Base de dados : MEDLINE
Pesquisa : C10.114 [Categoria DeCS]
Referências encontradas : 939 [refinar]
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[PMID]:29309416
[Au] Autor:Memon AB; Javed A; Caon C; Srivastawa S; Bao F; Bernitsas E; Chorostecki J; Tselis A; Seraji-Bozorgzad N; Khan O
[Ad] Endereço:Multiple Sclerosis Center, Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan, United States of America.
[Ti] Título:Long-term safety of rituximab induced peripheral B-cell depletion in autoimmune neurological diseases.
[So] Source:PLoS One;13(1):e0190425, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: B-cells play a pivotal role in several autoimmune diseases, including patients with immune-mediated neurological disorders (PIMND), such as neuromyelitis optica (NMO), multiple sclerosis (MS), and myasthenia gravis (MG). Targeting B-cells has been an effective approach in ameliorating both central and peripheral autoimmune diseases. However, there is a paucity of literature on the safety of continuous B-cell depletion over a long period of time. OBJECTIVE: The aim of this study was to examine the long-term safety, incidence of infections, and malignancies in subjects receiving continuous therapy with a B-cell depleting agent rituximab over at least 3 years or longer. METHODS: This was a retrospective study involving PIMND who received continuous cycles of rituximab infusions every 6 to 9 months for up to 7 years. The incidence of infection related adverse events (AE), serious adverse events (SAE), and malignancies were observed. RESULTS: There were a total of 32 AE and 4 SAE with rituximab treatment. The 3 SAE were noted after 9 cycles (48 months) and 1 SAE was observed after 11 cycles (60 months) of rituximab. There were no cases of Progressive multifocal leukoencephalopathy (PML) and malignancies observed throughout the treatment period. Rituximab was well tolerated without any serious infusion reactions. Also, rituximab was found to be beneficial in treating PIMND over a 7-year period. CONCLUSIONS: This study demonstrates that long-term depletion of peripheral B-cells appears safe and efficacious in treating PIMND. Longer and larger prospective studies with rituximab are needed to carefully ascertain risks associated with chronic B-cell depletion, including malignancies. Recognizing that this is a small, retrospective study, such data nonetheless complement the growing literature documenting the safety and tolerability of B-cell depleting agents in neurological diseases.
[Mh] Termos MeSH primário: Doenças Autoimunes do Sistema Nervoso/tratamento farmacológico
Linfócitos B/efeitos dos fármacos
Fatores Imunológicos/uso terapêutico
Rituximab/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Doenças Autoimunes do Sistema Nervoso/imunologia
Feminino
Seres Humanos
Fatores Imunológicos/farmacologia
Depleção Linfocítica
Masculino
Estudos Retrospectivos
Rituximab/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunologic Factors); 4F4X42SYQ6 (Rituximab)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190425


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[PMID]:29173974
[Au] Autor:Pugnet G; Castilla-Llorente C; Puyade M; Terriou L; Badoglio M; Deligny C; Guillaume-Jugnot P; Labeyrie C; Benzidia I; Faivre H; Lansiaux P; Marjanovic Z; Bourhis JH; Faucher C; Furst S; Huynh A; Martin T; Vermersch P; Yakoub-Agha I; Farge D
[Ad] Endereço:CHU de Toulouse, hôpital Purpan, service de médecine interne, 1, place Baylac, 31059 Toulouse, France.
[Ti] Título:[Indications and follow-up for autologous hematopoietic stem cell transplantation in autoimmune and autoinflammatory diseases: Guidelines from the Francophone Society of Bone Marrow Transplantation and Cellular Therapy (SFGM-TC)].
[Ti] Título:Indications et suivi des autogreffes de cellules souches hématopoïétiques dans les maladies auto-immunes et auto-inflammatoires : recommandations de la Société francophone de greffe de moelle et de thérapie cellulaire (SFGM-TC)..
[So] Source:Bull Cancer;104(12S):S169-S180, 2017 Dec.
[Is] ISSN:1769-6917
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:The Francophone Society of Bone Marrow Transplantation and Cellular Therapy (SFGM-TC) organized the 7th allogeneic hematopoietic stem cell transplantation clinical practices harmonization workshop series in September 2017 in Lille, France and updated recommendations for indications and follow-up in autologous hematopoietic stem cell transplantation in autoimmune and autoinflammatory diseases, previously published under the auspices of SFGM-TC.
