Research Papers

@article{Rollet-Kurhajec2015,
title = {Hepatic Fibrosis Progression in HIV-Hepatitis C Virus Co-Infection--The Effect of Sex on Risk of Significant Fibrosis Measured by Aspartate-to-Platelet Ratio Index},
author = {Kathleen C. Rollet-Kurhajec and Erica E. M. Moodie and Sharon Walmsley and Curtis Cooper and Neora Pick and Marina B. Klein},
editor = {Jason Blackard},
url = {https://www.ncbi.nlm.nih.gov/pubmed/26090666},
doi = {10.1371/journal.pone.0129868},
year = {2015},
date = {2015-06-05},
journal = {PLoS One},
abstract = {BACKGROUND:
In Hepatitis C virus (HCV) mono-infection, male sex is associated with faster liver fibrosis progression but the effects of sex have not been well studied in HIV-HCV co-infected patients. We examined the influence of sex on progression to significant liver fibrosis in HIV-HCV co-infected adults receiving antiretroviral therapy (ART) using the aspartate aminotransferase-to-platelet ratio index (APRI) as a surrogate biomarker of liver fibrosis.
METHODS:
We evaluated 308 HIV infected, HCV RNA positive participants of a Canadian multicentre prospective cohort receiving antiretrovirals and without significant liver fibrosis or end-stage liver disease at baseline. We used multivariate discrete-time proportional hazards models to assess the effect of sex on time to significant fibrosis (APRI≥1.5) adjusting for baseline age, alcohol use, cigarette smoking, HCV duration, and APRI and time-updated CD4 count and HIV RNA.
RESULTS:
Overall, 55 (18%) participants developed an APRI ≥ 1.5 over 544 person-years of at-risk follow-up time; 18 (21%) women (incidence rate (IR)=14.0/100 PY; 7.5-20.4) and 37 (17%) men (IR=8.9/100 PY; 6.0-11.8). Women had more favourable profiles with respect to traditional risk factors for liver disease progression (younger, shorter duration of HCV infection and less alcohol use). Despite this, female sex was associated with a greater than two-fold increased risk of fibrosis progression (adjusted hazard rate (HR) =2.23; 1.22-4.08).
CONCLUSIONS:
HIV-HCV co-infected women receiving antiretroviral therapy were at significantly greater risk of progressing to liver fibrosis as measured by APRI compared with men. Enhanced efforts to engage and treat co-infected women for HCV are needed.},
keywords = {Fibrosis, Hepatic Fibrosis, HIV-HCV co-infection, Sex},
pubstate = {published},
tppubtype = {article}
}

@article{Cooper2015,
title = {HIV virological rebounds but not blips predict liver fibrosis progression in antiretroviral-treated HIV/hepatitis C virus-coinfected patients},
author = {Curtis Cooper and Kathleen C. Rollet-Kurhajec and Jim Young and Colins Vasquez and Mark Tyndall and John Gill and Neora Pick and Sharon Walmsley and Marina B. Klein},
url = {https://www.ncbi.nlm.nih.gov/pubmed/24837567},
doi = {10.1111/hiv.12168},
year = {2015},
date = {2015-01-15},
journal = {HIV Med},
volume = {16},
number = {1},
pages = {24-31},
abstract = {OBJECTIVES:
Antiretroviral interruption is associated with liver fibrosis progression in HIV/hepatitis C virus (HCV) coinfection. It is not known what level of HIV viraemia affects fibrosis progression.
METHODS:
We evaluated 288 HIV/HCV-coinfected cohort participants with undetectable HIV RNA (<50 HIV-1 RNA copies/mL) on two consecutive visits while on combination antiretroviral therapy (cART) without fibrosis [aspartate aminotransferase to platelet ratio index (APRI) <1.5], end-stage liver disease or HCV therapy. An HIV blip was defined as a viral load of ≥ 50 and <1000 copies/mL, preceded and followed by undetectable values. HIV rebound was defined as: (i) HIV RNA ≥ 50 copies/mL on two consecutive visits, or (ii) a single HIV RNA measurement ≥ 1000 copies/mL. Multivariate discrete-time proportional hazards models were used to assess the effect of different viraemia levels on liver fibrosis progression (APRI ≥ 1.5).
RESULTS:
The mean age of the patients was 45 years, 74% were male, 81% reported a history of injecting drug use, 51% currently used alcohol and the median baseline CD4 count was 440 [interquartile range (IQR) 298, 609] cells/μL. Fifty-seven (20%) participants [12.4/100 person-years (PY); 95% confidence interval (CI) 9.2-15.7/100 PY] progressed to an APRI ≥ 1.5 over a mean 1.1 (IQR 0.6, 2.0) years of follow-up time at risk. Virological rebound [hazard ratio (HR) 2.3; 95% CI 1.1, 4.7] but not blips (HR 0.5; 95% CI 0.2, 1.1) predicted progression to APRI ≥ 1.5. Each additional 1 log10 copies/mL HIV RNA exposure (cumulative) was associated with a 20% increase in the risk of fibrosis progression (HR 1.2; 95% CI 1.0-1.3).
CONCLUSIONS:
Liver fibrosis progression was associated with HIV rebound, but not blips, and with increasing cumulative exposure to HIV RNA, highlighting the importance of achieving and maintaining HIV suppression in the setting of HIV/HCV coinfection.
© 2014 The Authors. HIV Medicine published by John Wiley & Sons Ltd on behalf of British HIV Association.},
keywords = {Fibrosis, HCV, HIV, Virological blips, Virological rebound},
pubstate = {published},
tppubtype = {article}
}