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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
Author(s) -
Susanna LallukkaBrück,
Elina Isokuortti,
Panu K. Luukkonen,
Antti Hakkarainen,
Nina Lundbom,
Jussi Sutinen,
Hannele YkiJärvinen
Publication year - 2019
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1093/cid/ciz435
Subject(s) - transient elastography , nonalcoholic fatty liver disease , lipodystrophy , medicine , gastroenterology , insulin resistance , fatty liver , diabetes mellitus , steatosis , type 2 diabetes , type 2 diabetes mellitus , insulin , liver biopsy , endocrinology , viral load , human immunodeficiency virus (hiv) , disease , antiretroviral therapy , immunology , biopsy
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.

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