Objectives: The aim of the present study was to determine the efficacy of oral magnesium (Mg) supplementation on endothelial function through evaluation of carotid intima-media thickness (cIMT), brachial artery flow-mediated dilatation (FMD), and C-reactive protein (CRP) among hemodialysis (HD) patients. Methods: This randomized, controlled, double-blind clinical trial consisted of 54 patients on HD. One group was treated orally with 440 mg of Mg oxide 3 times per week for 6 months (n = 29). The control group (n = 25) was given placebo using the same administration protocol. cIMT, FMD, serum calcium levels, phosphorus, lipid, CRP, and bicarbonate were measured at baseline and at 6 months in both groups. Results: At 6 months, cIMT was significantly decreased in the Mg group (0.84 ± 0.13 mm at baseline and 0.76 ± 0.13 mm at 6 months, p = 0.001). However, in the placebo group, cIMT was significantly increased (0.73 ± 0.13 and 0.79 ± 0.12 mm, respectively, p = 0.003). When hypertension, diabetes mellitus, smoking, hyperlipidemia, and systemic lupus erythematosus were controlled for in the analysis, the effect of Mg remained significant in both groups (p = 0.000). Conclusion: Our results indicate that Mg might not improve endothelial function (CRP level and FMD) and that a decreased cIMT as a marker of atherosclerosis may be due to the inhibition of calcification through the regulation parathormone, calcium, and phosphorus.

Early treatment of MS with IFN-beta1b may stabilize clinical disease by attenuating levels of inflammatory cytokines and MMPs. Serial measurement of inflammatory mediators may serve as sensitive markers to gauge therapeutic responses to IFN-beta1b during the first year of treatment.

For patients with positive MRI at the time of their initial neurologic event, both gadolinium-enhancing lesions and the Barkhof criteria are predictors for development of CDMS over a short interval. However, these results, based on a combined CDMS/MRI outcome, suggest that the majority of these patients are already in the earliest stages of MS, regardless of whether any further MRI criteria are met.

Background Although multiple sclerosis (MS) is thought to represent an excessive and inappropriate immune response to several central nervous system (CNS) autoantigens, increasing evidence also suggests that MS may also be a neurovascular inflammatory disease, characterized by endothelial activation and shedding of cell membrane microdomains known as ‘microparticles’ into the circulation. Objective To investigate the relationships between these endothelial biomarkers and MS. Methods We examined the relative abundance of CD31+/PECAM-1, CD51+CD61+ (αV–β3) and CD54+ (ICAM-1) bearing microparticles in sera of healthy individuals, patients with relapsing–remitting MS, and secondary-progressive MS. We also investigated the correlation among circulating levels of different microparticle species in MS with conventional MRI (T2- and T1-lesion volumes and brain atrophy), as well as novel MR modalities [assessment of iron content on susceptibility-weighted imaging (SWI)-filtered phase]. Results Differences in circulating microparticle levels were found among MS groups, and several microparticle species (CD31+/CD51+/CD61+/CD54+) were found to correlate with conventional MRI and SWI features of MS. Conclusion These results indicate that circulating microparticles’ profiles in MS may support mechanistic roles for microvascular stress and injury which is an underlying contributor not only to MS initiation and progression, but also to pro-inflammatory responses.