Nutrition and the HIV-associated lipodystrophy syndrome

Abstract

HIV-associated lipodystrophy syndrome (HALS), comprising metabolic and morphological alterations, is a known side effect of highly active antiretroviral therapy (HAART). Evidence for the role of nutrition in the management of the systemic parameters of HALS is currently limited. In the present paper we review the current knowledge base surrounding HALS, focusing particularly on the role of nutrition in mitigating the systemic parameters of the syndrome. Reported prevalence of HALS was found to vary from 9 to 83 % due to lack of a standardised definition, as well as variations in assessment methods and in the study population used. HALS is associated with both morphological (lipoatrophy, lipohypertrophy) and metabolic (dyslipidaemia, glucose intolerance, diabetes, hypertension, endothelial dysfunction and atherosclerosis) alterations, which may occur singly or in combination, and are associated with an increased risk of CVD. HAART-induced adipocyte inflammation, oxidative stress and macrophage infiltration, as well as altered adipocyte function and mitochondrial toxicity, have been shown to be central to the development of HALS. The adipocyte, therefore, represents a plausible target for treatment. Pharmacological and surgical treatment interventions have shown effect. However, their use is associated with numerous adverse effects and complications. Targeted lifestyle interventions may provide a useful alternative for managing HALS owing to their safety and tolerability. A Mediterranean-style diet has been found to be effective in improving the systemic parameters of HALS. Furthermore, the effects of n-3 PUFA supplementation are encouraging and future randomised controlled trials investigating the beneficial effects of n-3 PUFA in HALS are justified.

Redistribuição de gordura corporal e alterações no metabolismo de lipídeos e glicose em pessoas vivendo com HIV/AIDS

“…Despite their benefits and efficacy, the interaction between HAART with the infection itself and inflammation caused by HIV is associated with severe adverse effects, such as metabolic alterations and abnormal redistribution of body fat. These changes are called HIV lipodystrophy syndrome (HIVLS) 4 . The abnormal redistribution of body fat (lipodystrophy) in PLWHA using HAART is characterized by loss of subcutaneous fat, mainly on the face, gluteal region and limbs (lipoatrophy), as well as by accumulation of fat on the back of the cervix, breasts and visceral region (lipohypertrophy).…”

Lipodystrophy syndrome in HIV-infected patients – a cohort study in Lower Silesia, Poland

“…In comparison with the control group, the LDL cholesterol level was noticeably lower and TG concentration was significantly higher in patients with severe lipodystrophy (LS2). The vast majority of authors describing lipid dysfunction in HIV-infected patients also observe hypertriglyceridemia [1,25,26,30,[35][36][37]. Mercie et al also discovered a significantly higher TG concentration in LS patients than in no-LS subgroup [25].…”

Highly Active Antiretroviral Therapy-Associated Metabolic Syndrome and Lipodystrophy: Pathophysiology and Current Therapeutic Interventions

“…Lipoatrophy is associated with the loss of subcutaneous fat mainly in the face, arms, buttocks and lower limbs whereas lipohypertrophy is characterised by fat accumulation in the adipose tissues at the back of the neck "buffalo hump" or dorsocervical region, abdominal adiposity and mammary hypertrophy/gynecomastia [8][9][10]. The etiology of lipodystrophy syndrome is poorly understood but the incidence is estimated at 2-60% and 30% in adults and children on HAART, respectively [9,[11][12][13].…”

“…Risk factors currently associated with HAARTrelated lipodystrophy include duration of therapy, female gender (lipohypertrophy), increased age, race (common in Manuscript accepted for publication March 31, 2017 HAART-Associated Metabolic Syndrome J Endocrinol Metab. 2017;7(4): [103][104][105][106][107][108][109][110][111][112][113][114][115][116] Caucasians), low CD4 + counts, use of PIs and NRTIs (mainly thymidine analogues) in addition to HIV pathogenesis, genetic and environment factors [11,18,19]. Metabolic complications associated with lipodystrophy following HAART include glucose intolerance and insulin resistance, increased plasma total cholesterol (TC) and triglycerides (TG), decreased plasma concentrations of high-density lipoprotein cholesterol (HDL-C), and increased low-density lipoprotein cholesterol (LDL-C) [3,[19][20][21].…”