[Mh] Termos MeSH primário: Doenças Autoimunes/terapia
Doença de Crohn/terapia
Escleroderma Sistêmico/terapia
[Mh] Termos MeSH secundário: Autoenxertos
Doenças Autoimunes do Sistema Nervoso/terapia
Seguimentos
França
Mobilização de Células-Tronco Hematopoéticas/normas
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Transplante de Células-Tronco Hematopoéticas/normas
Seres Humanos
Imunossupressores/efeitos adversos
Lúpus Eritematoso Sistêmico/terapia
Sociedades Médicas
Condicionamento Pré-Transplante/normas
[Pt] Tipo de publicação:CONSENSUS DEVELOPMENT CONFERENCE; JOURNAL ARTICLE; PRACTICE GUIDELINE; REVIEW
[Nm] Nome de substância:
0 (Immunosuppressive Agents)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:28835460
[Au] Autor:Achleitner M; Kleefisch M; Hennig A; Peschke K; Polikarpova A; Oertel R; Gabriel B; Schulze L; Lindeman D; Gerbaulet A; Fiebig U; Lee-Kirsch MA; Roers A; Behrendt R
[Ad] Endereço:Institute for Immunology, Medical Faculty Carl Gustav Carus, Technical University of Dresden, 01307 Dresden, Germany.
[Ti] Título:Lack of Trex1 Causes Systemic Autoimmunity despite the Presence of Antiretroviral Drugs.
[So] Source:J Immunol;199(7):2261-2269, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biallelic mutations of three prime repair exonuclease 1 (TREX1) cause the lupus-like disease Aicardi-Goutières syndrome in which accumulation of a yet unknown endogenous DNA substrate of TREX1 triggers a cyclic GMP-AMP synthase-dependent type I IFN response and systemic autoimmunity. Products of reverse transcription originating from endogenous retroelements have been suggested to be a major substrate for TREX1, and reverse transcriptase inhibitors (RTIs) were proposed as a therapeutic option in autoimmunity ensuing from defects of TREX1. In this study, we treated mice with RTIs. The serum RTI levels reached were sufficient to block retrotransposition of endogenous retroelements. However, the treatment did not reduce the spontaneous type I IFN response and did not ameliorate lethal inflammation. Furthermore, long interspersed nuclear elements 1 retrotransposition was not enhanced in the absence of Trex1. Our data do not support the concept of retroelement-derived cDNA as key triggers of systemic autoimmunity in Trex1-deficient humans and mice and motivate the continuing search for the pathogenic IFN-inducing Trex1 substrate.
[Mh] Termos MeSH primário: Autoimunidade
Exodesoxirribonucleases/metabolismo
Fosfoproteínas/metabolismo
Inibidores da Transcriptase Reversa/sangue
[Mh] Termos MeSH secundário: Animais
Doenças Autoimunes do Sistema Nervoso/imunologia
DNA Complementar
Exodesoxirribonucleases/deficiência
Exodesoxirribonucleases/genética
Células HeLa
Seres Humanos
Inflamação
Interferon Tipo I/biossíntese
Interferon Tipo I/imunologia
Camundongos
Mutação
Malformações do Sistema Nervoso/imunologia
Fosfoproteínas/deficiência
Fosfoproteínas/genética
Retroelementos
Inibidores da Transcriptase Reversa/efeitos adversos
Inibidores da Transcriptase Reversa/uso terapêutico
Transcrição Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Interferon Type I); 0 (Phosphoproteins); 0 (Retroelements); 0 (Reverse Transcriptase Inhibitors); EC 3.1.- (Exodeoxyribonucleases); EC 3.1.16.- (three prime repair exonuclease 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700714


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[PMID]:28684423
[Au] Autor:Chen J; Martindale JL; Cramer C; Gorospe M; Atasoy U; Drew PD; Yu S
[Ad] Endereço:From the Arkansas Biosciences Institute, Department of Biological Sciences, Arkansas State University, Jonesboro, Arkansas 72467, jing.chen@jefferson.edu.
