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Secondary Immunodeficiency and Risk of Infection Following Immune Therapies in Neurology
F. Szepanowski, C. Warnke, G. Meyer Zu Hörste, AK. Mausberg, HP. Hartung, C. Kleinschnitz, M. Stettner
Jazyk angličtina Země Nový Zéland
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
NLK
ProQuest Central
od 2008-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2008-01-01 do Před 1 rokem
Psychology Database (ProQuest)
od 2008-01-01 do Před 1 rokem
- MeSH
- alemtuzumab aplikace a dávkování škodlivé účinky MeSH
- dimethyl fumarát aplikace a dávkování škodlivé účinky MeSH
- fingolimod hydrochlorid aplikace a dávkování škodlivé účinky MeSH
- imunoglobulin G krev imunologie MeSH
- imunologické faktory aplikace a dávkování škodlivé účinky MeSH
- imunosupresiva aplikace a dávkování škodlivé účinky MeSH
- imunoterapie škodlivé účinky MeSH
- infekce krev chemicky indukované imunologie MeSH
- koinfekce MeSH
- lidé MeSH
- natalizumab aplikace a dávkování škodlivé účinky MeSH
- neurologie metody trendy MeSH
- rituximab aplikace a dávkování škodlivé účinky MeSH
- rizikové faktory MeSH
- věkové faktory MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
Secondary immunodeficiencies (SIDs) are acquired conditions that may occur as sequelae of immune therapy. In recent years a number of disease-modifying therapies (DMTs) has been approved for multiple sclerosis and related disorders such as neuromyelitis optica spectrum disorders, some of which are frequently also used in- or off-label to treat conditions such as chronic inflammatory demyelinating polyneuropathy (CIDP), myasthenia gravis, myositis, and encephalitis. In this review, we focus on currently available immune therapeutics in neurology to explore their specific modes of action that might contribute to SID, with particular emphasis on their potential to induce secondary antibody deficiency. Considering evidence from clinical trials as well as long-term observational studies related to the patients' immune status and risks of severe infections, we delineate long-term anti-CD20 therapy, with the greatest data availability for rituximab, as a major risk factor for the development of SID, particularly through secondary antibody deficiency. Alemtuzumab and cladribine have relevant effects on circulating B-cell counts; however, evidence for SID mediated by antibody deficiency appears limited and urgently warrants further systematic evaluation. To date, there has been no evidence suggesting that treatment with fingolimod, dimethyl fumarate, or natalizumab leads to antibody deficiency. Risk factors predisposing to development of SID include duration of therapy, increasing age, and pre-existing low immunoglobulin (Ig) levels. Prevention strategies of SID comprise awareness of risk factors, individualized treatment protocols, and vaccination concepts. Immune supplementation employing Ig replacement therapy might reduce morbidity and mortality associated with SIDs in neurological conditions. In light of the broad range of existing and emerging therapies, the potential for SID warrants urgent consideration among neurologists and other healthcare professionals.
Brain and Mind Centre University of Sydney Sydney NSW Australia
Department of Neurology Medical Faculty University of Duesseldorf Duesseldorf Germany
Department of Neurology Palacky University Olomouc Czech Republic
Department of Neurology University of Cologne Cologne Germany
Department of Neurology University of Muenster Muenster Germany
Citace poskytuje Crossref.org
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