Weight gain in patients starting Dolutegravir-based ART according to baseline CD4 count after 48 weeks of follow up

Cardoso-Neto, Érico C.; Netto, Eduardo Martins; Brites, Carlos

doi:10.1016/j.bjid.2023.102807

Cited by 3 publications

(1 citation statement)

References 13 publications

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“…A recent metaanalysis of randomized controlled trials comparing integrase inhibitors with other antiretroviral classes (EFV-based or PI-based therapies) in naive HIV patients, demonstrated that INSTIs led to decreased TC (MD −13.44 mg/dL), LDL (MD −1.37 mg/dL), HDL (MD −5.03 mg/dL), and TG levels (MD −20.70 mg/dL). However, a well-established risk of considerable weight gain among HIV individuals has been associated with INSTI-based treatment, compared to PIs and NNRTIs [131][132][133]. The pathophysiological pathway behind the aforementioned outcome is yet to be established; however, a low CD4 count, high viral load, and substantial weight loss before the initiation of HAART were associated with greater weight gain, implying that superior immune reconstitution in individuals with more advanced HIV infection appears to be an independent risk factor for INSTI-induced fat accumulation [134,135].…”

Section: Integrase Inhibitorsmentioning

confidence: 99%

Pathophysiology and Clinical Management of Dyslipidemia in People Living with HIV: Sailing through Rough Seas

Papantoniou,

Arvanitakis,

Markakis

et al. 2024

Life

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Infections with human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS) represent one of the greatest health burdens worldwide. The complex pathophysiological pathways that link highly active antiretroviral therapy (HAART) and HIV infection per se with dyslipidemia make the management of lipid disorders and the subsequent increase in cardiovascular risk essential for the treatment of people living with HIV (PLHIV). Amongst HAART regimens, darunavir and atazanavir, tenofovir disoproxil fumarate, nevirapine, rilpivirine, and especially integrase inhibitors have demonstrated the most favorable lipid profile, emerging as sustainable options in HAART substitution. To this day, statins remain the cornerstone pharmacotherapy for dyslipidemia in PLHIV, although important drug–drug interactions with different HAART agents should be taken into account upon treatment initiation. For those intolerant or not meeting therapeutic goals, the addition of ezetimibe, PCSK9, bempedoic acid, fibrates, or fish oils should also be considered. This review summarizes the current literature on the multifactorial etiology and intricate pathophysiology of hyperlipidemia in PLHIV, with an emphasis on the role of different HAART agents, while also providing valuable insights into potential switching strategies and therapeutic options.

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