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[PMID]:29269693
[Au] Autor:Yasuda K; Murase N; Ohtani R; Oka N; Nakamura M
[Ad] Endereço:Department of Neurology, National Hospital Organization Kyoto Medical Center.
[Ti] Título:[A case of chronic inflammatory demyelinating polyradiculoneuropathy, showing radicular pain due to tuberous hypertrophy of the spinal roots and plexuses after 20 years interval without relapsing sensorimotor symptoms].
[So] Source:Rinsho Shinkeigaku;58(1):21-24, 2018 Jan 26.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 40-year-old man visited our department because of chest and back pain. He had a history of diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) 20 years ago. He received immunosuppressive therapy and had no relapses after that. On Admission, MRI showed tuberous hypertrophy of the spinal roots, intercostal nerves, and brachial and lumbar plexuses. The genetic analysis showed no mutations in any of Charcot-Marie-Tooth related genes. He was finally diagnosed with CIDP and administration of high dose intravenous methylprednisolone relieved his chest and back pain within a few days. We present a rare case of CIDP in which showed marked enlarged spinal roots in long clinical course and have a relapse with radicular pain without sensorimotor symptoms.
[Mh] Termos MeSH primário: Dor nas Costas/etiologia
Plexo Braquial/patologia
Dor no Peito/etiologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/complicações
Raízes Nervosas Espinhais/patologia
[Mh] Termos MeSH secundário: Adulto
Dor nas Costas/tratamento farmacológico
Plexo Braquial/diagnóstico por imagem
Dor no Peito/tratamento farmacológico
Seres Humanos
Hipertrofia
Infusões Intravenosas
Imagem por Ressonância Magnética
Masculino
Metilprednisolona/administração & dosagem
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico por imagem
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/tratamento farmacológico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/patologia
Pulsoterapia
Raízes Nervosas Espinhais/diagnóstico por imagem
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001073


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[PMID]:28747620
[Au] Autor:Finsterer J; Aliyev R
[Ad] Endereço:Department of Neurology, Krankenanstalt Rudolfstiftung, Vienna, Austria.
[Ti] Título:Chronic Inflammatory Demyelinating Polyneuropathy Variant with Creatine-Kinase Elevation and Vanishing Effect of Immunoglobulins.
[So] Source:Am J Case Rep;18:834-838, 2017 Jul 27.
[Is] ISSN:1941-5923
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Whether creatine-kinase (CK) is elevated or not in chronic inflammatory demyelinating polyneuropathy (CIDP) and its variants is not comprehensively investigated. CASE REPORT We report the case of a 47-year-old male who developed weakness of the left lower leg and the right index finger at age 42 years. At age 44 years, paresthesias and dysesthesias of both lower legs and mild right lower leg weakness additionally developed. CK was recurrently elevated since age 42 years but paraprotein and anti-myelin-associated glycoprotein (MAG)-antibodies were negative. Nerve conduction studies at age 43 years showed an axonal and demyelinating lesion with conduction blocks. Cerebrospinal fluid (CSF) investigations revealed mild pleocytosis and elevated protein, which is why CIDP variant was diagnosed. Immunoglobulins were administered with success. Because of recurrent relapses, immunoglobulins were increased at age 45 years, resulting in stabilization. Currently, the patient is infusing immunoglobulins subcutaneously himself. CONCLUSIONS CIDP variants may go along with CK elevation, an axonal lesion, pleocytosis, and asymmetry of the lesion. A vanishing effect of immunoglobulins over time may be characteristic of CIDP variants.
[Mh] Termos MeSH primário: Creatina Quinase/sangue
Imunoglobulinas Intravenosas/uso terapêutico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/tratamento farmacológico
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
Meia-Idade
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/sangue
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
Recidiva
Autoadministração
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulins, Intravenous); EC 2.7.3.2 (Creatine Kinase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE


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[PMID]:28984777
[Au] Autor:Ju W; Qi B; Wang X; Yang Y
[Ad] Endereço:aDepartment of Neurology bDepartment of Orthopedic Trauma, the First Hospital of Jilin University, Changchun, Jilin, China.
[Ti] Título:Anti-Ma2-associated limbic encephalitis with coexisting chronic inflammatory demyelinating polyneuropathy in a patient with non-Hodgkin lymphoma: A case report.