[Ti] Título:The RNA-binding protein HuR contributes to neuroinflammation by promoting C-C chemokine receptor 6 (CCR6) expression on Th17 cells.
[So] Source:J Biol Chem;292(35):14532-14543, 2017 Sep 01.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In both multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), the C-C chemokine receptor 6 (CCR6) is critical for pathogenic T helper 17 (Th17) cell migration to the central nervous system (CNS). Whereas many cytokines and their receptors are potently regulated via post-transcriptional mechanisms in response to various stimuli, how CCR6 expression is post-transcriptionally regulated in Th17 cells is unknown. Here, using RNA-binding protein HuR conditional knock-out (KO) and wild-type (WT) mice, we present evidence that HuR post-transcriptionally regulates CCR6 expression by binding to and stabilizing mRNA and by promoting CCR6 translation. We also found that HuR down-regulates several microRNA expressions, which could target the 3'-UTR of Ccr6 mRNA for decay. Accordingly, knock-out of HuR reduced CCR6 expression on Th17 cells and impaired their migration to CNS compared with the response of WT Th17 cells and thereby ameliorated EAE. Together, these findings highlight how HuR contributes to Th17 cell-mediated autoimmune neuroinflammation and support the notion that targeting HuR might be a potential therapeutic intervention for managing autoimmune disorders of the CNS.
[Mh] Termos MeSH primário: Proteína Semelhante a ELAV 1/metabolismo
Regulação da Expressão Gênica
RNA Mensageiro/metabolismo
Receptores CCR6/agonistas
Linfócitos T Auxiliares-Indutores/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Doenças Autoimunes do Sistema Nervoso/imunologia
Doenças Autoimunes do Sistema Nervoso/metabolismo
Doenças Autoimunes do Sistema Nervoso/patologia
Linhagem Celular
Movimento Celular
Células Cultivadas
Sistema Nervoso Central/imunologia
Sistema Nervoso Central/metabolismo
Sistema Nervoso Central/patologia
Proteína Semelhante a ELAV 1/antagonistas & inibidores
Proteína Semelhante a ELAV 1/genética
Encefalomielite/imunologia
Encefalomielite/metabolismo
Encefalomielite/patologia
Seres Humanos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
MicroRNAs/metabolismo
Biossíntese de Proteínas
Interferência de RNA
Estabilidade de RNA
Receptores CCR6/antagonistas & inibidores
Receptores CCR6/genética
Receptores CCR6/metabolismo
Linfócitos T Auxiliares-Indutores/citologia
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Auxiliares-Indutores/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (CCR6 protein, mouse); 0 (ELAV-Like Protein 1); 0 (ELAVL1 protein, human); 0 (Elavl1 protein, mouse); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (Receptors, CCR6)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.782771


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[PMID]:28502830
[Au] Autor:Herold N; Rudd SG; Sanjiv K; Kutzner J; Myrberg IH; Paulin CBJ; Olsen TK; Helleday T; Henter JI; Schaller T
[Ad] Endereço:Childhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, and Karolinska University Hospital, Stockholm, Sweden; Theme of Children's and Women's Health, Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden. Electronic addres
[Ti] Título:With me or against me: Tumor suppressor and drug resistance activities of SAMHD1.
[So] Source:Exp Hematol;52:32-39, 2017 Aug.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Sterile alpha motif and histidine/aspartic acid domain-containing protein 1 (SAMHD1) is a (deoxy)guanosine triphosphate (dGTP/GTP)-activated deoxyribonucleoside triphosphate (dNTP) triphosphohydrolase involved in cellular dNTP homoeostasis. Mutations in SAMHD1 have been associated with the hyperinflammatory disease Aicardi-Goutières syndrome (AGS). SAMHD1 also limits cells' permissiveness to infection with diverse viruses, including human immunodeficiency virus (HIV-1), and controls endogenous retroviruses. Increasing evidence supports the role of SAMHD1 as a tumor suppressor. However, SAMHD1 also can act as a resistance factor to nucleoside-based chemotherapies by hydrolyzing their active triphosphate metabolites, thereby reducing response of various malignancies to these anticancer drugs. Hence, informed cancer therapies must take into account the ambiguous properties of SAMHD1 as both an inhibitor of uncontrolled proliferation and a resistance factor limiting the efficacy of anticancer treatments. Here, we provide evidence that SAMHD1 is a double-edged sword for patients with acute myelogenous leukemia (AML). Our time-dependent analyses of The Cancer Genome Atlas (TCGA) AML cohort indicate that high expression of SAMHD1, even though it critically limits the efficacy of high-dose ara-C therapy, might be associated with more favorable disease progression.
