach-Cuétara, López-Torres, Salgado-Mercado, & Bräu, 2006; Souza, Tovo, Mattos, & Chaves, 2008; Bochud et al, 2009). …”

Section: Discussionsupporting

confidence: 61%

Hepatitis C virus (HCV) disease progression in people who inject drugs (PWID): A systematic review and meta-analysis

Smith

Combellick

Jordan

et al. 2015

International Journal of Drug Policy

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Background Understanding HCV disease progression rates among people who inject drugs (PWID) is important to setting policy to expand access to detection, diagnosis and treatment, and in forecasting the burden of disease. In this paper we synthesize existing data on the natural history of HCV among PWID, including fibrosis progression rates (FPR) and the incidence of compensated cirrhosis (CC), decompensated cirrhosis (DC), and hepatocellular carcinoma (HCC). Methods We conducted electronic and manual searches for published and unpublished literature. Reports were eligible if they (i) included participants who were chronically infected with HCV and reported current or previous injection drug use; (ii) presented original data on disease progression in a study sample comprised of at least 90% PWID; (iii) published between January 1, 1990, and December 31, 2013; and (iv) included data from upper-middle- or high-income countries. Quality ratings were assigned using an adaptation of the Quality In Prognosis Studies (QUIPS) tool. We estimated pooled FPRs using the stage-constant and stage-specific methods, and pooled incidence rates of CC, DC, and HCC. Results Twenty-one reports met the study inclusion criteria. Based on random-effect models, the pooled stage-constant FPR was 0.117 METAVIR units per year (95% CI, 0.099 −0.135), and the stage-specific FPRs were F0→F1, 0.128 (95% CI 0.080, 0.176); F1→F2, 0.059 (95% CI 0.035, 0.082); F2→F3, 0.078 (95% CI 0.056, 0.100); and F3→F4, 0.116 (95% CI 0.070, 0.161). The pooled incidence rates of CC, DC, and HCC were 6.6 (95% CI 4.8, 8.4), 1.8 (95% CI 0.3, 3.3), and 0.3 (95% CI −0.1, 0.6) events per 1,000 person-years, respectively. Following the stage-constant estimate, average time to cirrhosis is 34 years post-infection, and time to METAVIR stage F3 is 26 years; using the stage-specific estimates, time to cirrhosis is 46 years and time to F3 is 38 years. Conclusion Left untreated, PWID with chronic HCV infection will develop liver sequelae (including HCC) in mid- to late-adulthood. Delaying treatment with the new drug regimens until advanced fibrosis develops prolongs the period of infectiousness to perhaps thirty years. Scaling up of effective HCV prevention and early engagement in care and treatment will facilitate the elimination HCV as a source of serious disease in PWID.

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Section: Discussionsupporting

confidence: 61%

Hepatitis C virus (HCV) disease progression in people who inject drugs (PWID): A systematic review and meta-analysis

Smith

Combellick

Jordan

et al. 2015

International Journal of Drug Policy

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“…In a more recent study, Macias observed that 28% progressed one fibrosis stage and 16% increased at least 2 stages over a period over three years [22]. To account for the differences in time between biopsies, we also calculated the FPR and again observed no significant differences in those with and without HIV supportive of other retrospective studies [12,26]. Interestingly, not only did we not observe a pattern of progression; 4 of our patients without SVR (7%) experienced improvement of 2 units in the Ishak fibrosis score.…”

Section: Discussionsupporting

confidence: 61%

“…Because most studies of fibrosis progression in coinfected patients were either retrospective with only estimates of disease duration or after anti-HCV therapy [7–17], the natural history of HCV in those coinfected with HIV remains poorly defined. Although several studies included either paired biopsy analysis [15,21,22,24] or indirect comparisons to those with HCV alone [12,16,25,26], no studies of paired biopsies report direct comparisons of coinfected patients to matched patients with HCV alone.…”

Section: Discussionmentioning

confidence: 99%

“…Studies on disease progression by paired biopsy analysis in those with coinfection suggest that 16–50% have fibrosis progression [15,21,22,24]. However, few studies directly compare fibrosis progression by paired biopsy between those with coinfection and those with HCV alone [25,26]. To address this gap in knowledge, we performed a longitudinal cohort study to compare fibrosis progression by paired biopsy in patients with HIV-HCV and HCV alone and assessed factors associated with fibrosis progression in those with HIV-HCV coinfection.…”

Section: Introductionmentioning

confidence: 99%

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Similar Progression of Fibrosis Between HIV/HCV–Infected and HCV–Infected Patients: Analysis of Paired Liver Biopsy Samples

