Catálogo de publicaciones - revistas
Multiple Sclerosis Journal
Resumen/Descripción – provisto por la editorial
No disponible.
Palabras clave – provistas por la editorial
No disponibles.
Disponibilidad
Institución detectada | Período | Navegá | Descargá | Solicitá |
---|---|---|---|---|
No detectada | desde feb. 1999 / hasta dic. 2023 | SAGE Journals |
Información
Tipo de recurso:
revistas
ISSN impreso
1352-4585
ISSN electrónico
1477-0970
Editor responsable
SAGE Publishing (SAGE)
País de edición
Estados Unidos
Fecha de publicación
1995-
Cobertura temática
Tabla de contenidos
Safety of anti-varicella zoster virus vaccination in patients with multiple sclerosis treated with natalizumab: A case series
Caterina Lapucci; Vincenzo Daniele Boccia; Tommaso Sirito; Maria Cellerino; Malgorzata Mikulska; Laura Sticchi; Matilde Inglese
<jats:p> The vaccination with live attenuated vaccines is generally not recommended during natalizumab (NTZ), as it is included among immunosuppressive/immunomodulating therapies. Nevertheless, considering the lack of evidence of a non-Central Nervous System (CNS) immunosuppressive effect of NTZ, after a risk/benefit evaluation, we decided to vaccinate four multiple sclerosis (MS) patients (three with an indication to switch to ocrelizumab for high-risk Progressive Multifocal Leukoencephalopathy (PML) and one for pregnancy planning). No vaccine-related adverse events of any type nor varicella zoster virus (VZV) infections were observed. To the best of our knowledge, these case series represent the first description of the good safety profile of anti-VZV vaccination in MS patients during NTZ treatment. </jats:p>
Palabras clave: Neurology (clinical); Neurology.
Pp. No disponible
Microfibrillar-associated protein 4 as a potential marker of acute relapse in inflammatory demyelinating diseases of the central nervous system: Pathological and clinical aspects
Sara Samadzadeh; Mads Nikolaj Olesen; Martin Wirenfeldt; Sören Möller; Tatsuro Misu; Kerstin Soelberg; Jette Lautrup Frederiksen; Steffen Heegaard; Sara Mariotto; Kazuo Fujihara; Klemens Ruprecht; Thomas Levin Andersen; Romain Marignier; Søren Thue Lillevang; Eoin P Flanagan; Sean J Pittock; Ho Jin Kim; Jeffrey L Bennett; Friedemann Paul; Grith Lykke Sorensen; Brian G Weinshenker; Hans Lassmann; Nasrin Asgari
<jats:sec><jats:title>Background:</jats:title><jats:p> Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein not previously described in the human central nervous system (CNS). </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> We determined MFAP4 CNS expression and measured cerebrospinal fluid (CSF) and serum levels. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> Tissue was sampled at autopsy from patients with acute multiple sclerosis (MS) ( n = 3), progressive MS ( n = 3), neuromyelitis optica spectrum disorder (NMOSD) ( n = 2), and controls ( n = 9), including 6 healthy controls (HC). MFAP4 levels were measured in 152 patients: 49 MS, 62 NMOSD, 22 myelin oligodendrocyte glycoprotein-associated disease (MOGAD), and 19 isolated optic neuritis (ION). </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> MFAP4 localized to meninges and vascular/perivascular spaces, intense in the optic nerve. At sites of active inflammation, MFAP4 reactivity was reduced in NMOSD and acute MS and less in progressive MS. CSF MFAP4 levels were reduced during relapse and at the onset of diseases (mean U/mL: MS 14.3, MOGAD 9.7, and ION 14.6 relative to HC 17.9. ( p = 0.013, p = 0.000, and p = 0.019, respectively). Patients with acute ON ( n = 68) had reduced CSF MFAP4 (mean U/mL: 14.5, p = 0.006). CSF MFAP4 levels correlated negatively with relapse severity (rho = −0.41, p = 0.017). </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> MFAP4 immunoreactivity was reduced at sites of active inflammation. CSF levels of MFAP4 were reduced following relapse and may reflect disease activity. </jats:p></jats:sec>
Palabras clave: Neurology (clinical); Neurology.
