Longitudinal evolution of HIV-1-associated lipodystrophy is correlated to serum cortisol:DHEA ratio and IFN-α

Background We have previously shown that lipid alterations in HIV‐1‐associated lipodystrophy (LD) are correlated with decreased serum dehydroepiandosterone (DHEA) and increased cortisol:DHEA ratio and IFN‐α levels. Objective To evaluate in a longitudinal study whether steroid and cytokine modificati...

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Bibliographic Details
Published in:European journal of clinical investigation 2002-10, Vol.32 (10), p.775-784
Main Authors: Christeff, N., De Truchis, P., Melchior, J.-C., Perronne, C., Gougeon, M.-L.
Format: Article
Language:English
Subjects:
Adult
Antiretroviral Therapy, Highly Active
Apolipoprotein A-I - analysis
Apolipoproteins B - analysis
Cholesterol - blood
Cholesterol, HDL - blood
Cholesterol, VLDL - blood
Cortisol
Dehydroepiandrosterone - blood
DHEA ratio
Disease Progression
HIV Infections - blood
HIV Infections - drug therapy
HIV-1
HIV-1-infected men
HIV-Associated Lipodystrophy Syndrome - blood
HIV-Associated Lipodystrophy Syndrome - etiology
Humans
Hydrocortisone - blood
IFN-α
Insulin - blood
Interferon-alpha - blood
lipodystrophy
Longitudinal Studies
Male
Statistics, Nonparametric
Triglycerides - blood
VLDL cholesterol
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Summary:Background We have previously shown that lipid alterations in HIV‐1‐associated lipodystrophy (LD) are correlated with decreased serum dehydroepiandosterone (DHEA) and increased cortisol:DHEA ratio and IFN‐α levels. Objective To evaluate in a longitudinal study whether steroid and cytokine modifications are associated with the evolution of physical changes and lipid alterations associated with LD. Methods Thirty‐four HIV‐1‐positive men were followed during 32·5 ± 4·0 months and tested at four time‐points. The patients were subdivided into five groups according to physical changes and anthropometric measurements: LD‐negative, initially LD‐negative becoming LD‐positive, LD‐positive unchanged, aggravated or improved. Serum lipids, apolipoproteins, adrenal steroids and cytokines were measured and compared with baseline values. Results (1) LD aggravation is associated with persistent elevated lipids, a decrease in serum DHEA, an increase in cortisol:DHEA ratio and persistent high levels of IFN‐α. (2) LD improvement is associated with normalization of serum lipids, an increase in serum DHEA leading to normalization in cortisol:DHEA ratio, and normalization of IFN‐α levels. (3) In LD‐positive men evolution of VLDL cholesterol is negatively correlated with DHEA (r = −0·56, P 
ISSN:0014-2972
1365-2362
DOI:10.1046/j.1365-2362.2002.01068.x