[So] Source:Medicine (Baltimore);96(40):e8228, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: We report the rare case of a 74-year-old man with anti-Ma2-associated paraneoplastic neurologic syndrome (PNS), and review and analyze the clinical manifestations, diagnosis, and treatment of the disease. PATIENT CONCERNS: The patient presented with a 5-month history of muscle weakness, progressive body aches, and weakness and numbness in both lower extremities. Before his hospitalization, he had experienced cognitive function decline; ptosis, inward gaze, and vertical gaze palsy in the right eye; and occasional visual hallucinations. Brain and spinal cord magnetic resonance imaging (MRI) yielded normal results. Anti-Ma2 antibodies were detected in both serum and cerebrospinal fluid. A 4-hour electroencephalogram showed irregular sharp slow waves and δ waves in the temporal region. Electromyography showed peripheral nerve demyelination. Positron-emission tomography/computed tomography (PET-CT) examination revealed hypermetabolism in the lymph nodes of the whole body. Biopsy of the lymph nodes showed non-Hodgkin lymphoma. DIAGNOSIS: A clinical diagnosis of lymphoma and PNS was made. INTERVENTIONS: The patient was treated with intravenous dexamethasone (15 mg/day) for 3 days. LESSONS: We have presented a rare case of a PNS involving both the central and peripheral nervous systems. The clinical features of this case indicated anti-Ma2-associated encephalitis and chronic inflammatory demyelinating polyneuropathy. PET-CT played a critical role in enabling early diagnosis and prompt treatment in this case.
[Mh] Termos MeSH primário: Encefalite Límbica/imunologia
Linfoma não Hodgkin/complicações
Síndromes Paraneoplásicas do Sistema Nervoso/complicações
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/imunologia
[Mh] Termos MeSH secundário: Idoso
Anticorpos/sangue
Anticorpos/líquido cefalorraquidiano
Antígenos de Neoplasias/imunologia
Seres Humanos
Encefalite Límbica/complicações
Linfoma não Hodgkin/imunologia
Masculino
Proteínas do Tecido Nervoso/imunologia
Síndromes Paraneoplásicas do Sistema Nervoso/imunologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/complicações
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Antigens, Neoplasm); 0 (Ma2 antigen); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008228


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[PMID]:28877025
[Au] Autor:Rush RP; Saltman AP; Prica AA; Breiner A; Detsky AS
[Ad] Endereço:From the Department of Medicine (R.P.R., A.P.S., A.A.P., A.B., A.S.D.) and Institute for Health Policy Management and Evaluation (A.S.D.), University of Toronto, and the Department of Medicine, University Health Network and Mount Sinai Hospital (A.A.P., A.B., A.S.D.), Toronto, and the Department of
[Ti] Título:Connecting the Dots.
[So] Source:N Engl J Med;377(10):978-984, 2017 Sep 07.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Linfoma Difuso de Grandes Células B/diagnóstico
Debilidade Muscular/etiologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
[Mh] Termos MeSH secundário: Animais
Dor nas Costas/etiologia
Diagnóstico Diferencial
Evolução Fatal
Feminino
Seres Humanos
Linfoma Difuso de Grandes Células B/complicações
Linfoma Difuso de Grandes Células B/patologia
Imagem por Ressonância Magnética
Meia-Idade
Ovário/diagnóstico por imagem
Ovário/patologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/etiologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/patologia
Tomografia por Emissão de Pósitrons
Raízes Nervosas Espinhais/patologia
Coluna Vertebral/diagnóstico por imagem
Ultrassonografia
Útero/diagnóstico por imagem
Útero/patologia
Perda de Peso
[Pt] Tipo de publicação:CASE REPORTS; CLINICAL CONFERENCE; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMcps1613804


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[PMID]:28855494
[Au] Autor:Fujisawa M; Sano Y; Omoto M; Ogasawara JI; Koga M; Takashima H; Kanda T
[Ad] Endereço:Department of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medical Science.
[Ti] Título:Charcot-Marie-Tooth disease type 2 caused by homozygous MME gene mutation superimposed by chronic inflammatory demyelinating polyneuropathy.
