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<jats:sec> <jats:title>Background:</jats:title> <jats:p>Ecological comparisons suggest that neuromyelitis optic spectrum disorder (NMOSD) is more common in African Caribbean and Asian compared to White people.</jats:p> </jats:sec> <jats:sec> <jats:title>Objective:</jats:title> <jats:p>The aim is to rigorously assess susceptibility across multiple racial and ethnic groups from the same cohort.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods:</jats:title> <jats:p>We conducted a retrospective cohort study of &gt; 39 million person-years of observation from members of Kaiser Permanente Southern California. The electronic health records of individuals with at least one International Classification of Diseases (ICD) code for NMOSD were reviewed to identify persons who met 2015 diagnostic criteria for NMOSD.</jats:p> </jats:sec> <jats:sec> <jats:title>Results:</jats:title> <jats:p>We identified 153 NMOSD cases, 105 incident and 105 prevalent. The age- and sex-standardized incidence (2013–2022) and prevalence (2019) according to the 2020 US Census per 100,000 person-years was significantly higher in Black persons (incidence = 0.90, 95% confidence interval (CI) = 0.59–1.21; prevalence = 8.44, 95% CI = 5.52–11.36) compared to all other racial and ethnic groups. The incidence was similar among Asian/Pacific Islander (0.32, 95% CI = 0.16–0.48) compared to Hispanic people (0.19, 95% CI = 0.13–0.25) and lowest in White people (incidence = 0.13, 95% CI = 0.07–0.19).</jats:p> </jats:sec> <jats:sec> <jats:title>Discussion:</jats:title> <jats:p>NMOSD susceptibility is highest in Black people, followed by Asian/Pacific Islands, then Hispanic people, and lowest in White people. Studies in diverse groups of minoritized people are needed to determine whether this increased susceptibility is due to shared genetic ancestry, the ill-health consequences of racism, or both.</jats:p> </jats:sec>

<jats:sec> <jats:title>Background:</jats:title> <jats:p>It is essential to exclude alternative diagnoses to diagnose multiple sclerosis (MS). However, detailed descriptions of alternative diagnoses in patients with suspected MS presenting with clinically isolated syndrome (CIS) are limited.</jats:p> </jats:sec> <jats:sec> <jats:title>Objectives:</jats:title> <jats:p>To describe alternative diagnoses in patients presenting with CIS suggestive of MS.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods:</jats:title> <jats:p>We conducted a descriptive analysis of patients from the Barcelona CIS cohort including subjects under 50 years of age with a CIS suggestive of MS but later diagnosed with conditions other than MS. We collected clinical, biological, and radiological data, and described the alternative etiologies identified.</jats:p> </jats:sec> <jats:sec> <jats:title>Results:</jats:title> <jats:p>Among 1468 patients in the Barcelona CIS cohort, 100 (6.8%) were diagnosed with an alternative condition. The most common neurological syndrome was optic neuritis (43.0%). Four patients (4.0%) had inflammatory-demyelinating lesions in at least two typical MS topographies on baseline magnetic resonance imaging (MRI), and 2 (2.0%) met the 2017 McDonald MS criteria. The most common etiologies were immune-mediated diseases (42.0%), especially MOGAD, followed by functional neurological disorders (15.0%) and vascular disease (10.0%).</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion:</jats:title> <jats:p>The range of alternative diagnoses encountered during the MS diagnostic process highlights the need to rule out better explanations than MS. However, current MS diagnostic criteria effectively identify patients without MS in this context.</jats:p> </jats:sec>

<jats:sec> <jats:title>Background:</jats:title> <jats:p>Research on the optimal duration of immunosuppressive therapy (IST) and the outcome upon its discontinuation in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) remains limited.</jats:p> </jats:sec> <jats:sec> <jats:title>Objective:</jats:title> <jats:p>To evaluate the outcomes following IST discontinuation in MOGAD.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods:</jats:title> <jats:p>This multicenter retrospective study collected data from 333 MOGAD patients in Korea. Among 273 patients who received IST, 41 who discontinued IST were analyzed.</jats:p> </jats:sec> <jats:sec> <jats:title>Results:</jats:title> <jats:p> The median age at disease onset was 38.3 years (interquartile range (IQR), 27.6–53.1). Before IST withdrawal, 21 (51%) patients exhibited relapsing courses. Over a median follow-up of 23.5 months (IQR, 12.1–39.5) after discontinuation, 10 patients (24.4%) relapsed after a median of 8.2 months (IQR, 6.3–11.5). All relapses occurred in patients with a prior relapsing course (10/21, 47.6%); none with prior monophasic courses relapsed. Among 21 prior relapsing patients, relapse after discontinuation group had a shorter IST duration than non-relapse group (median, 9.4 vs 50.9 months, <jats:italic>p</jats:italic> = 0.036). None of the 41 patients had severe disability (Expanded Disability Status Scale (EDSS) score ⩾ 4.0 or Visual Functional System score ⩾ 5) at the last visit. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion:</jats:title> <jats:p>IST discontinuation did not necessarily lead to relapse and could be considered with an individualized approach based on factors such as disease course and IST duration.</jats:p> </jats:sec>

<jats:sec> <jats:title>Background:</jats:title> <jats:p>Measuring brain volume changes over time is an objective and dependable surrogate marker for the pathological processes that damage the brain in relapsing-remitting multiple sclerosis (RRMS). These measures are particularly valuable for monitoring the long-term impact of immunomodulatory treatments such as cladribine.</jats:p> </jats:sec> <jats:sec> <jats:title>Objectives:</jats:title> <jats:p>To evaluate the long-term impact of oral cladribine treatment on brain volume loss in patients with RRMS.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods:</jats:title> <jats:p>This real-world study processed magnetic resonance imaging (MRI) scans using FreeSurfer’s recon-all-clinical pipeline leveraging SynthSeg for brain segmentation. Piecewise linear regression was used to analyze brain atrophy changes over 4.5 years before and after cladribine treatment and estimate the time breakpoint of atrophy rate change.</jats:p> </jats:sec> <jats:sec> <jats:title>Results:</jats:title> <jats:p>A total of 448 MRI exams from 102 RRMS patients were analyzed. Before the initiation of cladribine treatment, brain atrophy rates were significantly steep with an α1 slope between −1.27 and −0.62 for the Thalamus, DGM, Subcortical GM, Cerebral WM, and BP. Over 2 years after treatment, breakpoints marked a shift in atrophy rates, with post-breakpoint slopes (α2) becoming non-significant, reflecting stabilization of brain atrophy.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions:</jats:title> <jats:p>Cladribine treatment in highly active RRMS patients protects the brain from atrophy, with stabilization occurring over 2 years after initiation. The extended observation period highlights its sustained benefits compared with shorter clinical trials.</jats:p> </jats:sec>