[Mh] Termos MeSH primário: Doenças Autoimunes do Sistema Nervoso/genética
Resistência a Medicamentos/genética
Proteínas Monoméricas de Ligação ao GTP/genética
Mutação
Malformações do Sistema Nervoso/genética
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Antimetabólitos Antineoplásicos/uso terapêutico
Doenças Autoimunes do Sistema Nervoso/metabolismo
Azacitidina/análogos & derivados
Azacitidina/uso terapêutico
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Citarabina/uso terapêutico
Seres Humanos
Leucemia Mieloide/tratamento farmacológico
Leucemia Mieloide/genética
Leucemia Mieloide/metabolismo
Proteínas Monoméricas de Ligação ao GTP/metabolismo
Malformações do Sistema Nervoso/metabolismo
Proteína 1 com Domínio SAM e Domínio HD
Análise de Sobrevida
Resultado do Tratamento
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Tumor Suppressor Proteins); 04079A1RDZ (Cytarabine); 776B62CQ27 (decitabine); EC 3.1.5.- (SAM Domain and HD Domain-Containing Protein 1); EC 3.1.5.- (SAMHD1 protein, human); EC 3.6.5.2 (Monomeric GTP-Binding Proteins); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE


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[PMID]:28385184
[Au] Autor:Constantinescu R; Krýsl D; Andrén K; Asztély F; Bergquist F; Zetterberg H; Andreasson U; Axelsson M; Menachem EB; Jons D; Mahamud U; Malmeström C; Rosengren L; Blennow K
[Ad] Endereço:Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden; Department of Neurology, Sahlgrenska University Hospital, 413 45 Göteborg, Sweden. Electronic address: radu.constantinescu@vgregion.se.
[Ti] Título:Cerebrospinal fluid markers of neuronal and glial cell damage in patients with autoimmune neurologic syndromes with and without underlying malignancies.
[So] Source:J Neuroimmunol;306:25-30, 2017 May 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Autoimmune neurologic syndromes can be paraneoplastic (associated with malignancies and/or onconeural antibodies), or non-paraneoplastic. Their clinical presentation is often similar. As prognosis is related to malignancy treatment, better biomarkers are needed to identify patients with malignancy. We investigated cerebrospinal fluid (CSF) markers of neuronal (neurofilament light chain, NFL and total tau protein, T-tau) and glial (glial fibrillary acidic protein) damage. CSF-NFL and T-tau were increased in both paraneoplastic and non-paraneoplastic autoimmune syndromes. Patients with manifest malignancies were older, had less epilepsy, more focal central and peripheral neurological signs and symptoms, and worse long-term outcome, than those without malignancy. CSF-NFL-levels predicted long-term outcome but were not diagnostic for malignancy, after age adjustment.
[Mh] Termos MeSH primário: Doenças Autoimunes do Sistema Nervoso/líquido cefalorraquidiano
Doenças Autoimunes do Sistema Nervoso/complicações
Neoplasias/líquido cefalorraquidiano
Neoplasias/complicações
Proteínas do Tecido Nervoso/líquido cefalorraquidiano
Proteínas tau/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Doenças Autoimunes do Sistema Nervoso/diagnóstico por imagem
Biomarcadores/líquido cefalorraquidiano
Encéfalo/diagnóstico por imagem
Encéfalo/patologia
Criança
Pré-Escolar
Eletroencefalografia
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Neoplasias/diagnóstico por imagem
Estudos Retrospectivos
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Nerve Tissue Proteins); 0 (tau Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE


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[PMID]:28334850
[Au] Autor:Li P; Du J; Goodier JL; Hou J; Kang J; Kazazian HH; Zhao K; Yu XF
[Ad] Endereço:Institute of Virology and AIDS Research, First Hospital of Jilin University, Changchun, Jilin 130061, China.
