10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV 6-8 November 2008, London, UK

BMI AND LIPODYSTROPHY: A COMPLEX INTERPLAY ON ADIPOCYTE-DERIVED HORMONES ON HIV-INFECTED PATIENTS

Antiviral Therapy 2008; 13(Suppl. 4):A27 (abstract no. P-07)

P Freitas¹, D Carvalho¹, C Gonçalves², AJ Madureira³, AC Santos⁴, S Xerinda³, MJ Matos¹, R Marques⁵, F Correia¹, R Serrão⁵, I Azevedo², I Ramos³, H Barros⁴, A Sarmento⁵ and JL Medina^1
1Department of Endocrinology, Hospital de São João, Faculdade de Medicina do Porto, Portugal; ²Laboratório Nobre, Hospital de São João, Faculdade de Medicina do Porto, Portugal; ³Department of Radiology, Hospital de São João, Faculdade de Medicina do Porto, Portugal; ⁴Department of Hygiene and Epidemiology, Hospital de São João, Faculdade de Medicina do Porto, Portugal; ⁵Department of Infectious Diseases, Hospital de São João, Faculdade de Medicina do Porto, Portugal

INTRODUCTION: Adipocyte-derived hormones (ADH) could be the link between the distribution of adipose tissue and the metabolic changes, namely insulin resistance (IR), related to HIV lipodystrophy.

AIMS: To evaluate ADH (adiponectin, leptin, resistin and TNF-α), ghrelin and IR in HIV patients undergoing antiretroviral therapy with and without clinically defined lipodystrophy, with and without lipodystrophy defined by fat mass ratio (FMR) by DEXA, according to different types of fat distribution (without clinical lipodystrophy [CL] and without abdominal prominence [AP], without CL and with PA, with CL and without AP, and with CL and with AP). AP was defined by waist circumference (WC) by IDF-2005.

METHODS: A total of 163 patients were evaluated for the presence of CL, lipodystrophy defined by FMR and abdominal fat according to CT.

RESULTS: When lipodystrophy was clinically defined, no statistically significant differences were found in resistin, adiponectin, TNF-α, ghrelin, HOMA and Quicki, between patients with and without CL. Leptin was significantly lower in patients with CL (without CL 9.42 ±10.27 versus 4.25 ±4.08 ng/ml, P<0.001). All the former results were similar when patients were divided by gender. When lipodystrophy was defined by FMR, the results were similar in the total of patients. When divided by gender, the results were similar, except for adiponectin (without L 8,682.6 ±9,476.9 versus L 4,282.3 ±4,153.5 ng/ml, P=0.029), leptin (no statistically significant differences), HOMA (increase) and Quicki (decrease) in males with lipodystrophy. According to the types of fat distribution no differences were found for resistin, TNF-α and ghrelin; adiponectin was lower in patients with AP and leptin was higher in those without AP. In patients without CL, those with AP had lower adiponectin (without AP 8,856.0 ±8,849.7 versus with AP 3,808.7 ±4,569.8 ng/ml, P=0.004), higher leptin (without AP 4.50 ±4.26 versus with AP 11.74 ±11.44 ng/ml, P=0.001) and higher insulin resistance (HOMA without AP 1.4 ±0.7 versus with AP 3.4 ±3.4, P=0.005). In the patients with CL, those with AP had higher leptin (without AP 2.46 ±1.79 versus with AP 6.13 ±4.93 ng/ml, P<0.001); no differences were found in HOMA and Quicki in those with and without AP. In the total of patients, we found correlations between leptin and body mass index (BMI; r=0.493, P<0.001), WC (r=0.440, P<0.001), total fat (r=0.803, P<0.001), trunk fat (r=0.774, P<0.001), lower limb fat (r=0.734, P<0.001), visceral/ subcutaneous fat mass by CT (r=-0.451, P<0.001) and FMR (r=-0.265, P=0.001); between adiponectin and total fat (r=-0.209, P=0.013), trunk fat (r=-0.195, P=0.020) and lower limb fat (r=-0.168, P=0.047); between resistin and BMI (r=-0.177, P=0.024): and between ghrelin and HOMA (r=-0.205, P=0.013) and Quicki (r=0.211, P=0.011). We found the same correlations formerly described for leptin, independently of the presence of CL.

CONCLUSIONS: The lipodystrophy of HIV-infected patients is a complex model with an interplay of adiposity and fat redistribution on ADH.

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2008-11-06
P-07

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