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JAC Advance Access published online on June 18, 2008
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkn251
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Review

HIV-associated lipodystrophy: a review of underlying mechanisms and therapeutic options

Jane E. Mallewa1,*, Edmund Wilkins1, Javier Vilar1, Macpherson Mallewa2, Dominic Doran3, David Back4 and Munir Pirmohamed5

1 Department of Infectious Diseases, North Manchester General Hospital, Delaunays Road, Manchester M8 5RB, UK 2 Division of Child Health, Royal Liverpool Children’s Hospital, University of Liverpool, Eaton Road, Liverpool L12 2AP, UK 3 Department of Sports Science, Liverpool John Moores University, Henry Cotton Campus, 15–21 Webster Street, Liverpool L3 2ET, UK 4 Department of Pharmacology and Therapeutics, University of Liverpool, 70 Pembroke Place, Liverpool L69 3GF, UK 5 Department of Pharmacology and Therapeutics, University of Liverpool, Ashton Street, Liverpool L69 3GE, UK

* Corresponding author. Tel: +44-1516410099/7841203427; Fax: +44-1617202562; E-mail: janemallewa{at}yahoo.com

Lipodystrophy (LD) is a common adverse effect of HIV treatment with highly active antiretroviral therapy, which comprises morphological and metabolic changes. The underlying mechanisms for LD are thought to be due to mitochondrial toxicity and insulin resistance, which results from derangements in levels of adipose tissue-derived proteins (adipocytokines) that are actively involved in energy homeostasis. Several management strategies for combating this syndrome are available, but they all have limitations. They include: switching from thymidine analogues to tenofovir or abacavir in lipoatrophy, or switching from protease inhibitors associated with hyperlipidaemia to a protease-sparing option; injection into the face with either biodegradable fillers such as poly-L-lactic acid and hyaluronic acid (a temporary measure requiring re-treatment) or permanent fillers such as bio-alcamid (with the risk of foreign body reaction or granuloma formation); and structured treatment interruption with the risk of loss of virological control and disease progression. There is therefore a need to explore alternative therapeutic options. Some new approaches including adipocytokines, uridine supplementation, glitazones, growth hormone (or growth hormone-releasing hormone analogues), metformin and statins (used alone or in combination) merit further investigation.

Key Words: adipocytokines , antiretroviral therapy , protease inhibitors , nucleoside reverse transcriptase inhibitors


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