Assuntos
Autoanticorpos/imunologia , Encefalite/imunologia , Lobo Frontal/diagnóstico por imagem , Glicoproteína Mielina-Oligodendrócito/imunologia , Paraparesia/imunologia , Biópsia , Encéfalo/diagnóstico por imagem , Encéfalo/patologia , Encefalite/diagnóstico por imagem , Encefalite/tratamento farmacológico , Encefalite/patologia , Lobo Frontal/patologia , Glucocorticoides/uso terapêutico , Humanos , Imageamento por Ressonância Magnética , Masculino , Metilprednisolona/uso terapêutico , Pessoa de Meia-Idade , Paraparesia/diagnóstico por imagem , Paraparesia/tratamento farmacológico , Paraparesia/patologia , Prednisolona/uso terapêuticoRESUMO
Biologic therapy with tumor necrosis factor (TNF)-alpha antagonists for rheumatoid arthritis has been well established. We describe two patients with rheumatoid arthritis who developed chronic inflammatory demyelinating polyneuropathy (CIDP) during their course of therapy with TNF-alpha antagonists. A 45-year-old woman and a 49-year-old man, both with a history of rheumatoid arthritis, were treated with etanercept and infliximab, respectively. Clinical signs of peripheral neuropathy developed 2 weeks and 12 months after the initiation of TNF-alpha antagonists. Electrodiagnostic studies at variable points during the disease course showed signs of acquired demyelination consistent with CIDP. Cerebrospinal fluid examination showed albuminocytologic dissociation (total protein concentration 118 mg/dl and 152 mg/dl, respectively). Both patients failed to improve after discontinuation of the offending agent, and they responded poorly to corticosteroids. However, there was clinical and electrophysiologic recovery after initiation of intravenous immunoglobulin (IVIg) therapy. CIDP may occur early or late during the treatment course with TNF-alpha antagonists. IVIg may reverse and stabilize the inflammatory process.
Assuntos
Antirreumáticos/efeitos adversos , Artrite Reumatoide/tratamento farmacológico , Nervos Periféricos/efeitos dos fármacos , Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/induzido quimicamente , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Anticorpos Monoclonais/efeitos adversos , Artrite Reumatoide/imunologia , Artrite Reumatoide/fisiopatologia , Eletrodiagnóstico , Etanercepte , Feminino , Humanos , Imunoglobulina G/efeitos adversos , Imunoglobulinas Intravenosas/administração & dosagem , Terapia de Imunossupressão/efeitos adversos , Terapia de Imunossupressão/métodos , Infliximab , Masculino , Pessoa de Meia-Idade , Debilidade Muscular/induzido quimicamente , Debilidade Muscular/imunologia , Debilidade Muscular/fisiopatologia , Músculo Esquelético/inervação , Músculo Esquelético/fisiopatologia , Condução Nervosa/efeitos dos fármacos , Condução Nervosa/imunologia , Dor/induzido quimicamente , Dor/imunologia , Dor/fisiopatologia , Paraparesia/induzido quimicamente , Paraparesia/imunologia , Paraparesia/fisiopatologia , Nervos Periféricos/imunologia , Nervos Periféricos/patologia , Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/imunologia , Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/fisiopatologia , Receptores do Fator de Necrose Tumoral , Recuperação de Função Fisiológica/efeitos dos fármacos , Recuperação de Função Fisiológica/imunologia , Resultado do Tratamento , Fator de Necrose Tumoral alfa/metabolismoRESUMO
OBJECTIVE: The objective of this study was to evaluate the effect of intravenous immunoglobulin (IVIg) therapy in diabetic lumbosacral radiculoplexus neuropathy (DLRPN) patients who did not respond to analgesic drug therapy and corticosteroids. Background. DLRPN is a rare painful condition that may occur in diabetes mellitus (DM). At the moment, there are limited therapeutic options for DLRPN. METHODS: We recruited five patients affected by type 2 DM and DLRPN. They were selected from a cohort of 13 consecutive DLRPN patients. Inclusion criteria were severe pain (visual analog scale [VAS] > 4/10) and no response to pain symptomatic therapy and corticosteroids. Patients were treated with IVIg (0.4 g/kg/day for 5 days). Outcome measures were VAS, time of onset and duration of pain relief, the Medical Research Council (MRC) scale for lower limb muscle strength, and walking distance. Electrophysiology and needle electromyography (EMG) were retested after IVIg. RESULTS: Four of the patients had positive pain response after IVIg. VAS reduction started 5-10 days after IVIg infusion. Two patients underwent additional IVIg infusions due to pain reappearance after 7-18 months, again with positive response. VAS, MRC scale, and walking distance significantly improved at 1 month (Wilcoxon nonparametric test, two-tailed, P < 0.05). Electrodiagnostic testing was unchanged, but needle EMG showed reduction of denervation signs after IVIg. CONCLUSIONS: IVIg may rapidly reduce pain and improve motor function in DLRPN despite previous negative response to corticosteroids. IVIg may be repeated in those patients who experience disease relapse. Future double-blind trials are needed to evaluate the role of IVIg in DLRPN.