Sterling

Wegelin

Smith

et al. 2010

Clinical Gastroenterology and Hepatology

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Background and Aims Fibrosis progression might be accelerated in patients that are co-infected with HIV and hepatitis C virus (HIV/HCV). However, no studies have directly compared fibrosis progression by paired liver biopsy between patients infected with HIV and HCV vs. those infected with only HCV. Methods Liver biopsy samples were collected from patients with HIV/HCV (n=306) and those with HCV; biopsies from 59 without a sustained virologic response (SVR) or cirrhosis were matched with those from patients with only HCV (controls) for initial fibrosis stage, demographics, and HCV treatment. For HIV/HCV patients, categorical variables at baseline and the area under the curve of continuous variables per unit time were analyzed for associations with fibrosis progression. Results Liver biopsies from HIV/HCV patients had more piecemeal necrosis than controls (P=.001) and increased lobular inflammation (P=.002); HIV/HCV patients also had shorter intervals between liver biopsies (4.7 vs. 5.9 yrs, P<.0001). Between the 1st and 2nd biopsies, fibrosis remained unchanged or progressed 1 or 2 units in 55%, 18%, and 18% of HIV/HCV patients, respectively, compared with 45%, 30%, and 9% of controls. The fibrosis progression rate was similar between HIV/HCV and control patients (0.12±0.40 vs. 0.091±0.29 units/yr; P=.72). In paired biopsies from 66 patients, including those with SVR, there were no associations between fibrosis progression and demographics; numbers of CD4+ T cells; levels of aspartate aminotransferase or alanine aminotransferase; use of highly-active anti-retroviral therapy; response to HCV therapy (no treatment, SVR, or non-response); baseline levels of FIB-4; or histological features including inflammation, fibrosis, or steatosis. Conclusions Based on analysis of liver biopsy samples, fibrosis progression was similar between HIV/HCV- and HCV-infected patients; no clinical or laboratory parameters predicted disease progression.

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“…Of them, 6242 were positive for HIV and 10508 were negative for HIV. Fourteen studies assessed the histological cirrhosis [9,18,19,21,[27][28][29][30][31][32]38,39,41,42] , 7 studies assessed the death [17,22,23,[34][35][36]40] , 3 studies assessed the decompensated liver disease [15,26,37] , 2 studies assessed the outcome of decompensated liver disease and death [16][17][18][19][20][21][22][23][24][25] , 1 study assessed the outcome of histological cirrhosis, hepatocellular carcinoma and death [20] , 1 study assessed the outcome of histological cirrhosis and death [24] , and 1 study assessed the outcome of hepatocellular carcinoma and death [33] , respectively. Most studies did not provide a racial distribution.…”

Section: Deng Lp Et Al Impact Of Hiv Infection On Hcv Infectionmentioning

confidence: 99%

Impact of human immunodeficiency virus infection on the course of hepatitis C virus infection: A meta-analysis

Deng¹,

Gui²,

Zhang³

et al. 2009

WJG

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AIM:To analyze the influence of human immunodeficiency virus (HIV) infection on the course of hepatitis C virus (HCV) infection. METHODS:We performed a meta-analysis to quantify the effect of HIV co-infection on progressive liver disease in patients with HCV infection. Published studies in the English or Chinese-language medical literature involving cohorts of HIV-negative and -positive patients coinfected with HCV were obtained by searching the PUBMED, EMBASE and CBM. Data were extracted independently from relevant studies by 2 investigators and used in a fixed-effect meta analysis to determine the difference in the course of HCV infection in the 2 groups. RESULTS:Twenty-nine trails involving 16 750 patients were identified including the outcome of histological fibrosis or cirrhosis or de-compensated liver disease or hepatocellular carcinoma or death. These studies yielded a combined adjusted odds ratio (OR) of 3.40 [95% confidence interval (CI) = 2.45 and 4.73]. Of note, studies that examined histological fibrosis/ cirrhosis, decompensated liver disease, hepatocellular carcinoma or death had a pooled OR of 1.47 (95% CI = 1.27 and 1.70), 5.45 (95% CI = 2.54 and 11.71), 0.76 (95% CI = 0.50 and 1.14), and 3.60 (95% CI = 3.12 and 4.15), respectively. CONCLUSION:Without highly active antiretroviral therapies (HAART), HIV accelerates HCV disease progression, including death, histological fibrosis/ cirrhosis and decompensated liver disease. However, the rate of hepatocellular carcinoma is similar in persons who had HCV infection and were positive for HIV or negative for HIV.

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There is no difference in hepatic fibrosis rates of patients infected with hepatitis C virus and those co-infected with HIV

Cited by 11 publications

References 35 publications

Hepatitis C virus (HCV) disease progression in people who inject drugs (PWID): A systematic review and meta-analysis

Hepatitis C virus (HCV) disease progression in people who inject drugs (PWID): A systematic review and meta-analysis

Similar Progression of Fibrosis Between HIV/HCV–Infected and HCV–Infected Patients: Analysis of Paired Liver Biopsy Samples

Impact of human immunodeficiency virus infection on the course of hepatitis C virus infection: A meta-analysis

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