AEGiS-Glasgow [PL7.1] Pathogenesis and treatment of metabolic complications of HIV therapy

Seventh International Congress on Drug Therapy in HIV Infection

Glasgow, UK - 14-17 November 2004

[PL7.1] Pathogenesis and treatment of metabolic complications of HIV therapy

Int Cong Drug Therapy HIV 2004 Nov 14-18;7:Abstract No. PL7.1

Peter Reiss
Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

Fat maldistribution (lipodystrophy), dyslipidemia and insulin resistance unfortunately are frequent adverse effects of current combination therapy for HIV infection, and thereby importantly jeopardize the sustained effectiveness of treatment. Nucleoside analog reverse transcriptase and protease inhibitors are both thought to contribute to the pathogenesis of lipoatrophy in particular, although there is some evidence which may suggest that both drug classes could also be involved in the pathogenesis of lipid changes and insulin resistance. Although a number of potential mechanisms have been suggested from in vitro studies, including inhibition of fat cell differentiation and mitochondrial toxicity, much remains unclear as to the precise derangements giving rise to fat maldistribution in patients. Of note, neither all protease inhibitors nor all nucleoside analogs are equal with respect to their propensity to induce these metabolic complications. Although interventions aimed at established fat maldistribution thus far have not been very effective, the earlier mentioned demonstrated differences between particular drugs do offer promise for establishing combination therapy strategies (e.g. involving novel NRTI backbones such as abacavir+lamivudine or tenofovir+emtricitabine) which may be associated with a reduced or at least delayed incidence of lipodystrophy.

SESSION 7: ADVERSE EVENTS I

2004-11-14
PL7.1

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