Purpose of review
Increased total body fat with truncal redistribution is common in antiretroviral therapy (ART)-controlled persons living with HIV(PLWH), leading to insulin resistance, prediabetes/diabetes and dyslipidaemia. We address these topics here.
Most antiretrovirals are associated with gain in trunk fat, including visceral adipose tissue (VAT). Protease-inhibitors could inhibit white fat ability to dissipate energy (i.e. beiging) favouring fat gain. Expansion of VAT is associated with a pro-inflammatory profile linked to the tryptophan-kynurenine pathway and CD4+ subtypes. ART-associated increased adipose tissue (AT) quantity leads to decreased AT density, insulin resistance and dyslipidaemia that could be improved by lifestyle modifications.
PLWH present high level of insulin resistance, regardless of their treatment, and a higher prevalence of prediabetes, but not diabetes, than noninfected persons. Otherwise, HbA1c values appear inaccurate to diagnose prediabetes/diabetes in PLWH.
ART-related-dyslipidaemia is characterized by elevated LDL-C and/or high triglycerides and reduced HDL-C. Whereas treatment with protease inhibitors generally results in worsened lipid values, treatment with integrase-strand-transfer-inhibitors is associated with a better profile. Tenofovir-alafenamide is associated with higher lipid levels than tenofovir-disoproxil-fumarate. Treatment of LDL-C-dyslipidaemia could benefit, in statin-insufficiently controlled patients, from the class of proprotein-convertase-subtilsin-kenin-type-9 (PCSK-9) inhibitors.
Lifestyle modifications are mandatory to reduce fat and improve dysglycaemia/dyslipidaemia. New drugs can efficiently control diabetes and LDL-C-dyslipidaemia.