Liver fibrosis in HIV

Rockstroh, Jürgen K.; Mohr, Raphael; Behrens, Georg M. N.; Spengler, Ulrich

doi:10.1097/coh.0000000000000064

Cited by 57 publications

(37 citation statements)

References 30 publications

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“…In these publications a wide range of prevalence for abnormal LS values were identified (Han et al, 2013; Lui et al, 2016; Merchante et al, 2010; Rockstroh et al, 2014). Using these applied cutoff values we had a similarly wide prevalence range (9.9–44.55%).…”

Section: Discussionmentioning

confidence: 99%

“…Age is a well-known risk factor for LF in non-alcoholic fatty liver disease (NAFLD) and HCV-infected patients (Chan, Patel & Choi, 2016). However, data about age-related fibrosis in the HIV mono-infected population are scarce (Rockstroh et al, 2014). To date, only a few descriptive studies identified significant association with age and LF in this patient population (Blanco et al, 2011; Han et al, 2013; Merchante et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…In HCV-infected patients, the CD4/8 ratio as a contributing factor to LF has also been considered (Feuth et al, 2014). Furthermore, CD4 cells can stimulate anti-fibrotic natural killer cell activity, therefore, loss and impaired activity of CD4 cells may contribute to the progression of LF (Rockstroh et al, 2014). Data suggesting HIV-induced effects on the pathogenesis of fibrosis generation has been described mainly in patients with HIV/HCV co-infection (Rockstroh et al, 2014) but the mechanism has still not been exactly determined.…”

Section: Discussionmentioning

confidence: 99%

“…While hepatitis B or C co-infections remain the most important cause of liver damage, liver related mortality also affects those infected only with HIV (Antiretroviral Therapy Cohort Collaboration, 2010). Long term antiretroviral and non-antiretroviral medications, HIV induced long term inflammation, metabolic complications and direct cytopathic effects may also contribute to the pathogenesis of liver fibrosis (LF) (Rockstroh et al, 2014). An increasing number of papers have been published on fibrosis in HIV/hepatitis virus co-infected patients (Audsley et al, 2016; Brunet et al, 2016; Costiniuk et al, 2016; Fernández-Montero et al, 2013; Gonzalez et al, 2015; Ioannou et al, 2015; Kliemann et al, 2016; Konerman et al, 2014; Kooij et al, 2016; Li Vecchi et al, 2013; Macías et al, 2013a; Macías et al, 2013b; Njei et al, 2016; Sanmartín et al, 2014; Vergara et al, 2007) but only a few studies have appeared on the analysis of data obtained from HIV mono-infected individuals (Akhtar et al, 2008; DallaPiazza et al, 2010; Han et al, 2013; Lui et al, 2016; Rivero-Juárez et al, 2013; Shur et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

“…These tests were demonstrated to be acceptable in predicting the absence of fibrosis or mild fibrosis (LF < 2 METAVIR score) and the presence of advanced fibrosis (LF > 3 METAVIR score) (González Guilabert, Hinojosa Mena-Bernal & del pozo González, 2010). Cross-sectional studies in HIV mono-infected patients reported high rates (11–47%) of significant LF suggesting that HIV itself may contribute independently to liver damage (Rockstroh et al, 2014). Ongoing LF is not always accompanied by elevated liver enzymes.…”

Section: Introductionmentioning

confidence: 99%

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Hepatic fibrosis and factors associated with liver stiffness in HIV mono-infected individuals

Sulyok

Ferenci

Makara

et al. 2017

PeerJ

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BackgroundLiver disease has become an important cause of morbidity and mortality even in those HIV-infected individuals who are devoid of hepatitis virus co-infection. The aim of this study was to evaluate the degree of hepatic fibrosis and the role of associated factors using liver stiffness measurement in HIV mono-infected patients without significant alcohol intake.MethodsWe performed a cross-sectional study of 101 HIV mono-infected patients recruited prospectively from March 1, 2014 to October 30, 2014 at the Center for HIV, St István and St László Hospital, Budapest, Hungary. To determine hepatic fibrosis, liver stiffness was measured with transient elastography. Demographic, immunologic and other clinical parameters were collected to establish a multivariate model. Bayesian Model Averaging (BMA) was performed to identify predictors of liver stiffness.ResultsLiver stiffness ranged from 3.0–34.3 kPa, with a median value of 5.1 kPa (IQR 1.7). BMA provided a very high support for age (Posterior Effect Probability-PEP: 84.5%), moderate for BMI (PEP: 49.3%), CD4/8 ratio (PEP: 44.2%) and lipodystrophy (PEP: 44.0%). For all remaining variables, the model rather provides evidence against their effect. These results overall suggest that age and BMI have a positive association with LS, while CD4/8 ratio and lipodystrophy are negatively associated.DiscussionOur findings shed light on the possible importance of ageing, overweight and HIV-induced immune dysregulation in the development of liver fibrosis in the HIV-infected population. Nonetheless, further controlled studies are warranted to clarify causal relations.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hepatic fibrosis and factors associated with liver stiffness in HIV mono-infected individuals

Sulyok

Ferenci

Makara

et al. 2017

PeerJ

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Human immunodeficiency virus and liver disease: An update

2015

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HIV infection affects approximately 1.2 million persons in the United States and 35 million worldwide. Progression to advanced liver disease remains a leading cause death among HIV-infected persons in the U.S. and elsewhere. Though mortality from HIV complications has been dramatically reduced wherever effective combination antiretroviral therapy is utilized, there has been little impact on liver related mortality. Causes of liver disease in the setting of HIV infection include viral hepatitis, NAFLD/NASH, drug-associated toxicities, and other metabolic/genetic disorders which interact in an environment modulated by persistent immune activation and altered cytokine display. Despite significant advances in treatment of HCV and suppression of HBV, treatment and management principles remain challenging. Limited resources, fragmented healthcare and high levels of injection drug use, alcohol use and depression remain relevant issues in the HIV-infected patient.

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HCV spontaneous clearers showed low senescence profile in people living with HIV under long ART

Lara-Aguilar

Crespo-Bermejo

Llamas-Adán

et al. 2023

Journal of Medical Virology

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Coinfection with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) increases immune activation, inflammation, and oxidative stress that could lead to premature senescence. Different HCV infections, either acute or chronic infection, could lead to distinct premature cellular senescence in people living with HIV (PLWHIV). Observational study in 116 PLWHIV under antiretroviral treatment with different HCV status: (i) n = 45 chronically infected with HCV (CHC); (ii) n = 36 individuals who spontaneously clarify HCV (SC); (iii) n = 35 HIV controls. Oxidative stress biomarkers were analyzed at lipid, DNA, protein, and nitrates levels, as well as

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Liver fibrosis in HIV

Cited by 57 publications

References 30 publications

Hepatic fibrosis and factors associated with liver stiffness in HIV mono-infected individuals

Hepatic fibrosis and factors associated with liver stiffness in HIV mono-infected individuals

Human immunodeficiency virus and liver disease: An update

HCV spontaneous clearers showed low senescence profile in people living with HIV under long ART

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