Assuntos
Neuropatias Diabéticas/tratamento farmacológico , Neuropatias Diabéticas/imunologia , Imunoglobulinas Intravenosas/administração & dosagem , Plexo Lombossacral/imunologia , Radiculopatia/tratamento farmacológico , Radiculopatia/imunologia , Vasculite/tratamento farmacológico , Idoso , Estudos de Coortes , Neuropatias Diabéticas/fisiopatologia , Esquema de Medicação , Eletromiografia , Feminino , Humanos , Plexo Lombossacral/irrigação sanguínea , Plexo Lombossacral/fisiopatologia , Masculino , Pessoa de Meia-Idade , Debilidade Muscular/tratamento farmacológico , Debilidade Muscular/imunologia , Debilidade Muscular/fisiopatologia , Medição da Dor , Paraparesia/tratamento farmacológico , Paraparesia/imunologia , Paraparesia/fisiopatologia , Radiculopatia/fisiopatologia , Índice de Gravidade de Doença , Resultado do Tratamento , Vasculite/complicações , Vasculite/imunologiaRESUMO
Ochronosis is a late developing complication of alkaptonuria, a black brownish pigment in the fibrous and cartilaginous tissues. Although most previous studies reported alkaptonuria and back pain due to ochronosis, thoracic myelopathy is an extremely rare complication. In this report, a paraparetic patient who has ochronotic spondiloarthropathy with the presence of HLA B27 antigen is described. He had low back and leg pain and morning stiffness for 5 yrs. Last year, these were followed by tingling, numbness, and weakness the in lower extremities and he was operated on with preliminary diagnosis of prolapsed disc herniation and cord compression. Surgery is suggested for disc herniations related to ochronotic spondyloarthropathy if it is necessary or neurologic symptoms are present. However, his pain and weakness have partially recovered after the operation. After medical and physical treatment, he showed clinically significant improvements. This case report demonstrates that the management of ochronosis needs a multidisciplinary approach with physiologic, neurologic, and psychologic effects and proper treatment may significantly improve functional outcomes in these patients.
Assuntos
Antígeno HLA-B27/sangue , Ocronose/complicações , Doenças da Medula Espinal/etiologia , Espondiloartropatias/complicações , Vértebras Torácicas , Humanos , Masculino , Pessoa de Meia-Idade , Ocronose/imunologia , Paraparesia/complicações , Paraparesia/imunologia , Doenças da Medula Espinal/imunologia , Espondiloartropatias/imunologiaRESUMO
To study alterations in the morphology of spinal perivascular macrophages (SPM) during experimental allergic encephalomyelitis (EAE), we labelled SPM by intracerebroventricular (i.c.v.) injection of horseradish peroxidase (HRP). As earlier electron microscopical analysis had shown severely damaged SPM, we suspected that each inflammatory process is accompanied by the death of SPM. To prove this hypothesis, we compared the numerical density of resident SPM (i.c.v. labelled in red by Fluoro-Ruby) with that of monocytes/macrophages recruited to the perivascular space (i.c.v. labelled in green by Fluoro-Emerald). At the peak of paraparesis, the density of resident SPM was reduced by 33%. Since this reduction contrasted sharply with earlier data indicating a massive increase in the density of SPM during EAE, we checked our findings after general or selective suppression of the immune response to myelin autoantigens with the drugs dexamethasone and copaxone, respectively. Dexamethasone treatment commenced after evident paraparesis accelerated recovery, but did not influence SPM density. Immunisation with copaxone completely prevented the occurrence of EAE (monitored by video-based motion analysis of tail motility); the subsequent histological analysis revealed no reduction in SPM density. Based on this inverse correlation between the severity of EAE and the density of resident macrophages, we conclude that SPM plays an important role in the pathogenesis of EAE.
