RESUMO
BACKGROUND: Growing bodies of evidence suggest that angiogenesis plays a crucial role in the development and progression of multiple sclerosis (MS). Vascular endothelial growth factor (VEGF) is one of the key factors involved in angiogenesis. Because of this importance, we investigated the serum levels of VEGF in MS patients according to their clinical phase and subtype of MS in this study. MATERIAL AND METHODS: This case-control study was done on 47 definite MS patients with the first clinical attack and 47 randomly selected individuals without any underlying inflammatory and autoimmune disease as the control group. The total serum VEGF level was measured from the subject's peripheral blood sample by ELISA during the first and second attacks of MS and 6 months after the first attack in the remission phase as well as the control group. In addition, the correlation between these variables and the influence of gender, age, and duration of the remission phase on such associations was evaluated by using the independent t test and Pearson's correlation coefficient. RESULTS: There was an increase in the serum level of VEGF in all phases of MS compared with non-MS individuals (p value <0.0001) and a significant correlation between the serum level of VEGF and the interval between first and second attacks (r = -720, p < 0.0001). A higher serum level of VEGF in the first attack leads to higher VEGF levels in the second and sixth mount of remission phases. CONCLUSION: Rise in the serum VEGF level may be involved in MS's relapsing phases and a shorter remission phase. Therefore, it could be used as a prognostic and predictive biomarker for MS disease.
Assuntos
Esclerose Múltipla , Humanos , Esclerose Múltipla/diagnóstico , Fator A de Crescimento do Endotélio Vascular , Estudos de Casos e Controles , Prognóstico , BiomarcadoresRESUMO
BACKGROUND AND AIM: Vascular dementia (VaD) is the second most common cause of dementia and currently there is scarcity of therapies for VaD. We aimed to investigate the efficacy and safety of MLC601 in the treatment of VaD. METHODS: In this multicenter, pilot, randomized, double-blind trial, 82 patients with VaD according to DSM-5 criteria received MLC601 or placebo capsules three times a day for 2 years. The primary efficacy end-point was evaluated by comparing Mini-Mental State Examination (MMSE) and Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-cog) score between the two groups over 2 years of study. Safety was also assessed by recording adverse events and abnormal laboratory results. RESULTS: Eighty-one patients completed the study and were included in the analysis. One patient was lost to follow-up in the placebo group. After 2 years, mean (±SD) changes in the MMSE score were -3.71 (±4.50) for MLC601 group and -9.33 (±4.80) for placebo group. ADAS-cog score showed (±SD) changes of 7.34 (±9.55) and 19.00 (±11.28) for MLC601 and placebo group, respectively. Repeated measures analyses showed that both MMSE and ADAS-cog scores were significantly better in the treatment group at 24 months (p<0.001). Ten (24.39%) patients reported predominantly transient gastrointestinal adverse events in MLC601 group. No patient left the study due to adverse events. There were no clinically significant abnormalities on laboratory tests. CONCLUSION: Patients treated with MLC601 over the 2 years showed dramatically better cognitive outcome compared with those treated with placebo. MLC601 was devoid of any serious adverse events and was well-tolerated.
RESUMO
In patients on maintenance hemodialysis several factors reduce the body stored carnitine which could lead to dyslipidemia, anemia, and general health in these patients. We evaluated the effect of oral L-carnitine supplementation on lipid profiles, anemia, and quality of life (QOL) in hemodialysis patients. In a randomized, double-blinded, placebo-controlled trial, end-stage renal disease (ESRD) patients on hemodialysis received either L-carnitine 1 g/d (n = 24) or placebo (27 patients) for 16 weeks. At the end of the study, there was a significant decrease in triglyceride (-31.1 ± 38.7 mg/dL, P = 0.001) and a significant increase in HDL (3.7 ± 2.8 mg/dL, P < 0.001) levels in the carnitine group. Decrease in total cholesterol (-6.6 ± 16.0 mg/dL, P = 0.075) and increase in hemoglobin (0.7 ± 1.7 g/dL, P = 0.081) concentrations in the carnitine group were not significant. There was no statistically significant changes in LDL in any group (P > 0.05). Erythropoietin dose was significantly decreased in both the carnitine (-4750 ± 5772 mg, P = 0.001) and the placebo group (-2000 ± 4296 mg, P < 0.05). No improvement was observed in QOL scores of two groups. In ESRD patients under maintenance hemodialysis, oral L-carnitine supplementation may reduce triglyceride and cholesterol and increase HDL and hemoglobin and subsequently reduce needed erythropoietin dose without effect on QOL.