[So] Source:Rinsho Shinkeigaku;57(9):515-520, 2017 09 30.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:We report a 59-year-old Japanese male who developed gradually worsening weakness and numbness of distal four extremities since age 50. His parents were first cousins, and blood and cerebral spinal examinations were unremarkable. Homozygous mutation of MME gene was detected and thus he was diagnosed as autosomal-recessive Charcot-Marie-Tooth disease 2T (AR-CMT2T); however, electrophysiological examinations revealed scattered demyelinative changes including elongated terminal latency in several peripheral nerve trunks. Sural nerve biopsy showed endoneurial edema and a lot of thinly myelinated nerve fibers with uneven distribution of remnant myelinated fibers within and between fascicles. Immunoglobulin treatment was initiated considering the possibility of superimposed inflammation and demyelination, and immediate clinical as well as electrophysiological improvements were noted. Our findings indicate that AR-CMT2T caused by MME mutation predisposes to a superimposed inflammatory demyelinating neuropathy. This is the first report which documented the co-existence of CMT2 and chronic inflammatory demyelinating polyneuropathy (CIDP); however, in the peripheral nervous system, neprilysin, a product of MME gene, is more abundant in myelin sheath than in axonal component. The fragility of myelin sheath due to mutated neprilysin may trigger the detrimental immune response against peripheral myelin in this patient.
[Mh] Termos MeSH primário: Doença de Charcot-Marie-Tooth/complicações
Doença de Charcot-Marie-Tooth/genética
Estudos de Associação Genética
Mutação
Neprilisina/genética
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/complicações
[Mh] Termos MeSH secundário: Doença de Charcot-Marie-Tooth/diagnóstico
Doença de Charcot-Marie-Tooth/terapia
Homozigoto
Seres Humanos
Imunoglobulinas Intravenosas/administração & dosagem
Masculino
Meia-Idade
Bainha de Mielina/enzimologia
Bainha de Mielina/imunologia
Neprilisina/metabolismo
Condução Nervosa
Nervos Periféricos/patologia
Nervos Periféricos/fisiopatologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/terapia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulins, Intravenous); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001036


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[PMID]:28768822
[Au] Autor:Kuwabara S; Mori M; Misawa S; Suzuki M; Nishiyama K; Mutoh T; Doi S; Kokubun N; Kamijo M; Yoshikawa H; Abe K; Nishida Y; Okada K; Sekiguchi K; Sakamoto K; Kusunoki S; Sobue G; Kaji R; Glovenin-I CIDP Study Group
[Ad] Endereço:Department of Neurology, Chiba University Hospital, Chiba, Japan.
[Ti] Título:Intravenous immunoglobulin for maintenance treatment of chronic inflammatory demyelinating polyneuropathy: a multicentre, open-label, 52-week phase III trial.
[So] Source:J Neurol Neurosurg Psychiatry;88(10):832-838, 2017 Oct.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Short-term efficacy of induction therapy with intravenous immunoglobulin (Ig) in patients with chronic inflammatory demyelinating polyneuropathy (CIDP) is well established. However, data of previous studies on maintenance therapy were limited up to 24-week treatment period. We aimed to investigate the efficacy and safety of longer-term intravenous Ig therapy for 52 weeks. METHODS: This study was an open-label phase 3 clinical trial conducted in 49 Japanese tertiary centres. 49 patients with CIDP who fulfilled diagnostic criteria were included. After an induction intravenous Ig therapy (0.4 g/kg/day for five consecutive days), maintenance dose intravenous Ig (1.0 g/kg) was given every 3 weeks for up to 52 weeks. The primary outcome measures were the responder rate at week 28 and relapse rate at week 52. The response and relapse were defined with the adjusted Inflammatory Neuropathy Cause and Treatment scale. RESULTS: At week 28, the responder rate was 77.6% (38/49 patients; 95% CI 63% to 88%), and the 38 responders continued the maintenance therapy. At week 52, 4 of the 38 (10.5%) had a relapse (95% CI 3% to 25%). During 52 weeks, 34 (69.4%) of the 49 enrolled patients had a maintained improvement. Adverse events were reported in 94% of the patients; two patients (66-year-old and 76-year-old men with hypertension or diabetes) developed cerebral infarction (lacunar infarct with good recovery), and the other adverse effects were mild and resolved by the end of the study period. CONCLUSIONS: Maintenance treatment with 1.0 g/kg intravenous Ig every 3 weeks is an efficacious therapy for patients with CIDP, and approximately 70% of them had a sustained remission for 52 weeks. Thrombotic complications should be carefully monitored, particularly in elderly patients with vascular risk factors. TRIAL REGISTRATION NUMBER: ClinicalTrials.gov (NCT01824251).
