Fibroblast growth factor 21 is independently associated with severe hepatic steatosis in non-obese HIV-infected patients.


Journal

Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857

Informations de publication

Date de publication:
08 2019
Historique:
received: 23 01 2019
revised: 20 03 2019
accepted: 21 03 2019
pubmed: 28 3 2019
medline: 18 9 2020
entrez: 28 3 2019
Statut: ppublish

Résumé

Severe hepatic steatosis shows a high prevalence and contributes to morbidity and mortality in human immunodeficiency virus (HIV) infected patients. Known risk factors include obesity, dyslipidaemia and features of metabolic syndrome. Fibroblast growth factor 21 (FGF-21) is involved with hepatic glucose and lipid metabolism. This study aimed to evaluate FGF-21 as a biomarker for severe hepatic steatosis in non-obese HIV-infected patients. This is a prospective, cross-sectional, monocentric study including HIV-infected out-patients. Hepatic steatosis was measured via controlled attenuation parameter (CAP) using FibroScan 502 touch (ECHOSENS, France). Severe hepatic steatosis was defined at CAP ≥ 253 dB/m. Peripheral blood samples were collected and plasma was analysed for FGF-21. Demographic and clinical characteristics were collected from patient's health records. In total, 73 non-obese HIV-monoinfected patients were included in this study. Prevalence of severe hepatic steatosis was 41%. Patients with severe hepatic steatosis showed significantly higher levels of FGF-21. Univariate analysis revealed FGF-21, BMI, hyperlipidaemia, ALT levels and arterial hypertension as significant, while multivariate analysis showed only FGF-21, arterial hypertension and ALT levels as significant independent risk factors for severe hepatic steatosis. This study presents FGF-21 as an independent and stronger predictor of severe hepatic steatosis than blood lipids in HIV-infected patients. Moreover, arterial hypertension and ALT levels predict severe steatosis even in non-obese HIV-monoinfected patients. Furthermore, this study supports existing metabolic risk factors and expands them to non-obese HIV-infected patients.

Sections du résumé

BACKGROUND
Severe hepatic steatosis shows a high prevalence and contributes to morbidity and mortality in human immunodeficiency virus (HIV) infected patients. Known risk factors include obesity, dyslipidaemia and features of metabolic syndrome. Fibroblast growth factor 21 (FGF-21) is involved with hepatic glucose and lipid metabolism. This study aimed to evaluate FGF-21 as a biomarker for severe hepatic steatosis in non-obese HIV-infected patients.
METHODS
This is a prospective, cross-sectional, monocentric study including HIV-infected out-patients. Hepatic steatosis was measured via controlled attenuation parameter (CAP) using FibroScan 502 touch (ECHOSENS, France). Severe hepatic steatosis was defined at CAP ≥ 253 dB/m. Peripheral blood samples were collected and plasma was analysed for FGF-21. Demographic and clinical characteristics were collected from patient's health records.
RESULTS
In total, 73 non-obese HIV-monoinfected patients were included in this study. Prevalence of severe hepatic steatosis was 41%. Patients with severe hepatic steatosis showed significantly higher levels of FGF-21. Univariate analysis revealed FGF-21, BMI, hyperlipidaemia, ALT levels and arterial hypertension as significant, while multivariate analysis showed only FGF-21, arterial hypertension and ALT levels as significant independent risk factors for severe hepatic steatosis.
CONCLUSION
This study presents FGF-21 as an independent and stronger predictor of severe hepatic steatosis than blood lipids in HIV-infected patients. Moreover, arterial hypertension and ALT levels predict severe steatosis even in non-obese HIV-monoinfected patients. Furthermore, this study supports existing metabolic risk factors and expands them to non-obese HIV-infected patients.

Identifiants

pubmed: 30916873
doi: 10.1111/liv.14107
doi:

Substances chimiques

FGF21 protein, human 0
Fibroblast Growth Factors 62031-54-3

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1514-1520

Informations de copyright

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Auteurs

Michael Praktiknjo (M)

Department of Medicine I, University of Bonn, Bonn, Germany.

Natalie Djayadi (N)

Department of Medicine I, University of Bonn, Bonn, Germany.

Raphael Mohr (R)

Department of Medicine I, University of Bonn, Bonn, Germany.

Robert Schierwagen (R)

Department of Medicine I, University of Bonn, Bonn, Germany.

Jenny Bischoff (J)

Department of Medicine I, University of Bonn, Bonn, Germany.

Leona Dold (L)

Department of Medicine I, University of Bonn, Bonn, Germany.

Alessandra Pohlmann (A)

Department of Medicine I, University of Bonn, Bonn, Germany.

Carolynne Schwarze-Zander (C)

Department of Medicine I, University of Bonn, Bonn, Germany.

Jan-Christian Wasmuth (JC)

Department of Medicine I, University of Bonn, Bonn, Germany.

Christoph Boesecke (C)

Department of Medicine I, University of Bonn, Bonn, Germany.

Jürgen K Rockstroh (JK)

Department of Medicine I, University of Bonn, Bonn, Germany.

Jonel Trebicka (J)

Department of Medicine I, University of Bonn, Bonn, Germany.
Department of Medicine I, University of Frankfurt, Frankfurt, Germany.
Department of Gastroenterology, Odense Hospital, University of Southern Denmark, Odense, Denmark.
European Foundation for the Study of Chronic Liver Failure - EF Clif, Barcelona, Spain.
Institute for Bioengineering of Catalonia, Barcelona, Spain.

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Classifications MeSH