Vol 56, No 1 (2005)
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Published online: 2006-03-22

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Serum leptin and adiponectin concentrations in patients infected with human immunodeficiency virus type 1 (HIV-1) on antiretroviral therapy

Magdalena Leszczyszyn-Pynka, Sławomir Pynka, Anna Boroń-Kaczmarska, Krystyna Pilarska
Endokrynol Pol 2005;56(1):19-24.


The lipodystrophy syndrome with dyslipidaemia and insuline resistance is side-effect of combined antiretroviral therapy (CART).
Aim of the study: to describe the influence of CART on leptin and adiponectin concentration in connection with lipids levels in HIV-infected patients on antiretroviral therapy.
BMI, serum leptin, adiponectin, triglycerides, total cholesterol, HDL- and LDL-cholesterol concentrations were measured in 56 HIV(+) patients before and on CART; average of treatment duration 38.4 ± 13.2 months. Significant increase of BMI (p=0.0268) of (22.6 ± 3.3 before and 23.5 ± 3.4 kg/m2 on therapy, respectively) and all analyzed lipids were found. Mean adiponectin concentration in treated patients was significantly (7.256 ± 3.551 µg/ml) lower than mean value before treatment (8.395 ± 3.568 µg/ml; p=0.0011). Mean values of leptin concentrations did not differ significantly (before therapy 3.721 ± 0.347 log10; on therapy 3.1737 ± 0.353 log10). Significant positive correlation between BMI and leptin concentrations was found before, as well as during CART (r=0.5333; p<0.0001), but negative correlation between adiponectin and leptin concentrations (r=-0.2677; p=0.042). Leptin and adiponectin concentrations did not revealed significant correlation with lipids levels before therapy. The decrease of adiponectin concentration on CART correlated negatively with total (r=-0.2912; p=0.0310) and LDL-cholesterol (r=-0.310; p=0.0225).CART lasting longer than 2 years resulted in the decrease of adiponectin concentration, with lack of influence on leptin concentration in analyzed group.
The increase of total cholesterol and LDL-cholesterol in correlation with the decrease of adiponectin concentration confirms that CART induces metabolic disturbances related to higher risk of atherosclerosis and its sequel.

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