Natural Course of Nonalcoholic Fatty Liver Disease and Type 2 Diabetes in Patients With Human Immunodeficiency Virus With and Without Combination Antiretroviral Therapy-associated Lipodystrophy: A 16-Year Follow-up Study.


Journal

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213

Informations de publication

Date de publication:
10 04 2020
Historique:
received: 14 11 2018
accepted: 24 05 2019
pubmed: 28 5 2019
medline: 7 1 2021
entrez: 28 5 2019
Statut: ppublish

Résumé

Abnormal glucose metabolism and nonalcoholic fatty liver disease (NAFLD) are common in patients with human immunodeficiency virus (HIV+ patients), but longitudinal data are lacking. We determined the natural course of NAFLD (liver fat [LFAT]) and type 2 diabetes mellitus (T2DM) in HIV+ patients with and without lipodystrophy (LD+ and LD-, respectively) during a 16-year longitudinal study. LFAT (by proton magnetic resonance spectroscopy) and clinical characteristics were measured in 41 HIV+ patients at baseline and after 16 years. Liver fibrosis was estimated by measuring liver stiffness using transient elastography (TE) and magnetic resonance elastography (MRE) at 16 years. We also longitudinally studied 28 healthy subjects. During follow-up, the HIV+ patients gained more body fat (8.6% ± 0.7%) than the control patients (4.5% ± 0.6%, P < .001). Features of insulin resistance increased significantly in the HIV+ patients but not the control patients. A significant proportion (20%, P < .01 vs 0% at baseline) of the HIV+ but none of the control patients developed T2DM. LFAT was significantly higher at baseline in the LD+ (4.3 [1.9-11.8]) than the LD- (1.0 [0.5-1.5]; P < .001) HIV+ patients. LFAT remained stable during follow-up in all groups. At follow-up, liver stiffness measured with TE was similar among all HIV, LD+, LD-, and control patients and between the LD+ and LD- patients measured with MRE. Advanced fibrosis by MRE was observed in 3 of LD+ and none of LD- patients. During 16 years of follow-up, progression of NAFLD is rare compared to development of T2DM in HIV+ patients.

Sections du résumé

BACKGROUND
Abnormal glucose metabolism and nonalcoholic fatty liver disease (NAFLD) are common in patients with human immunodeficiency virus (HIV+ patients), but longitudinal data are lacking. We determined the natural course of NAFLD (liver fat [LFAT]) and type 2 diabetes mellitus (T2DM) in HIV+ patients with and without lipodystrophy (LD+ and LD-, respectively) during a 16-year longitudinal study.
METHODS
LFAT (by proton magnetic resonance spectroscopy) and clinical characteristics were measured in 41 HIV+ patients at baseline and after 16 years. Liver fibrosis was estimated by measuring liver stiffness using transient elastography (TE) and magnetic resonance elastography (MRE) at 16 years. We also longitudinally studied 28 healthy subjects.
RESULTS
During follow-up, the HIV+ patients gained more body fat (8.6% ± 0.7%) than the control patients (4.5% ± 0.6%, P < .001). Features of insulin resistance increased significantly in the HIV+ patients but not the control patients. A significant proportion (20%, P < .01 vs 0% at baseline) of the HIV+ but none of the control patients developed T2DM. LFAT was significantly higher at baseline in the LD+ (4.3 [1.9-11.8]) than the LD- (1.0 [0.5-1.5]; P < .001) HIV+ patients. LFAT remained stable during follow-up in all groups. At follow-up, liver stiffness measured with TE was similar among all HIV, LD+, LD-, and control patients and between the LD+ and LD- patients measured with MRE. Advanced fibrosis by MRE was observed in 3 of LD+ and none of LD- patients.
CONCLUSIONS
During 16 years of follow-up, progression of NAFLD is rare compared to development of T2DM in HIV+ patients.

Identifiants

pubmed: 31131845
pii: 5498863
doi: 10.1093/cid/ciz435
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1708-1716

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

Auteurs

Susanna Lallukka-Brück (S)

Minerva Foundation Institute for Medical Research.
Department of Medicine, University of Helsinki, and Helsinki University Hospital.

Elina Isokuortti (E)

Minerva Foundation Institute for Medical Research.
Department of Medicine, University of Helsinki, and Helsinki University Hospital.

Panu K Luukkonen (PK)

Minerva Foundation Institute for Medical Research.
Department of Medicine, University of Helsinki, and Helsinki University Hospital.

Antti Hakkarainen (A)

Helsinki University Hospital Medical Imaging Center, Helsinki University Hospital.

Nina Lundbom (N)

Helsinki University Hospital Medical Imaging Center, Helsinki University Hospital.

Jussi Sutinen (J)

Department of Infectious Diseases, University of Helsinki, and Helsinki University Hospital, Finland.

Hannele Yki-Järvinen (H)

Minerva Foundation Institute for Medical Research.
Department of Medicine, University of Helsinki, and Helsinki University Hospital.

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