HIV HAART AIDS SIDA VIH HIV
insulin resistance C-Reactive protein (CRP)
  Espaņol (soon!) - September 7, 2008
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 Conference
"Lipodistrophy and Related Issues"
Dr. Stephano Vella (biography)
English - 2002-04-15 - 25 minutes
(28 slides)
(2 questions)

Summary :
The major metabolic abnormalities that complicate the management of HIV infection include serum lipid abnormalities, body fat maldistribution, dysregulation of glucose metabolism, lactic acidemia, and reduced bone mineral density. It has not been determined whether these observed changes are all components of a single syndrome related to HIV treatment or whether they have different etiologies. Concern has been expressed about long-term cardiovascular morbidity in subjects who experience increases in atherogenic serum lipids, insulin resistance/dysglycemia, and body fat redistribution, but at present this risk is undefined.

From a pathogenetic point of view, if these conditions are part of a single syndrome or represent distinct syndromes, and whether the etiology is unique or multifactorial remain unanswered questions. Predictors of fat redistribution syndromes are numerous and may include: age > 40 years, longer time since HIV diagnosis, longer time since nadir CD4+, NRTI use > 6 months, protease inhibitor use > 2 years, nadir CD4%, Body Mass Index loss > 1.0 kg/m2. Overall, etiology remains unknown; and appears to be multifactorial and influenced by ARV use and host factors.

Morphologic changes include both fat accumulation (lipohypertrophy: dorsocervical fat, visceral adiposity, breast enlargement) and fat loss (lipoatrophy: facial fat loss, subcutaneous fat loss of extremities). Morphologic changes have a substantial impact on quality of life Management approaches are largely empirical. Only few of them are based on short term controlled studies: antiretroviral therapy switches, exercise and diet, anabolic steroids, recombinant human growth hormone (rhGH), testosterone, metformin, tiazolidinediones and plastic surgery.

Lipid abnormalities are also frequent and varies by drug (even within the same class). Recommended initial evaluations includes baseline and fasting cholesterol (total, HDL, LDL, triglycerides) and the assessment of cardiovascular risk and lifestyle factors (family history, exercise, diabetes, smoking, obesity, alcohol use, comorbidities such as pancreatitis).

Dyslipidemia management approaches include the assessment of cardiovascular risk followed by dietary and lifestyle changes and, possibly, using lipid-lowering agents (statins, fibrates). The impact of the mofication of antiretroviral therapy is still under investigation, despite some short term favourable trial results (e.g. substitute NNRTIs for PIs or substitute abacavir for PIs). In conclusion, initial management approach should be lifestyle modification (diet, exercise). Lipid-lowering agents can be added as necessary (but beware of drug-drug interactions and toxicities). Switching to non-PI regimens may be most effective for triglyceride elevations, but long-term efficacy is unclear. Finally, cardiovascular sequelae are minimal short-term; but long-term outcome is unknown.

   


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