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Lipid and glucose metabolism in HIV-1-infected children treated with protease inhibitors
  1. N M Vink1,
  2. A M C van Rossum1,
  3. N G Hartwig1,
  4. R de Groot1,
  5. S Geelen2
  1. 1Department of Pediatrics, University Hospital Rotterdam/ Sophia Children's Hospital Dr Molewaterplein 60, 3015 GJ Rotterdam, The Netherlands rdegroot{at}alkg.azr.nl
  2. 2Department of Pediatrics, Wilhelmina Children's Hospital, Utrecht, The Netherlands

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The use of protease inhibitors (PIs) in patients with HIV-1/AIDS has been associated with peripheral lipodystrophy, hyperlipidemia and insulin resistance.1,2 However, all studies have been done in adults. The aim of this study was to evaluate the influence of highly active antiretroviral therapy (HAART) on serum levels of fasting triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL), free fatty acids (FFAs) and glucose in twenty HIV-1 infected children treated during a minimum period of 18 months with an indinavir (IDV) or nelfinavir (NFV) containing regimen of HAART.

The lipid values were evaluated at two timepoints: within the first month of HAART (“baseline values”) and after 18 months or more (range 18–24 months). Serum levels of fasting glucose was only evaluated at follow up.

In summary, we found an increase in serum levels of total cholesterol and LDL after PI use in HIV-1-infected children, as was previously observed in adults.1 However, in contrast with adults, a marked increase in HDL and normal glucose levels was observed.2 The total cholesterol/HDL ratio, fasting triglyceride and FFA levels remained stable over time.

To date, it has not been revealed whether these metabolic changes are the result of HAART or if HIV-1 infection itself is responsible. Hypertriglyceridemia and low levels of total cholesterol, HDL and LDL have been detected in HIV-1-infected patients without prior antiretroviral therapy, especially in the late phase of the disease.3 Thus, the significant rise of total cholesterol, HDL and LDL in HIV-1 infected children may not only be attributed to the effects of HAART, but may be also partially be the result of a normalisation of pre-existing lipid abnormalities.

It is difficult to discriminate the metabolic effects of PIs from those of other antiretroviral drugs in this study. Most children received a combination of a PI, zidovudine, and lamivudine, which are also reported to cause lipodystrophy and lipid abnormalities.4 Eleven children were pretreated with zidovudine before the start of HAART. These children had significantly lower levels of total cholesterol and LDL at baseline than naive children, suggesting that zidovudine itself may have an effect on the lipid metabolism.

After these results we unfortunately have to conclude that HAART also effects the lipid and glucose metabolism in children.

Acknowledgments

We would like to thank L Zwang and M A C van Fessem for performing the laboratory analyses, W C J Hop for statistical advice, G J Bruining, F Pistoor, H J Scherpbier, and T F W Wolfs for their co-operation.

References

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