In vitro data support the use of uridine in patients exposed to d4T or ZDV [22], although no changes in fat or blood mtDNA were observed in a pilot trial on the safety and effect of uridine on mitochondrial indices [15]. The

in vitro effects of uridine on tNRTI-affected adipocytes exposed to drugs such as abacavir and tenofovir are unknown. Further, uridine absorption may have been suboptimal even though uridine plasma levels increased 17-fold 1 week after patients commenced treatment with uridine. Previous studies have shown that NucleomaxX increased serum uridine concentrations in humans from about selleck inhibitor 5 to >150 μM [23]. Poor adherence to a three-times-per-day sachet is possible, but mean adherence was over 90%. Lastly, although we used the same dose that was effective in adults receiving a tNRTI, the optimal dose of uridine is not known and it is conceivable that a higher dose might be effective in this population. We also observed no increase in limb fat mass with pravastatin. HMG-CoA reductase

inhibitors (statins) are predominantly used to manage hypercholesterolaemia but have a range of additional effects (e.g. anti-inflammatory FG-4592 concentration effects) beyond cholesterol reduction [24]. Participants in the study by Mallon et al. were similar to ours (mostly men taking a protease inhibitor but no longer a tNRTI) with the notable exceptions that they all had hypercholesterolaemia (>6.5 mmol/L) and were not selected for lipoatrophy [16]. Our study was powered to

detect clinically detectable increases in limb fat mass, and could not reliably determine whether change in limb fat was greater in those with higher total cholesterol levels (ρ=0.17; P=0.51). Lean mass increased in uridine recipients, although creatine kinase plasma levels did not change. We did not assess dietary intake, but the absence of changes in weight, albumin level and cholesterol level suggests that there was no major change in nutritional status with uridine. We did not observe any severe or unexpected safety signal with uridine or pravastatin; in particular, there was no loss of Sorafenib molecular weight virological control. Also, the sugar cane-derived dietary supplement did not appear to have had a deleterious effect on glucose homeostasis. Only four patients interrupted their assigned treatment allocation, and five patients were switched to one uridine sachet daily, mainly because of diarrhoea. Diarrhoea might also explain the slight decrease observed in plasma potassium levels. Eleven per cent of our patients developed grade 3 and 4 hypertriglyceridaemia after study commencement; these changes were asymptomatic and did not require any change in therapy. This increase was mainly associated with the recent initiation of LPV/r; such an increase has been observed in previous studies. In conclusion, neither of the two trial regimens investigated in our study proved to be effective in this patient population.