[P-06] Leptin, a marker of evolution to lipodystrophy? Results of a 1-year follow-up in HIV-infected patients

10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV

6-8 November 2008, London, UK

LEPTIN, A MARKER OF EVOLUTION TO LIPODYSTROPHY? RESULTS OF A 1-YEAR FOLLOW-UP IN HIV-INFECTED PATIENTS

Antiviral Therapy 2008; 13(Suppl. 4):A26 (abstract no. P-06)

P Freitas¹, D Carvalho¹, C Gonçalves², AC Santos³, MJ Matos¹, S Xerinda⁴, R Marques⁴, F Correia¹, R Serrão⁴, I Azevedo², H Barros³, A Sarmento⁴ and JL Medina¹
¹Departments of Endocrinology, Hospital de São João, Faculdade de Medicina do Porto, Portugal; ²Laboratório Nobre, Hospital de São João, Faculdade de Medicina do Porto, Portugal; ³Hygiene and Epidemiology, Hospital de São João, Faculdade de Medicina do Porto, Portugal; ⁴Infectious Diseases, Hospital de São João, Faculdade de Medicina do Porto, Portugal

INTRODUCTION: Adipocyte-derived hormones (ADH) might help to explain the relationship between the distribution of adipose tissue and the progressive metabolic changes associated to HIV-related lipodystrophy, namely insulin resistance.

AIMS: We aimed to evaluate ADH in HIV-infected patients undergoing antiretroviral therapy (ART) and to measure their evolution over a 1-year follow-up in the total of patients and in patients with and without clinically defined lipodystrophy.

METHODS: A total of 131 HIV-infected patients undergoing ART were evaluated for the presence of CL and ADH (adiponectin, leptin, resistin and tumour necrosis factor-a [TNF-α]), ghrelin and insulin resistance (HOMA and Quicki) were measured. The results are presented as mean ±sd. Means were compared using Student’s t-test or non-parametric Mann–Whitney U test.

RESULTS: After a 1-year follow-up, we found that in the total of patients, a decrease in adiponectin (6,117.9 ±6,757.9 versus 1,407.6 ±1,019.6 ng/ml, P<0.001), TNF-α (55.4 ±40.3 versus 27.6 ±21.2 pg/ml, P<0.001), ghrelin (133.8 ±135.2 versus 94.77 ±122.1 pg/ml, P=0.006), an increase in resistin (1.06 ±0.48 versus 1.45 ±0.99 ng/ml, P=0.001) and no differences in leptin levels. In those without CL, a decrease in adiponectin (5,221.9 ±6,398.1 versus 1,434.1 ±1,273.4 ng/ml, P=0.002), TNF-α (61.0 ±55.5 versus 29.5 ±22.8 pg/ml, P=0.004), an increase in resistin (1.11 ±0.83 versus 1.67 ±1.52 ng/ml, P=0.032) and no differences in leptin and ghrelin levels. In those with CL, a decrease in adiponectin (5,587.0 ±7,000.1 versus 1,681.7 ±1,732.1 ng/ml, P<0.001), TNF-α (56.1 ±40.6 versus 25.9 ±19.2 pg/ml, P<0.001), ghrelin (122.8 ±117.6 versus 82.1 ±108.3 pg/ml, P=0.003), an increase in resistin (1.29 ±1.24 versus 1.37 ±0.65 ng/ml, P=0.014) and no differences in leptin levels. No differences were found in the progression over a year of resistin, adiponectin, TNF-α and ghrelin between patients without and with clinical lipodystrophy. On the contrary, we found statistically significant differences for the evolution of leptin (Table 1).

Table 1. (Abstract P-06)

	Without clinical lipodystrophy (difference after 1 year)	With clinical lipodystrophy (difference after 1 year)	P-value

Resistin, ng/ml	0.58 ±1.52	0.30 ±0.78	NS
Adiponectin, ng/ml	-5,204.2 ±7,382.7	-4,542.9 ±6,167.3	NS
TNF-α, pg/ml	-36.6 ±65.0	-24.3 ±35.1	NS
Ghrelin, pg/ml	-8.36 ±208.6	-53.2 ±140.8	NS
Leptin, ng/ml	-1.1 ±4.1	0.79 ±3.39	0.028

NS, not significant; TNF-α, tumour necrosis factor-α.

CONCLUSIONS: ADH and ghrelin, except leptin, showed a similar evolution on 1-year follow-up in HIV-infected patients with or without lipodystrophy. The decrease of leptin in patients without lipodystrophy seems to indicate a decrease in subcutaneous fat in these patients and could be a marker of progression to lipodystrophy.

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2008-11-06
P-06

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