Trends in Incidences and Risk Factors for Hepatocellular Carcinoma and Other Liver Events in HIV and Hepatitis C Virus–coinfected Individuals From 2001 to 2014: A Multicohort Study

Gjærde, Lars Klingen; Shepherd, Leah; Jabłonowska, Elżbieta; Lazzarin, Adriano; Rougemont, Mathieu; Darling, Katharine E A; Battegay, Manuel; Braun, Dominique L; Martel-Laferrière, Valérie; Lundgren, Jens D; Rockstroh, Jürgen K.; Gill, John; Rauch, Andri; Mocroft, Amanda; Klein, Marina B.; Peters, Lars

doi:10.1093/cid/ciw380

Cited by 47 publications

(45 citation statements)

References 32 publications

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“…Liver related clinical events encompassed ascites, end stage hepatic encephalopathy, bacterial peritonitis, esophageal variceal bleeding, hepatorenal syndrome, liver transplantation, death from any liver related cause [13], and hepatocellular carcinoma [14]. Poisson regression was used to investigate the relationship between use of TDF and liver related events or non-liver related death among those persons on cART.…”

Section: Discussionmentioning

confidence: 99%

Uptake of Tenofovir-Based Antiretroviral Therapy among HIV–HBV-Coinfected Patients in the EuroSIDA Study

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Uptake of Tenofovir-Based Antiretroviral Therapy among HIV–HBV-Coinfected Patients in the EuroSIDA Study

et al. 2017

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“…Elevated expression of IL-34 and macrophage colony-stimulating factor (M-CSF) from HCV-infected hepatocytes stimulates maturation of peripheral monocytes into macrophages, which contributes to HSC activation by enhancing TGFβ and PDGFβ signaling, blocking antifibrotic NK cell-derived IFNγ, and inducing MMP-1 [101]. Human immunodeficiency virus (HIV) co-infection is clinically known to accelerate fibrosis progression in HCV-infected individuals, and it can be slowed down by antiretroviral therapies [102, 103]. HIV can directly infect HSCs, and viral envelop protein, gp120, promotes collagen I expression via CXCR4 [104, 105].…”

Section: Mechanisms Of Hsc Activationmentioning

confidence: 99%

Hepatic stellate cells as key target in liver fibrosis

Higashi

Friedman

Hoshida

2017

Advanced Drug Delivery Reviews

976

894

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Progressive liver fibrosis, induced by chronic viral and metabolic disorders, leads to more than one million deaths annually via development of cirrhosis, although no antifibrotic therapy has been approved to date. Transdifferentiation (or “activation”) of hepatic stellate cells is the major cellular source of matrix protein-secreting myofibroblasts, the major driver of liver fibrogenesis. Paracrine signals from injured epithelial cells, fibrotic tissue microenvironment, immune and systemic metabolic dysregulation, enteric dysbiosis, and hepatitis viral products can directly or indirectly induce stellate cell activation. Dysregulated intracellular signaling, epigenetic changes, and cellular stress response represent candidate targets to deactivate stellate cells by inducing reversion to inactivated state, cellular senescence, apoptosis, and/or clearance by immune cells. Cell type- and target-specific pharmacological intervention to therapeutically induce the deactivation will enable more effective and less toxic precision antifibrotic therapies.

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“…HCC amongst individuals with HIV infection has been associated with lower CD4 T cell counts, and high HBV DNA [125, 126] , however the increased risk of HCC in coinfection in the era of TDF containing HBV active ART suggests that other factors are also important. In patients with HBV monoinfection, HBV DNA suppression with NRTI has been demonstrated to lower but not eliminate the risk of HCC [127, 128] .…”

Section: Natural History Of Hiv-hbv Co-infection In the Era Of Hbvmentioning

confidence: 99%

HIV-hepatitis B virus coinfection

Singh¹,

Crane

Audsley

et al. 2017

Aids

176

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HIV infection has a significant impact on the natural history of chronic HBV infection, with increased levels of HBV DNA, accelerated progression of liver disease and increased liver-associated mortality compared to HBV mono-infection. Widespread uptake and early initiation of HBV-active antiretroviral therapy (ART) has substantially improved the natural history of HIV-HBV co-infection but the prevalence of liver disease remains elevated in this population. In this paper, we review recent studies examining the natural history and pathogenesis of liver disease and seroconversion in HIV-HBV co-infection in the era of HBV-active ART and the effects of HIV directly on liver disease. We also review novel therapeutics for the management of HBV with a particular emphasis on clinical strategies being developed for an HBV cure and an HIV cure and their impact on HIV-HBV co-infected individuals.

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Trends in Incidences and Risk Factors for Hepatocellular Carcinoma and Other Liver Events in HIV and Hepatitis C Virus–coinfected Individuals From 2001 to 2014: A Multicohort Study

Abstract: In HIV/HCV-coinfected individuals, the crude incidence of HCC increased from 2001 to 2014, while other liver events declined. Individuals with cirrhosis or low current CD4 cell count are at highest risk of developing HCC or other liver events.

Cited by 47 publications

References 32 publications

Uptake of Tenofovir-Based Antiretroviral Therapy among HIV–HBV-Coinfected Patients in the EuroSIDA Study

Uptake of Tenofovir-Based Antiretroviral Therapy among HIV–HBV-Coinfected Patients in the EuroSIDA Study

Hepatic stellate cells as key target in liver fibrosis

HIV-hepatitis B virus coinfection

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