[Mh] Termos MeSH primário: Imunoglobulinas Intravenosas/uso terapêutico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/terapia
Resultado do Tratamento
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Imunoglobulinas Intravenosas/efeitos adversos
Japão
Masculino
Meia-Idade
Recidiva
Fatores de Tempo
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Immunoglobulins, Intravenous)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2017-316427


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[PMID]:28601286
[Au] Autor:Mathey EK; Garg N; Park SB; Nguyen T; Baker S; Yuki N; Yiannikas C; Lin CS; Spies JM; Ghaoui R; Barnett MH; Vucic S; Pollard JD; Kiernan MC
[Ad] Endereço:Brain & Mind Centre, University of Sydney, Sydney, Australia. Electronic address: emily.mathey@sydney.edu.au.
[Ti] Título:Autoantibody responses to nodal and paranodal antigens in chronic inflammatory neuropathies.
[So] Source:J Neuroimmunol;309:41-46, 2017 Aug 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Autoantibodies to nodal/paranodal proteins have been reported in patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). To determine the frequency of anti-paranodal antibodies in our cohort of CIDP patients and to validate the presence anti-nodal antibodies in MMN, sera were screened for IgG against human neurofascin 155, contactin-1, neurofascin 186 and gliomedin using ELISA. In CIDP patients, 7% were anti-NF155 IgG positive and 7% were anti-CNTN1 IgG positive. Positive results were confirmed using cell based assays and indirect immunofluorescence on teased nerve fibres. We did not detect IgG autoantibodies against these nodal/paranodal antigens in MMN patients.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Polineuropatias/sangue
Polineuropatias/diagnóstico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/sangue
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Autoanticorpos/imunologia
Moléculas de Adesão Celular/sangue
Moléculas de Adesão Celular/imunologia
Feminino
Células HeLa
Seres Humanos
Imunoglobulina G/sangue
Imunoglobulina G/imunologia
Masculino
Proteínas de Membrana/sangue
Proteínas de Membrana/imunologia
Meia-Idade
Fatores de Crescimento Neural/sangue
Fatores de Crescimento Neural/imunologia
Proteínas do Tecido Nervoso/sangue
Proteínas do Tecido Nervoso/imunologia
Polineuropatias/imunologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/imunologia
Ratos
Ratos Endogâmicos Lew
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Cell Adhesion Molecules); 0 (GLDN protein, human); 0 (Immunoglobulin G); 0 (Membrane Proteins); 0 (NFASC protein, human); 0 (Nerve Growth Factors); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170612
[St] Status:MEDLINE


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[PMID]:28575198
[Au] Autor:Delmont E; Manso C; Querol L; Cortese A; Berardinelli A; Lozza A; Belghazi M; Malissart P; Labauge P; Taieb G; Yuki N; Illa I; Attarian S; Devaux JJ
[Ad] Endereço:Referral Center for ALS and Neuromuscular Diseases, Timone University Hospital, Aix-Marseille University, France.
[Ti] Título:Autoantibodies to nodal isoforms of neurofascin in chronic inflammatory demyelinating polyneuropathy.
[So] Source:Brain;140(7):1851-1858, 2017 Jul 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chronic inflammatory demyelination polyneuropathy is a heterogeneous and treatable immune-mediated disorder that lacks biomarkers to support diagnosis. Recent evidence indicates that paranodal proteins (contactin 1, contactin-associated protein 1, and neurofascin-155) are the targets of autoantibodies in subsets of patients showing distinct clinical presentations. Here, we identified neurofascin-186 and neurofascin-140 as the main targets of autoantibodies in five patients presenting IgG reactivity against the nodes of Ranvier. Four patients displayed predominantly IgG4 antibodies, and one patient presented IgG3 antibodies that activated the complement pathway in vitro. These patients present distinct clinical features compared to those with anti-neurofascin-155 IgG4. Most patients had a severe phenotype associated with conduction block or decreased distal motor amplitude. Four patients had a subacute-onset and sensory ataxia. Two patients presented with nephrotic syndromes and one patient with an IgG4-related retroperitoneal fibrosis. Intravenous immunoglobulin and corticosteroids were effective in three patients, and one patient remitted following rituximab treatment. Clinical remission was associated with autoantibody depletion and with recovery of conduction block and distal motor amplitude suggesting a nodo-paranodopathy. Our data demonstrate that the pathogenic mechanisms responsible for chronic inflammatory demyelination polyneuropathy are broad and may include dysfunctions at the nodes of Ranvier in a subgroup of patients.
