[45] SERUM CORTISOL: DHEA RATIO IS THE BEST PREDICTOR OF CLINICAL EVOLUTION AND LIPID VARIATIONS ASSOCIATED TO LIPODYSTROPHY

3rd International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV

23-26 October 2001, Athens, Greece

SERUM CORTISOL: DHEA RATIO IS THE BEST PREDICTOR OF CLINICAL EVOLUTION AND LIPID VARIATIONS ASSOCIATED TO LIPODYSTROPHY

Antiviral Therapy 2001; 6(Suppl. 4):33 (abstract no. 45)

N Christeff¹, P de Truchis², J-C Melchior² and M-L Gougeon¹
¹ AIDS and Retroviruses Department, Institut Pasteur, Paris, France; ² Hospital Raymond Poincare, Garches, France.

OBJECTIVES: We have previously shown that lipid alterations associated to the Lipodystrophy syndrome (LD) in HIV-1-infected men on combined antiretroviral therapy (ART) are correlated with decreased DHEA, increased cortisol-DHEA ratio and increased serum IFN-α levels. In this study, we asked whether clinical evolution and changes in circulating lipids in LD-positive men is associated with changes in the parameters.

METHODS: Thirty-five HIV-1-positive men on ART, 20 of them presenting with LD, defined by clinical examination and computed tomography scan, were followed during 25.9±4.0 months and tested at two time points. LD patients were subdivided into three groups, unchanged (n=5), aggravated (n=9) and improved (n=6), according to their clinical evolution and anthropometric measurements, including waist-hip ratio and skinfold thickness in the four usual sites. Serum lipids (cholesterol, triglycerides and their subclasses and apolipoproteins), cortisol, DHEA and cytokines (IFN-α, TNF-α, IL-6) were measured and compared to baseline values of LD-negative patients.

RESULTS: We show that: (1) LD aggravation is associated to persistent elevated lipids a decrease in serum DHEA (-60%, P<0.02 and -66%, P<0.008), an increase in cortisol: DHEA ratio (+170%, P<0.009 and +200%, P<0.005) and persistent high levels of IFN-α. (2) LD improvement is associated to normalization of serum lipids, an increase in serum DHEA (+190%, P<0.001)leading to normalization of the cortisol: DHEA ratio and normalization of IFN-α levels. (3) The absence of LD evolution is associated with persistent elevated lipids, a slight increase in serum DHEA, a slight decrease in both cortisol-DHEA ratio and IFN-α. (4) Importantly, we found that, in aggravated and improved patients, there is a negative correlation between atherogenic lipids, such as VLDL cholesterol and VLDL triglycerides and serum DHEA (r=0.57, P<0.03 and r=-0.60, P<0.02, respectively) and a positive correlation between these lipids and cortisol-DHEA ratio (r=0.63, P<0.016 and P<0.54, P<0.046, respectively). (5) The follow-up of LD-negative men (n=15) revealed that those who began to develop LD (n=6) showed an increase in lipid levels, a decrease in serum DHEA, an increase in cortisol-DHEA ratio and an increase in IFN-α levels. In contrast, patients who remained LD-negative (n=9), maintained normal lipids, elevated cortisol, elevated DHEA leading to a normal cortisol-DHEA ratio, and normal levels of IFN-α.

CONCLUSIONS: This study suggests that cortisol-DHEA ratio is the best predictor of clinical evolution and atherogenic lipid alterations in LD patients.

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