Pp. No disponible
Extended interval dosing of ocrelizumab in patients with multiple sclerosis is not associated with meaningful differences in disease activity
Nicole Bou Rjeily; Kathryn C Fitzgerald; Ellen M Mowry
<jats:p> Risk concerns related to ocrelizumab treatment for multiple sclerosis (MS) during the COVID-19 pandemic caused infusion delays with extended interval dosing (EID). We reviewed medical records of patients on ocrelizumab to determine whether EID maintains its effectiveness compared to standard interval dosing (SID). Among 361 patients, 231 (64%) and 123 (34%) had at least one infusion with infusion intervals of ⩾8 months and ⩾12 months, respectively. There were no differences in demographics or clinical profiles between the SID and EID groups. No significant differences between rates of breakthrough activity among relapsing-remitting patients were observed between SID (three patients) and EID (seven patients). </jats:p>
Palabras clave: Neurology (clinical); Neurology.
Pp. No disponible
Longitudinal evaluation of serum MOG-IgG titers in MOGAD after initiation of maintenance immunoglobulin: A case series
Shuvro Roy; Eleni Vasileiou; Paula Barreras; Gelareh Ahmadi; Haiwen Chen; William Suslovic; Alexandra Kornbluh; Ilana Kahn; Elias S Sotirchos
<jats:sec><jats:title>Background:</jats:title><jats:p> Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a distinct demyelinating disease of the central nervous system. Immunoglobulin (Ig) has been used as a maintenance therapy to prevent relapses in MOGAD, but the impact of Ig on serum MOG-IgG titers is unclear. </jats:p></jats:sec><jats:sec><jats:title>Objective:</jats:title><jats:p> To characterize the variation in serum MOG-IgG titers after initiation of Ig treatment in people with MOGAD. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> We conducted a retrospective study of 10 patients with a diagnosis of MOGAD and available serum MOG-IgG titers before and after initiation of maintenance Ig treatment. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> We found that most of the patients remained MOG-IgG seropositive while on Ig treatment with a reduced or unchanged titer, despite a lack of disease activity. </jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p> This case series suggests that the mechanism of action of Ig therapy in MOGAD is not exclusively dependent on MOG-IgG titer reduction. </jats:p></jats:sec>
Palabras clave: Neurology (clinical); Neurology.
Pp. No disponible
Biological aging in multiple sclerosis
Yinan Zhang; Jeffrey Atkinson; Christin E Burd; Jennifer Graves; Benjamin M Segal
<jats:p> Multiple sclerosis (MS) is most likely to adopt a progressive clinical course during middle age or beyond, and the number of older adults with MS is steadily increasing. Developing new strategies to manage progressive forms of MS, which do not respond to currently available disease-modifying therapies (DMTs), will require a deeper understanding of the mechanisms by which biological aging interacts with pathogenic pathways to propel disability accumulation. In experimental autoimmune encephalomyelitis (EAE), a widely used preclinical mouse model of MS, middle-aged animals experience a more severe and protracted clinical course than their younger counterparts. This exacerbated disease course is accompanied by persistent neuroinflammation. Clinical studies of age-related biomarkers, such as telomere length, senescence markers, and DNA methylation, suggest that biological aging is accelerated in people with MS compared with age- and sex-matched healthy controls. Furthermore, distinguishing biological age from chronological may afford more precision in determining aging effects in MS. Here we review the current literature on aging biology and its impact on MS pathogenesis. Future research on this topic may lead to the development of novel biomarkers and senotherapy agents that slow neurological decline in people with progressive MS by targeting relevant aging-related pathways. </jats:p>
Palabras clave: Neurology (clinical); Neurology.