[Ti] Título:Aicardi-Goutières syndrome protein TREX1 suppresses L1 and maintains genome integrity through exonuclease-independent ORF1p depletion.
[So] Source:Nucleic Acids Res;45(8):4619-4631, 2017 May 05.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Maintaining genome integrity is important for cells and damaged DNA triggers autoimmunity. Previous studies have reported that Three-prime repair exonuclease 1(TREX1), an endogenous DNA exonuclease, prevents immune activation by depleting damaged DNA, thus preventing the development of certain autoimmune diseases. Consistently, mutations in TREX1 are linked with autoimmune diseases such as systemic lupus erythematosus, Aicardi-Goutières syndrome (AGS) and familial chilblain lupus. However, TREX1 mutants competent for DNA exonuclease activity are also linked to AGS. Here, we report a nuclease-independent involvement of TREX1 in preventing the L1 retrotransposon-induced DNA damage response. TREX1 interacted with ORF1p and altered its intracellular localization. Furthermore, TREX1 triggered ORF1p depletion and reduced the L1-mediated nicking of genomic DNA. TREX1 mutants related to AGS were deficient in inducing ORF1p depletion and could not prevent L1-mediated DNA damage. Therefore, our findings not only reveal a new mechanism for TREX1-mediated L1 suppression and uncover a new function for TREX1 in protein destabilization, but they also suggest a novel mechanism for TREX1-mediated suppression of innate immune activation through maintaining genome integrity.
[Mh] Termos MeSH primário: DNA/genética
Exodesoxirribonucleases/genética
Genoma Humano
Fosfoproteínas/genética
Proteínas/genética
Retroelementos
[Mh] Termos MeSH secundário: Doenças Autoimunes do Sistema Nervoso/genética
Doenças Autoimunes do Sistema Nervoso/imunologia
Doenças Autoimunes do Sistema Nervoso/patologia
Autoimunidade
DNA/imunologia
Quebras de DNA de Cadeia Dupla
Exodesoxirribonucleases/antagonistas & inibidores
Exodesoxirribonucleases/imunologia
Regulação da Expressão Gênica
Instabilidade Genômica
Células HEK293
Células HeLa
Seres Humanos
Mutação
Malformações do Sistema Nervoso/genética
Malformações do Sistema Nervoso/imunologia
Malformações do Sistema Nervoso/patologia
Fosfoproteínas/antagonistas & inibidores
Fosfoproteínas/imunologia
Fosforilação
Plasmídeos/química
Plasmídeos/metabolismo
Proteínas/imunologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Proteínas Recombinantes/genética
Proteínas Recombinantes/imunologia
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ORF1 protein, human); 0 (Phosphoproteins); 0 (Proteins); 0 (RNA, Small Interfering); 0 (Recombinant Proteins); 0 (Retroelements); 9007-49-2 (DNA); EC 3.1.- (Exodeoxyribonucleases); EC 3.1.16.- (three prime repair exonuclease 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx178


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[PMID]:28166327
[Au] Autor:Dubey D; Alqallaf A; Hays R; Freeman M; Chen K; Ding K; Agostini M; Vernino S
[Ad] Endereço:Department of Neurology and Neurotherapeutics, UT Southwestern Medical Center, Dallas, Texas2Department of Neurology, Parkland Health and Hospital System, Dallas, Texas.
[Ti] Título:Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology.
[So] Source:JAMA Neurol;74(4):397-402, 2017 Apr 01.
