Background: Many factors are believed to be positively associated with the incidence of relapses in people with multiple sclerosis (MS), including infections. However, their role is still controversial. We aimed to investigate whether symptomatic infections in people with MS increase the risk of relapse in the short, medium, or long term.
Materials And Methods: We enrolled consecutive patients with relapsing MS (RMS) from October to December 2018. From enrolment up to September 2020, an online questionnaire investigating the occurrence of infections was sent via WhatsApp monthly to the enrolled patients, while in-person visits were performed every six months. When patients complained of symptoms compatible with relapses, they attended an extra in-person visit.
Results: We enrolled 155 patients with RMS, and 88.38% of patients were treated with disease-modifying therapies. In the dataset, 126,381 total patient days, 78 relapses, and 1202 infections were recorded over a period of about 2 years. No increased risk of relapse after clinically manifest infections was found in the short-, medium-, or long-term period. No correlation was found between all infections and the number of relapses ( = 0.212). The main analyses were repeated considering only those infections that had at least two of the following characteristics: duration of infection ≥ 4 days, body temperature > 37° Celsius, and the use of drugs (antibiotics and/or antivirals), and no significant associations were observed.
Conclusions: No associations between infections and relapses were observed, likely suggesting that disease-modifying therapies may protect against the risk of relapse potentially triggered by infections.
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http://dx.doi.org/10.3390/jcm12031023 | DOI Listing |
BioDrugs
January 2025
Department of Neurology, Neuroscience Clinical Research Center (NCRC) and Integrated Myasthenia Gravis Center, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Charitéplatz 1, Germany.
Myasthenia gravis (MG) is a rare autoimmune disease characterised by exertion-induced muscle weakness that can lead to potentially life-threatening myasthenic crises. Detectable antibodies are directed against specific postsynaptic structures of the neuromuscular junction. MG is a chronic condition that can be improved through therapies, but to date, not cured.
View Article and Find Full Text PDFReumatismo
January 2025
Unit of Dermatology, Department of Medicine and Aging Science, G. d'Annunzio University, Chieti.
Objective: Psoriatic arthritis (PsA) can be treated with biological drugs targeting IL-17A, such as secukinumab, with good responses and long-term positive outcomes in clinical studies.
Methods: An observational study was conducted on adult subjects with PsA and comorbidities, treated with secukinumab after prior therapy with conventional disease-modifying anti-rheumatic drugs or biological agents that were discontinued due to lack of efficacy or adverse drug reactions. Patients were followed up with clinical visits at 3, 6, 9, and 12 months and evaluated for disease activity, pain, and quality of life, with respect to values recorded at baseline.
Mov Disord
January 2025
Department of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Background: Christianson syndrome (CS) is an x-linked recessive neurodevelopmental and neurodegenerative condition characterized by severe intellectual disability, cerebellar degeneration, ataxia, and epilepsy. Mutations to the gene encoding NHE6 are responsible for CS, and we recently demonstrated that a mutation to the rat gene causes a similar phenotype in the spontaneous rat model, which exhibits cerebellar degeneration with motor dysfunction. In previous work, we used the PhP.
View Article and Find Full Text PDFGlycation-induced oxidative stress underlies the numerous metabolic ravages of Alzheimer's disease (AD). Reduced glutathione levels in AD lead to increased oxidative stress, including glycation-induced pathology. Previously, we showed that the accumulation of reactive 1,2-dicarbonyls such as methylglyoxal, the major precursor of non-enzymatic glycation products, was reduced by the increased function of GSH-dependent glyoxalase-1 enzyme in the brain.
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