Pp. 1701-1708
Misdiagnosis in multiple sclerosis in a Brazilian reference center: Clinical, radiological, laboratory profile and failures in the diagnostic process—Cohort study
Eduardo Macedo de Souza Tieppo; Guilherme Diogo Silva; Tomás Fraga Ferreira da Silva; Roger Santana de Araujo; Mateus Boaventura de Oliveira; Mariana Gondim Peixoto Spricigo; Gabriela Almeida Pimentel; Igor Gusmão Campana; Bruno Batitucci Castrillo; Natalia Trombini Mendes; Larissa Silva Teixeira; Douglas Mendes Nunes; Carolina de Medeiros Rimkus; Tarso Adoni; Samira Luisa Apóstolos Pereira; Dagoberto Callegaro
<jats:sec><jats:title>Background:</jats:title><jats:p> Multiple sclerosis misdiagnosis remains a problem despite the well-validated McDonald 2017. For proper evaluation of errors in the diagnostic process that lead to misdiagnosis, it is adequate to incorporate patients who are already under regular follow-up at reference centers of demyelinating diseases. </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> To evaluate multiple sclerosis misdiagnosis in patients who are on follow-up at a reference center of demyelinating diseases in Brazil. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> We designed an observational study including patients in regular follow-up, who were diagnosed with multiple sclerosis at our specialized outpatient clinic in the Hospital of Clinics in the University of Sao Paulo, from 1996 to 2021, and were reassessed for misdiagnosis in 2022. We evaluated demographic information, clinical profile, and complementary exams and classified participants as “established multiple sclerosis,” “non-multiple sclerosis, diagnosed,” and “non-multiple sclerosis, undiagnosed.” Failures in the diagnostic process were assessed by the modified Diagnostic Error Evaluation and Research tool. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> A total of 201 patients were included. After analysis, 191/201 (95.02%) participants were confirmed as “established multiple sclerosis,” 5/201 (2.49%) were defined as “non-multiple sclerosis, diagnosed,” and 5/201 (2.49%) were defined as “non-multiple sclerosis, undiagnosed.” </jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p> Multiple sclerosis misdiagnosis persists in reference centers, emphasizing the need for careful interpretation of clinical findings to prevent errors. </jats:p></jats:sec>
Palabras clave: Neurology (clinical); Neurology.
Pp. 1755-1764
Prevalence of neuromyelitis optica spectrum disorder in the United States
Farren BS Briggs; Jacqueline Shaia
<jats:sec><jats:title>Background:</jats:title><jats:p> Neuromyelitis optic spectrum disorder (NMOSD) is a rare demyelinating, autoimmune disease and the burden in United States is not well characterized. </jats:p></jats:sec><jats:sec><jats:title>Objective:</jats:title><jats:p> The objective of this study was to determine the 2022 US prevalence of NMOSD. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> We constructed a cross-sectional study using aggregated electronic health record data for 25.7 million patients who had a 2022 clinical encounter. The data originated from the TriNetX US Collaborative Network of 55 healthcare organizations that span all 50 states. NMOSD prevalence was determined by querying for age-interval, sex, and race combinations, with direct standardization to the 2022 US Census data. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> There were 1772 NMOSD patients among 25,743,039 patients for a prevalence of 6.88/100,000. Prevalence was the highest in Blacks (12.99/100,000) who represented 27.7% of NMOSD patients, then Asians (9.41/100,000and Whites (5.58/100,000). Among females, the prevalence of NMOSD was 9.48/100,000, and Black and Asian females had a 2.65- and 1.94-times higher prevalence than White females. In males, the prevalence of NMOSD was 3.52/100,000 and it did not differ by race. We observed a 3/5:1 female-to-male ratio in NMOSD. The age- and sex-adjusted 2022 estimate of persons with NMOSD in the United States was 15,413 females and 6233 males. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> We estimate that there were near 22,000 Americans living with NMOSD in 2022. </jats:p></jats:sec>
Palabras clave: Neurology (clinical); Neurology.