[Is] ISSN:2168-6157
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Autoimmune epilepsy is an underrecognized condition, and its true incidence is unknown. Identifying patients with an underlying autoimmune origin is critical because these patients' condition may remain refractory to conventional antiseizure medications but may respond to immunotherapy. Objective: To determine the prevalence of neurological autoantibodies (Abs) among adult patients with epilepsy of unknown etiology. Design, Setting, and Participants: Consecutive patients presenting to neurology services with new-onset epilepsy or established epilepsy of unknown etiology were identified. Serum samples were tested for autoimmune encephalitis Abs as well as thyroperoxidase (TPO) and glutamic acid decarboxylase 65 (GAD65) Abs. An antibody prevalence in epilepsy (APE) score based on clinical characteristics was assigned prospectively. Data were collected from June 1, 2015, to June 1, 2016. Main Outcomes and Measures: Presence of neurological Abs. A score based on clinical characteristics was assigned to estimate the probability of seropositivity prior to antibody test results. Good seizure outcome was estimated on the basis of significant reduction of seizure frequency at the first follow-up or seizure freedom. Results: Of the 127 patients (68 males and 59 females) enrolled in the study, 15 were subsequently excluded after identification of an alternative diagnosis. Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases. More than 1 Ab was detected in 7 patients (6.3%): 3 (2.7%) had TPO-Ab and voltage-gated potassium channel complex (VGKCc) Ab, 2 (1.8%) had GAD65-Ab and VGKCc-Ab, 1 had TPO-Ab and GAD65-Ab, and 1 had anti-Hu Ab and GAD65-Ab. Thirty-two patients (28.6%) had a single Ab marker. Among 112 patients included in the study, 15 (13.4%) had TPO-Ab, 14 (12.5%) had GAD65-Ab, 12 (10.7%) had VGKCc (4 of whom were positive for leucine-rich glioma-inactivated protein 1 [LGI1] Ab), and 4 (3.6%) had N-methyl-D-aspartate receptor (NMDAR) Ab. Even after excluding TPO-Ab and low-titer GAD65-Ab, Abs strongly suggesting an autoimmune cause of epilepsy were seen in 23 patients (20.5%). Certain clinical features, such as autonomic dysfunction, neuropsychiatric changes, viral prodrome, faciobrachial dystonic spells or facial dyskinesias, and mesial temporal sclerosis abnormality on magnetic resonance imaging, correlated with seropositivity. The APE score was a useful tool in predicting positive serologic findings. Patients who were Ab positive were more likely to have good seizure outcome than were patients with epilepsy of unknown etiology (15 of 23 [65.2%] vs 24 of 89 [27.0%]; odds ratio, 4.8; 95% CI, 1.8-12.9; P = .002). In patients who were seropositive, reduction in seizure frequency was associated with use of immunomodulatory therapy. Conclusions and Relevance: Among adult patients with epilepsy of unknown etiology, a significant minority had detectable serum Abs suggesting an autoimmune etiology. Certain clinical features (encoded in the APE score) could be used to identify patients with the highest probability of harboring neurological Abs.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Doenças Autoimunes do Sistema Nervoso/complicações
Epilepsia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Autoantígenos/imunologia
Epilepsia/sangue
Epilepsia/epidemiologia
Epilepsia/imunologia
Feminino
Glutamato Descarboxilase/imunologia
Seres Humanos
Iodeto Peroxidase/imunologia
Proteínas de Ligação ao Ferro/imunologia
Masculino
Meia-Idade
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
Estudos Prospectivos
Receptores de N-Metil-D-Aspartato/imunologia
Estatísticas não Paramétricas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Autoantigens); 0 (Iron-Binding Proteins); 0 (Potassium Channels, Voltage-Gated); 0 (Receptors, N-Methyl-D-Aspartate); EC 1.11.1.7 (TPO protein, human); EC 1.11.1.8 (Iodide Peroxidase); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170530
[Lr] Data última revisão:
170530
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE
[do] DOI:10.1001/jamaneurol.2016.5429


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[PMID]:28120349
[Au] Autor:Flanagan EP; Hinson SR; Lennon VA; Fang B; Aksamit AJ; Morris PP; Basal E; Honorat JA; Alfugham NB; Linnoila JJ; Weinshenker BG; Pittock SJ; McKeon A
[Ad] Endereço:Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN.
[Ti] Título:Glial fibrillary acidic protein immunoglobulin G as biomarker of autoimmune astrocytopathy: Analysis of 102 patients.