[Mh] Termos MeSH primário: Autoanticorpos/imunologia
Moléculas de Adesão Celular/imunologia
Fatores de Crescimento Neural/imunologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/imunologia
[Mh] Termos MeSH secundário: Adolescente
Corticosteroides/uso terapêutico
Adulto
Idoso
Idoso de 80 Anos ou mais
Autoanticorpos/sangue
Estudos de Casos e Controles
Criança
Pré-Escolar
Feminino
Seres Humanos
Imunoglobulinas Intravenosas/uso terapêutico
Masculino
Meia-Idade
Condução Nervosa/fisiologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/sangue
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/tratamento farmacológico
Isoformas de Proteínas/imunologia
Nós Neurofibrosos/imunologia
Rituximab/uso terapêutico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Autoantibodies); 0 (Cell Adhesion Molecules); 0 (Immunoglobulins, Intravenous); 0 (NFASC protein, human); 0 (Nerve Growth Factors); 0 (Protein Isoforms); 4F4X42SYQ6 (Rituximab)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx124


  9 / 1206 MEDLINE  
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[PMID]:28506346
[Au] Autor:Sun RD; Fu B; Jiang J
[Ad] Endereço:Department of Electrophysiology, Wuhan Women and Children's Hospital, Wuhan 421000, China. jiangjunzm@163.com.
[Ti] Título:[Role of short-latency somatosensory evoked potential in the diagnosis of chronic inflammatory demyelinating polyneuropathy].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(5):545-548, 2017 May.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the role of short-latency somatosensory evoked potential (SSEP) in the diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP). METHODS: A total of 48 children with a confirmed or suspected CIDP and 40 healthy children were enrolled. Nerve electrophysiological examination and/or SSEP examination was performed (the children in the healthy control group only underwent SSEP examination). Four-lead electromyography was used for nerve electrophysiological examination, including at least 4 motor nerves and 2 sensory nerves. N6 (elbow potential), N13 (cervical cord potential), and N20 (cortex potential) of the median nerve and N8 (popliteal fossa potential), N22 (lumbar cord potential), and P39 (cortex potential) of the tibial nerve were observed by SSEP examination. RESULTS: Among the 48 children with CIDP, 35 had demyelination in both motor and sensory nerves, 8 had demyelination in sensory nerves, and 5 had axonal degeneration. SSEP examination showed that 7 had conduction abnormality in the trunk of the brachial plexus and/or the posterior root and 33 had damage in the lumbosacral plexus and/or the posterior root. The 40 children with abnormal findings of SSEP examination included 8 children with affected sensory nerves and 5 children with secondary axonal degeneration who did not meet the electrophysiological diagnostic criteria for CIDP. Compared with the healthy control group, the CIDP group had significantly prolonged latency periods of N13 and N22 (P<0.05). CONCLUSIONS: SSEP can be used for the auxiliary diagnosis of CIDP, especially in CIDP children with affected sensory nerves or secondary axonal degeneration.
[Mh] Termos MeSH primário: Potenciais Somatossensoriais Evocados
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
[Mh] Termos MeSH secundário: Axônios/fisiologia
Criança
Pré-Escolar
Feminino
Seres Humanos
Masculino
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/fisiopatologia
Tempo de Reação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE


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[PMID]:28481421
[Au] Autor:Mahdi-Rogers M; Brassington R; Gunn AA; van Doorn PA; Hughes RA
[Ad] Endereço:Department of Neurology, King's College Hospital, Denmark Hill, London, UK, SE5 9RS.
[Ti] Título:Immunomodulatory treatment other than corticosteroids, immunoglobulin and plasma exchange for chronic inflammatory demyelinating polyradiculoneuropathy.
