No abstract

To analyze the presence of chronic cerebrospinal venous insufficiency parameter and vascular abnormalities, in the internal jugular veins (IJVs) and/or vertebral veins in sitting and supine posture, in patients with Meniere's disease compared to healthy general population. A prospective study on 32 patients affected by definite Ménière was performed from February 2012 to January 2013. All subjects underwent an echo-color Doppler examination of the cerebrospinal venous flow. 21 of the 32 Menieric patients showed a statistically significant reflux in the intracranial veins versus healthy (65.6 vs 25%; P < 0.001). A high prevalence of IJVs stenosis with hemodynamic changes (increased velocity or absence of flow) was observed (66.7 vs 33.3%; P < 0.05). The other parameters considered did not show statistically significant differences among the two groups. The results obtained showed a vascular pattern of cerebrospinal venous system present in patients affected by definite Meniere. This vascular impairment significantly affects the vascular areas more directly involved in the venous drainage of the inner ear. Thus venous stasis may be considered a further pathogenetic mechanism for development of Meniere's disease.

Objectives. Impaired endothelial function represents the early stage of atherosclerosis, which is typically associated with systemic inflammatory diseases like rheumatoid arthritis (RA). As modulators of endothelial nitric oxide synthase expression, asymmetric-dimethylarginine (ADMA) and apelin might be measured in the blood of RA patients to detect early atherosclerotic changes. We conducted a prospective, case-control study to investigate serum ADMA and apelin profiles of patients with early-stage RA (ERA) before and after disease-modifying antirheumatic drug (DMARD) therapy. Methods. We enrolled 20 consecutively diagnosed, treatment-naïve patients with ERA and 20 matched healthy controls. Serum ADMA and apelin levels and the 28-joint disease activity scores (DAS28) were assessed before and after 12 months of DMARDs treatment. All patients underwent ultrasonographic assessment for intima-media tickness (IMT) evaluation. Results. In the ERA group, ADMA serum levels were significantly higher than controls at baseline (P = 0.007) and significantly decreased after treatment (P = 0.012 versus controls). Baseline serum apelin levels were significantly decreased in this group (P = 0.0001 versus controls), but they were not significantly altered by treatment. IMT did not show significant changes. Conclusions. ERA is associated with alterations of serum ADMA and apelin levels, which might be used as biomarkers to detect early endothelial dysfunction in these patients.

Endothelial dysfunction has been detected in RA patients and seems to be reversed by control of inflammation. Low circulating endothelial progenitor cells (EPCs) have been described in many conditions associated with increased cardiovascular risk, including RA. The aim of this study was to investigate the effect of inhibition of TNF on EPCs in RA patients. Seventeen patients with moderate-severe RA and 12 sex and age-matched controls were evaluated. Endothelial biomarkers were tested at baseline and after 3 months. EPCs were identified from peripheral blood mononuclear cells by cytofluorimetry using anti-CD34 and anti-vascular endothelial growth factor-receptor 2. Asymmetric dimethylarginine (ADMA) was tested by ELISA and flow-mediated dilatation (FMD) by ultrasonography. Circulating EPCs were significantly lower in RA patients than in controls (P = 0.001). After 3 months EPCs increased significantly (P = 0.0006) while ADMA levels significantly decreased (P = 0.001). An inverse correlation between mean increase in EPCs number and mean decrease of DAS28 after treatment was observed (r = −0.56, P = 0.04). EPCs inversely correlated with ADMA (r = −0.41, P = 0.022). No improvement of FMD was detected. Short-term treatment with anti-TNF was able to increase circulating EPCs concurrently with a proportional decrease of disease activity suggesting that therapeutic intervention aimed at suppressing the inflammatory process might positively affect the endothelial function.