[So] Source:Ann Neurol;81(2):298-309, 2017 Feb.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: A novel autoimmune central nervous system (CNS) disorder with glial fibrillary acidic protein (GFAP)-IgG as biomarker was recently characterized. Here, 102 patients with GFAP-IgG positivity are described. METHODS: The 102 included patients had: (1) serum, cerebrospinal fluid (CSF), or both that yielded a characteristic astrocytic pattern of mouse tissue immunostaining; (2) confirmation of IgG reactive with specific GFAP isoforms (α, É›, or κ) by cell-based assays; and (3) clinical data available. Control specimens (n = 865) were evaluated by tissue (n = 542) and cell-based (n = 323) assays. RESULTS: Median symptom onset age was 44 years (range = 8-103), and 54% were women. The predominant phenotype (83 patients; 81%) was inflammation of meninges, brain, spinal cord, or all 3 (meningoencephalomyelitis). Among patients, highest specificity for those phenotypes was observed for CSF testing (94%), and highest sensitivity was for the GFAPα isoform (100%). Rare GFAP-IgG positivity was encountered in serum controls by tissue-based assay (0.5%) or cell-based assay (1.5%), and in CSF controls by cell-based assay (0.9%). Among patients, striking perivascular radial enhancement was found on brain magnetic resonance imaging in 53%. Although cases frequently mimicked vasculitis, angiography was uniformly negative, and spinal imaging frequently demonstrated longitudinally extensive myelitic lesions. Diverse neoplasms encountered were found prospectively in 22%. Ovarian teratoma was most common and was predicted best when both N-methyl-D-aspartate receptor-IgG and aquaporin-4-IgG coexisted (71%). Six patients with prolonged follow-up had brisk corticosteroid response, but required additional immunosuppression to overcome steroid dependency. INTERPRETATION: GFAPα-IgG, when detected in CSF, is highly specific for an immunotherapy-responsive autoimmune CNS disorder, sometimes with paraneoplastic cause. Ann Neurol 2017;81:298-309.
[Mh] Termos MeSH primário: Astrócitos/patologia
Autoanticorpos/líquido cefalorraquidiano
Doenças Autoimunes do Sistema Nervoso/líquido cefalorraquidiano
Proteína Glial Fibrilar Ácida/imunologia
Síndromes Paraneoplásicas do Sistema Nervoso/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Biomarcadores/líquido cefalorraquidiano
Criança
Feminino
Seres Humanos
Imunoglobulina G
Imagem por Ressonância Magnética
Masculino
Camundongos
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Biomarkers); 0 (Glial Fibrillary Acidic Protein); 0 (Immunoglobulin G)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24881


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[PMID]:28116953
[Au] Autor:Allison T; Roncero I; Forsyth R; Coffman K; Pichon JL
[Ad] Endereço:1 Division of Neurology, Children's Mercy Hospital, Kansas City, MO, USA.
[Ti] Título:Brown-Vialetto-Van Laere Syndrome as a Mimic of Neuroimmune Disorders: 3 Cases From the Clinic and Review of the Literature.
[So] Source:J Child Neurol;32(6):528-532, 2017 May.
[Is] ISSN:1708-8283
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We present 3 patients identified at 2 different institutions with Brown-Vialetto-Van Laere syndrome. Each patient was initially diagnosed with a neuroimmune disorder for a period of a few weeks to a few months. In each case, genetic analysis revealed mutations in one of the riboflavin transporters, confirming Brown-Vialetto-Van Laere syndrome. It is likely that Brown-Vialetto-Van Laere syndrome is more common than previously reported, and because it mimics neuroimmune disorders, it may be misdiagnosed as such. It shares many features with diseases such as chronic inflammatory demyelinating neuropathy, may present with positive cerebrospinal fluid antibody titers, and may transiently respond to intravenous immunoglobulin. We review the literature on Brown-Vialetto-Van Laere syndrome and Fazio-Londe syndrome, 2 riboflavin transporter disorders, looking for clinical presentations that may lead to confusion with neuroimmune disorders. We emphasize the importance of correctly diagnosing the disease, as its treatment is relatively benign and will stop progression of the disease and may even reverse it.
[Mh] Termos MeSH primário: Doenças Autoimunes do Sistema Nervoso/fisiopatologia
Paralisia Bulbar Progressiva/diagnóstico
Perda Auditiva Neurossensorial/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Paralisia Bulbar Progressiva/genética
Pré-Escolar
Progressão da Doença
Feminino
Perda Auditiva Neurossensorial/genética
Seres Humanos
Proteínas de Membrana Transportadoras/genética
Mutação/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Membrane Transport Proteins); 0 (SLC52A3 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1177/0883073816689517



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