However, as adiponectin has anti-inflammatory activity [11], it could be involved in a compensatory mechanism to cushion the inflammatory effect and IR induced by leptin and resistin

during the first few years of HAART. This mechanism could explain the lack of association between changes in adipokine levels and the emergence of lipodystrophy. Our study has several important limitations that may have affected the data. (1) Study design: this was a retrospective study of a small cohort of HIV-infected CHIR 99021 children. (2) Previous ART: children had already been treated with NRTIs, which may have played a role in the development of metabolic syndrome and lipodystrophy. (3) Absence of uniform HAART: clearly, all drugs do not have the same effect on lipid metabolism, adipokine profiles and lipodystrophy. We could not separately analyse data for each drug because of the low number

of patients included in the study. (4) The ages of the children: GSI-IX manufacturer given the average age of the patients, many of them could have been entering puberty, and this may have affected body composition and serum adipokine levels. These four factors could be responsible for the wide range of values found for the markers evaluated. In addition, immunosuppression level and viral load control can affect metabolic syndrome [30]. Specifically, HIV viral load has been associated with levels of proinflammatory cytokines, adiponectin and leptin [31]. Also, low immune function (C3) may influence proinflammatory cytokine levels [32]. Thus, it is possible that the variability of the markers evaluated was the result of inefficient virological response and immune reconstitution. In conclusion, HIV-infected children showed an increase in serum adipokine levels, but this was not associated with the emergence of lipodystrophy during 48 months on HAART. This work was supported by grants from Fundación para la Investigación y la Prevención del SIDA en España (FIPSE 36650/07), Fondo

de Investigación Sanitaria (FIS) of Ministerio de Ciencia e Innovación (PI07/90201; PI08/0738) and Instituto de Salud Carlos III (UIPY 1467/07) to SR, and grants from Fundación para la Investigación y la Prevención oxyclozanide del SIDA en España (FIPSE 240800/09), Fondo de Investigación Sanitaria (FIS) of Ministerio de Ciencia e Innovación FIS (Intrasalud PI09/02029); Red RIS RD06-0006-0035; Fundación Caja Navarra, Comunidad de Madrid (S-SAL-0159-2006) and Task Force in Europe for Drug Development for the Young (TEDDY) to MAMF. In addition, we would like to acknowledge the Spanish HIV BioBank, which is a part of the Spanish AIDS Research Network, and the collaborating centres for the generous gifts of some of the clinical samples used in the study. Potential conflicts of interest and transparency declaration: The authors do not have any commercial or other associations that might pose a conflict of interest.