3rd International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV 23-26 October 2001, Athens, Greece

DECREASED SERUM LEPTIN IS ASSOCIATED WITH ONSET OF LIPOATROPHY

Antiviral Therapy 2001; 6(Suppl. 4):31 (abstract no. 42)

BC Calhoun¹, S Esper¹, AM DePaoli², SA Riddler¹, R Evans¹ and LA Kingsley^1
1 University of Pittsburgh, Pittsburgh, Pa., USA; and ² Amgen Inc., Thousand Oaks, Calif., USA

BACKGROUND: Very few data have been reported regarding HIV-associated lipodystrophy syndrome (HIV-LS) and serum leptin levels. The development of this syndrome may have a hormonal influence contributing to the accumulation, loss or redistribution of body fat.

OBJECTIVES: The purpose of this study was to determine whether the lipoatrophy phenotype of HIV-LS is associated with changes in serum leptin following initiation of HAART.

METHODS: Between 4/99 and 3100,146 HIV-positive gay men were evaluated for HIV-LS at the Pittsburgh site of the Multicenter AIDS Cohort Study (MACS). HIV-LS was assessed by physical examination and stratified by the two major phenotypes: lipoatrophy alone and lipoatrophy with central fat gain ('mixed' HIV-LS). Stored serum obtained prior to the initiation of highly active antiretroviral therapy (HAART) was used for baseline leptin levels and serum from a subsequent visit when HIV-LS was documented provided follow-up data.

RESULTS: Forty-two of 146 men were found to have moderate or severe lipoatrophy or lipohypertrophy in one or more body areas. Twenty-seven had lipoatrophy alone and 15 had 'mixed' changes; 39/146 with no body habitus changes served as controls. Those with HIV-LS were older, had longer use of protease inhibitors, had lower baseline CD4 counts, and had lost an average of 4 kg from baseline. Median baseline leptin levels were 3.6 ng/ml for both the lipoatrophy and 'mixed' groups and 4.1 ng/ml for controls. Serum leptin decreased significantly in those who developed lipoatrophy alone (3.6-2.8 ng/ml; Wilcoxon P=0.006), while stable leptin levels were observed in both those with 'mixed' HIV-LS (4.0 ng/ml; P=NS) and 39 HIV-positive controls who did not develop HIV-LS (3.7ng/ml; P=NS).

CONCLUSIONS: The development of the lipoatrophy phenotype of HIV-LS following HAART initiation is associated with a decrease in serum leptin. Whether this decrease is explained exclusively by peripheral fat loss needs further study. This might suggest a reduced leptin level could contribute to the lipoatrophy syndrome.

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