Pp. No disponible
Effectiveness of cladribine compared to fingolimod, natalizumab, ocrelizumab and alemtuzumab in relapsing-remitting multiple sclerosis
Izanne Roos; Sifat Sharmin; Charles Malpas; Serkan Ozakbas; Jeannette Lechner-Scott; Suzanne Hodgkinson; Raed Alroughani; Sara Eichau Madueño; Cavit Boz; Anneke van der Walt; Helmut Butzkueven; Katherine Buzzard; Olga Skibina; Matteo Foschi; Francois Grand’Maison; Nevin John; Pierre Grammond; Murat Terzi; Julie Prévost; Michael Barnett; Guy Laureys; Liesbeth Van Hijfte; Jose Luis Sanchez-Menoyo; Yolanda Blanco; Jiwon Oh; Pamela McCombe; Cristina Ramo Tello; Aysun Soysal; Alexandre Prat; Pierre Duquette; Bassem I Yamout; Samia Khoury; Vincent van Pesch; Richard Macdonell; Maria José Sá; Mark Slee; Jens Kuhle; Davide Maimone; Daniele LA Spitaleri; Barbara Willekens; Abdallah Al Asmi; Emma Tallantyre; Neil P Robertson; Alasdair Coles; J William L Brown; Tomas Kalincik
<jats:sec><jats:title>Background:</jats:title><jats:p> Comparisons between cladribine and other potent immunotherapies for multiple sclerosis (MS) are lacking. </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> To compare the effectiveness of cladribine against fingolimod, natalizumab, ocrelizumab and alemtuzumab in relapsing-remitting MS. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> Patients with relapsing-remitting MS treated with cladribine, fingolimod, natalizumab, ocrelizumab or alemtuzumab were identified in the global MSBase cohort and two additional UK centres. Patients were followed for ⩾6/12 and had ⩾3 in-person disability assessments. Patients were matched using propensity score. Four pairwise analyses compared annualised relapse rates (ARRs) and disability outcomes. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> The eligible cohorts consisted of 853 (fingolimod), 464 (natalizumab), 1131 (ocrelizumab), 123 (alemtuzumab) or 493 (cladribine) patients. Cladribine was associated with a lower ARR than fingolimod (0.07 vs. 0.12, p = 0.006) and a higher ARR than natalizumab (0.10 vs. 0.06, p = 0.03), ocrelizumab (0.09 vs. 0.05, p = 0.008) and alemtuzumab (0.17 vs. 0.04, p < 0.001). Compared to cladribine, the risk of disability worsening did not differ in patients treated with fingolimod (hazard ratio (HR) 1.08, 95% confidence interval (CI) 0.47–2.47) or alemtuzumab (HR 0.73, 95% CI 0.26–2.07), but was lower for patients treated with natalizumab (HR 0.35, 95% CI 0.13–0.94) and ocrelizumab (HR 0.45, 95% CI 0.26–0.78). There was no evidence for a difference in disability improvement. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> Cladribine is an effective therapy that can be viewed as a step up in effectiveness from fingolimod, but is less effective than the most potent intravenous MS therapies. </jats:p></jats:sec>
Pp. No disponible
Significantly increasing multiple sclerosis prevalence in Australia from 2010 to 2021
Julie A Campbell; Steve Simpson-Yap; Bruce V Taylor; Ingrid van der Mei; Laura Laslett; Glen Henson; Ting Zhao; Andrew J Palmer
<jats:sec><jats:title>Background:</jats:title><jats:p> Multiple sclerosis (MS) prevalence is increasing globally. </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> To determine whether increased prevalence is continuing within Australia using our validated prescription-based ascertainment method. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> We used methods employed in our 2010 and 2017 prevalence estimates. Disease-modifying therapy (DMT) prescriptions were extracted from Australia’s Pharmaceutical Benefits Scheme data for January–December 2021. DMT penetrance was calculated using data from the Australian MS Longitudinal Study. We divided the total number of monthly prescriptions by 12 or 2 (except alemtuzumab), adjusted for DMT penetrance and Australian population estimates. Prevalences in Australian states/territories were age-standardised. 