Assuntos
Células Apresentadoras de Antígenos/patologia , Encefalomielite Autoimune Experimental/imunologia , Macrófagos/imunologia , Paraparesia/imunologia , Medula Espinal/irrigação sanguínea , Medula Espinal/patologia , Animais , Células Apresentadoras de Antígenos/efeitos dos fármacos , Células Apresentadoras de Antígenos/imunologia , Células Apresentadoras de Antígenos/metabolismo , Contagem de Células , Movimento Celular/imunologia , Dexametasona/administração & dosagem , Regulação para Baixo/efeitos dos fármacos , Regulação para Baixo/imunologia , Encefalomielite Autoimune Experimental/sangue , Encefalomielite Autoimune Experimental/tratamento farmacológico , Encefalomielite Autoimune Experimental/patologia , Corantes Fluorescentes/metabolismo , Injeções Intraperitoneais , Macrófagos/efeitos dos fármacos , Macrófagos/metabolismo , Macrófagos/patologia , Masculino , Paraparesia/sangue , Paraparesia/patologia , Paraparesia/fisiopatologia , Ratos , Ratos Endogâmicos Lew , Índice de Gravidade de Doença , Medula Espinal/imunologia , Cauda/fisiologia , Fatores de TempoRESUMO
The authors report on a patient who developed acute-onset paraparesis after underoing a thoracotomy 40 years earlier for a carcinoid adenoma. No infectious or neoplastic origin could be found to explain the patient's current clinical course and radiographic findings. The postoperative events in this case are discussed, as well as the literature regarding postthoracotomy complications.
Assuntos
Tumor Carcinoide/cirurgia , Inflamação/imunologia , Neoplasias Pulmonares/cirurgia , Paraparesia/imunologia , Pneumonectomia , Complicações Pós-Operatórias/imunologia , Compressão da Medula Espinal/imunologia , Toracotomia , Espaço Epidural , Fístula/diagnóstico , Fístula/imunologia , Fístula/cirurgia , Humanos , Inflamação/diagnóstico , Inflamação/cirurgia , Masculino , Pessoa de Meia-Idade , Paraparesia/diagnóstico , Paraparesia/cirurgia , Doenças Pleurais/diagnóstico , Doenças Pleurais/imunologia , Doenças Pleurais/cirurgia , Complicações Pós-Operatórias/diagnóstico , Complicações Pós-Operatórias/cirurgia , Compressão da Medula Espinal/diagnóstico , Compressão da Medula Espinal/cirurgia , Doenças da Coluna Vertebral/diagnóstico , Doenças da Coluna Vertebral/imunologia , Doenças da Coluna Vertebral/cirurgia , Vértebras Torácicas/patologia , Vértebras Torácicas/cirurgiaAssuntos
Antineoplásicos Imunológicos/efeitos adversos , Axônios/efeitos dos fármacos , Nivolumabe/efeitos adversos , Paraparesia/imunologia , Polineuropatias/imunologia , Idoso , Antineoplásicos Imunológicos/administração & dosagem , Axônios/imunologia , Carcinoma de Células Renais/diagnóstico , Carcinoma de Células Renais/tratamento farmacológico , Carcinoma de Células Renais/imunologia , Carcinoma de Células Renais/secundário , Substituição de Medicamentos/efeitos adversos , Evolução Fatal , Humanos , Indazóis , Neoplasias Renais/diagnóstico , Neoplasias Renais/tratamento farmacológico , Neoplasias Renais/imunologia , Neoplasias Renais/patologia , Metástase Linfática/terapia , Masculino , Neurônios Motores/efeitos dos fármacos , Neurônios Motores/imunologia , Nivolumabe/administração & dosagem , Paraparesia/induzido quimicamente , Polineuropatias/induzido quimicamente , Pirimidinas/administração & dosagem , Neoplasias Cutâneas/diagnóstico , Neoplasias Cutâneas/tratamento farmacológico , Neoplasias Cutâneas/imunologia , Neoplasias Cutâneas/secundário , Sulfonamidas/administração & dosagemRESUMO
Experimental autoimmune neuritis (EAN) is a T cell-mediated autoimmune inflammatory demyelinating disease of the peripheral nervous system and an animal model of human inflammatory demyelinating polyradiculoneuropathy. AUY954, which targets selectively the sphingosine-1-phosphate receptor 1 (S1P(1)), is known to sequester lymphocytes into secondary lymphoid tissues. In EAN rats, AUY954 greatly prevented paraparesis if administrated from the day of immunization. T cell, B cell, and macrophage infiltration, inflammatory demyelination, and local expression of interleukine-17 and matrix metalloproteinase-9 in sciatic nerves of EAN rats were significantly decreased by AUY954 treatment. Therefore, S1P(1) modulation might be a potential treatment option for inflammatory neuropathies.
Assuntos
Síndrome de Guillain-Barré/tratamento farmacológico , Neurite Autoimune Experimental/tratamento farmacológico , Receptores de Lisoesfingolipídeo/efeitos dos fármacos , Tiofenos/farmacologia , beta-Alanina/análogos & derivados , Animais , