■虽然芬戈莫德,鞘氨醇1-磷酸受体激动剂,已被证明是一种有效的治疗方法,可降低复发缓解型多发性硬化症(RRMS)患者的复发率并减缓残疾进展,快速识别那些次优反应者是很重要的。
■主要目的是评估不同的临床,放射学,遗传和环境因素可能是使用芬戈莫德治疗24个月的MS患者的早期反应预测因子。次要目标是分析在2年的随访过程中,分析的环境因素对疾病进展和活动的可能贡献。
■一项对151名确诊为MS患者的回顾性研究,在芬戈莫德治疗24个月,开始时和六个月后的血清样本,开始时和24个月后的临床和放射学数据,包括在研究中。收集临床和放射学变量以建立NEDA-3(没有疾病活动的证据:没有复发的患者,残疾进展和新的T2病变或Gd病变)和EDA(疾病活动的证据:复发和/或进展和/或新的T2病变或钆阳性[Gd]病变的患者)状况。人类白细胞抗原II(HLA-II),还分析了来自EB病毒(EBV)的EBNA-1IgG和VCAIgG以及抗人疱疹病毒6A/B(HHV-6A/B)的抗体滴度。
■共有151名MS患者符合纳入标准:27.8%为NEDA-3(在之前接受高疗效治疗>24个月的患者中,有37.5%)。以下早期预测因素与NEDA-3状况有统计学意义:性别(男性;p=0.002),基线年龄(年龄较大;p=0.009),芬戈莫德开始前2年复发≤1(p=0.010),基线无Gd+病变(p=0.006)。关于研究中包括的环境因素对疾病的活动或进展的可能贡献,我们仅发现EBNA-1IgG滴度在20.0%的PIRA(独立于复发活动的进展)患者中降低与73.3%的RAW(复发相关恶化)患者(p=0.006;O.R.=11.0)。
■男性MS患者,年长的,并且在fingolimod开始时具有较低的临床和放射学活性,在使用该疗法两年后达到NEDA-3状态的可能性更大。还描述了EBV与疾病进展的有趣关联,但应该在更大的队列中进一步研究以证实这些结果。
UNASSIGNED: Although fingolimod, a sphingosine 1-phosphate receptor agonist, has shown to be an effective treatment reducing relapse rate and also slowing down the disability progression in relapsing-remitting multiple sclerosis (RRMS) patients, it is important to quickly identify those suboptimal responders.
UNASSIGNED: The main objective was to assess different clinical, radiological, genetic and environmental factors as possible early predictors of response in MS patients treated with fingolimod for 24 months. The secondary objective was to analyze the possible contribution of the environmental factors analyzed to the progression and activity of the disease along the 2-years of follow-up.
UNASSIGNED: A retrospective study with 151 patients diagnosed with MS, under fingolimod treatment for 24 months, with serum samples at initiation and six months later, and with clinical and radiological data at initiation and 24 months later, were included in the study. Clinical and radiological variables were collected to establish NEDA-3 (no evidence of disease activity: patients without relapses, disability progression and new T2 lesions or Gd+ lesions) and EDA (evidence of disease activity: patients with relapses and/or progression and/or new T2 lesions or gadolinium-positive [Gd+] lesions) conditions. Human leukocyte antigen II (HLA-II), EBNA-1 IgG and VCA IgG from Epstein-Barr virus (EBV) and antibody titers against Human herpesvirus 6A/B (HHV-6A/B) were also analyzed.
UNASSIGNED: A total of 151 MS patients fulfilled the inclusion criteria: 27.8% was NEDA-3 (37.5% among those previously treated with high efficacy therapies >24 months). The following early predictors were statistically significantly associated with NEDA-3 condition: sex (male; p=0.002), age at baseline (older; p=0.009), relapses 2-years before fingolimod initiation ≤1 (p=0.010), and absence of Gd+ lesions at baseline (p=0.006). Regarding the possible contribution of the environmental factors included in the study to the activity or the progression of the disease, we only found that EBNA-1 IgG titers decreased in 20.0% of PIRA (progression independent from relapse activity) patients vs. 73.3% of RAW (relapse-associated worsening) patients (p=0.006; O.R. = 11.0).
UNASSIGNED: MS patients that are male, older, and with a low clinical and radiological activity at fingolimod initiation have a greater probability to reach NEDA-3 condition after two years with this therapy. An intriguing association of EBV with the progression of the disease has also been described, but it should be further study in a larger cohort to confirm these results.