2021 prevalence estimates were compared with 2010 and 2017 prevalence estimates using Poisson regression. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> Number of people with MS in Australia in 2021 was 33,335; an increase of 7728 from 2017 (30.2%) and 12,092 from 2010 (56.6%) and increasing at a faster rate than population change (+10.1%, +14.1%). Age-standardised prevalence was 136.1/100,000 (increased from 103.7/100,000 in 2017). The previously demonstrated positive latitudinal gradient in 2010 and 2017 persisted in 2021, with Tasmania (southernmost state) having the highest prevalence (age-standardised: 203.5/100,000) while northernmost states had the lowest. </jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p> In line with global trends, MS prevalence is escalating in Australia, particularly in higher-latitude states. MS prevention is crucial to halt this disturbing trend. </jats:p></jats:sec>
Pp. No disponible
Maternal and fetal outcomes in an Italian multicentric cohort of women with multiple sclerosis exposed to dimethyl fumarate during pregnancy
Doriana Landi; Silvia Bartolomeo; Francesca Bovis; Maria Pia Amato; Simona Bonavita; Giovanna Borriello; Maria Buccafusca; Sebastiano Bucello; Paola Cavalla; Maria Cellerino; Diego Centonze; Eleonora Cocco; Antonella Conte; Antonio Cortese; Emanuele D’Amico; Massimiliano Di Filippo; Renato Docimo; Roberta Fantozzi; Elisabetta Ferraro; Massimo Filippi; Matteo Foschi; Antonio Gallo; Franco Granella; Antonio Ianniello; Roberta Lanzillo; Lorena Lorefice; Matteo Lucchini; Giacomo Lus; Giorgia Mataluni; Massimiliano Mirabella; Lucia Moiola; Francesca Napoli; Carolina Gabri Nicoletti; Francesco Patti; Paolo Ragonese; Sabrina Realmuto; Giuseppe Schirò; Elisabetta Signoriello; Leonardo Sinisi; Maria Laura Stromillo; Valentina Tomassini; Domizia Vecchio; Maria Pia Sormani; Girolama Alessandra Marfia
<jats:sec><jats:title>Background:</jats:title><jats:p> Evidence on the impact of dimethyl fumarate (DMF) during pregnancy in women with multiple sclerosis (MS) is limited. </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> To investigate disease activity and pregnancy outcomes in a retrospective cohort of women exposed to DMF in early pregnancy. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> Women discontinuing DMF after pregnancy confirmation were identified from 29 Italian MS Centers. Disease activity 12 months before conception, during pregnancy, and 12 months postpartum were recorded, exploring reactivation predictors. Pregnancy and fetal outcomes were assessed. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> The study analyzed 137 pregnancies (12 pregnancy losses, 125 live births) from 137 women (mean age 32.9 ± 4.7 years), discontinuing DMF within a median (interquartile range (IQR)) interval of 4.9 (3.7–5.7) weeks from conception. In live birth pregnancies, annualized relapse rate (ARR) significantly decreased during pregnancy (ARR = 0.07, 95% confidence interval (CI): 0.03–0.14, p = 0.021) compared to pre-conception (ARR = 0.21 (95% CI: 0.14–0.30)) and increased postpartum ((ARR = 0.22 (95% CI: 0.15–0.32), p = 0.006). Median time to first relapse (TTFR) was 3.16 (IQR: 1:87–5.42) months. Higher pre-conception relapse number (hazard ratio (HR) = 2.33, 95% CI: 1.08–5.02) and Expanded Disability Status Scale (EDSS; HR = 1.81, 95% CI: 1.17-2.74) were associated with shorter TTFR, while treatment resumption with longer TTFR (HR = 0.29, 95% CI: 0.11–0.74). Fetal outcomes were unaffected by DMF exposure. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> DMF discontinuation does not increase relapse risk during pregnancy. Early therapy restart prevents postpartum relapses. Early DMF exposure shows no adverse fetal outcomes. </jats:p></jats:sec>
Pp. No disponible