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[107]. They also reported that increased levels of arginase II degrade L-arginine, leading to further eNOS uncoupling. A recent study by Varadharaj et al. reported that eNOS dysfunction in OSA patients was reversible with BH4 treatment [108]. 8. ADMA in OSA A recent meta-analysis of 22 studies with a total of 6168 patients reported a correlation between ADMA levels and carotid intima-media thickness (pooled correlation coefficient of 0.29; P selleck chemicals serum ADMA levels when compared to controls (0.59 �� 0.14?��mol/L versus 0.40 �� 0.09?��mol/L, P Oxygenase of 121 nondiabetic patients with proteinuria, ADMA levels were independently related to FMD (>2.76?��mol/L; r2 = 0.27, P = 0.0002) and were correlated with both proteinuria (>2.5?g/d; r2 = 0.40, P this website levels were measured in these patients before and after CPAP and there was no significant difference (0.58 �� 0.10 versus 0.61 �� 0.12, P = 0.32) despite the reduction in serum levels of other inflammatory factors such as CRP (0.83 �� 0.95 versus 0.53 �� 0.56, P = 0.02) [76, 113]. Barcelo et al. investigated the influence of OSA on the diurnal variations in some markers of endothelial dysfunction such as ADMA and soluble CD40 ligand and found that ADMA levels were significantly related to arousal index (P = 0.046). They also suggested that ADMA levels might be dependant either on obesity index or metabolic dysfunction rather than on OSA alone [114]. In nonobese children with OSA, Gozal et al. reported no differences in ADMA levels compared to matched controls [0.79 �� 0.