[So] Source:Cochrane Database Syst Rev;5:CD003280, 2017 05 08.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a disease that causes progressive or relapsing and remitting weakness and numbness. It is probably caused by an autoimmune process. Immunosuppressive or immunomodulatory drugs would be expected to be beneficial. This review was first published in 2003 and has been updated most recently in 2016. OBJECTIVES: To assess the effects of immunomodulatory and immunosuppressive agents other than corticosteroids, immunoglobulin, and plasma exchange in CIDP. SEARCH METHODS: On 24 May 2016, we searched the Cochrane Neuromuscular Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL; 2016, Issue 4) in the Cochrane Library, MEDLINE, Embase, CINAHL, and LILACS for completed trials, and clinical trial registers for ongoing trials. We contacted the authors of the trials identified and other disease experts seeking other published and unpublished trials. SELECTION CRITERIA: We sought randomised and quasi-randomised trials of all immunosuppressive agents, such as azathioprine, cyclophosphamide, methotrexate, ciclosporin, mycophenolate mofetil, and rituximab, and all immunomodulatory agents, such as interferon (IFN) alfa and IFN beta, in participants fulfilling standard diagnostic criteria for CIDP. We included all comparisons of these agents with placebo, another treatment, or no treatment. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures expected by Cochrane. We wanted to measure the change in disability after one year as our primary outcome. Our secondary outcomes were change in disability after four or more weeks (from randomisation); change in impairment after at least one year; change in maximum motor nerve conduction velocity and compound muscle action potential amplitude after one year; and for participants who were receiving corticosteroids or intravenous immunoglobulin (IVIg), the amount of this medication given during at least one year after randomisation. Participants with one or more serious adverse events during the first year was also a secondary outcome. MAIN RESULTS: Four trials fulfilled the selection criteria: one of azathioprine (27 participants), two of IFN beta-1a (77 participants in total) and one of methotrexate (60 participants). The risk of bias was considered low in the trials of IFN beta-1a and methotrexate but high in the trial of azathioprine. None of the trials showed significant benefit in any of the outcomes selected by their authors. The results of the outcomes which approximated most closely to the primary outcome for this review were as follows.In the azathioprine trial there was a median improvement in the Neuropathy Impairment Scale (scale range 0 to 280) after nine months of 29 points (range 49 points worse to 84 points better) in the azathioprine and prednisone treated participants compared with 30 points worse (range 20 points worse to 104 points better) in the prednisone alone group. There were no reports of adverse events.In a cross-over trial of IFN beta-1a with 20 participants, the treatment periods were 12 weeks. The median improvement in the Guy's Neurological Disability Scale (range 1 to 10) was 0.5 grades (interquartile range (IQR) 1.8 grades better to zero grade change) in the IFN beta-1a treatment period and 0.5 grades (IQR 1.8 grades better to 1.0 grade worse) in the placebo treatment period. There were no serious adverse events in either treatment period.In a parallel group trial of IFN beta-1a with 67 participants, none of the outcomes for this review was available. The trial design involved withdrawal from ongoing IVIg treatment. The primary outcome used by the trial authors was total IVIg dose administered from week 16 to week 32 in the placebo group compared with the IFN beta-1a groups. This was slightly but not significantly lower in the combined IFN beta-1a groups (1.20 g/kg) compared with the placebo group (1.34 g/kg, P = 0.75). There were four participants in the IFN beta-1a group and none in the placebo group with one or more serious adverse events, risk ratio (RR) 4.50 (95% confidence interval (CI) 0.25 to 80.05).The methotrexate trial had a similar design involving withdrawal from ongoing corticosteroid or IVIg treatment. At the end of the trial (approximately 40 weeks) there was no significant difference in the change in the Overall Neuropathy Limitations Scale, a disability scale (scale range 0 to 12), the median change being 0 (IQR -1 to 0) in the methotrexate group and 0 (IQR -0.75 to 0) in the placebo group. These changes in disability might have been confounded by the reduction in corticosteroid or IVIg dose required by the protocol. There were three participants in the methotrexate group and one in the placebo with one or more serious adverse events, RR 3.56 (95% CI 0.39 to 32.23). AUTHORS' CONCLUSIONS: Low-quality evidence from randomised trials does not show significant benefit from azathioprine or interferon beta-1a and moderate-quality evidence from one randomised trial does not show significant benefit from a relatively low dose of methotrexate for the treatment of CIDP. None of the trials was large enough to rule out small or moderate benefit. The evidence from observational studies is insufficient to avoid the need for randomised controlled trials to discover whether these drugs are beneficial. Future trials should have improved designs, more sensitive outcome measures relevant to people with CIDP, and longer treatment durations.
[Mh] Termos MeSH primário: Fatores Imunológicos/uso terapêutico
Imunossupressores/uso terapêutico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/tratamento farmacológico
[Mh] Termos MeSH secundário: Anti-Inflamatórios/uso terapêutico
Azatioprina/uso terapêutico
Seres Humanos
Imunoglobulinas Intravenosas/uso terapêutico
Interferon beta-1a/uso terapêutico
Interferon beta/uso terapêutico
Metotrexato/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Immunoglobulins, Intravenous); 0 (Immunologic Factors); 0 (Immunosuppressive Agents); 77238-31-4 (Interferon-beta); MRK240IY2L (Azathioprine); XRO4566Q4R (Interferon beta-1a); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD003280.pub5



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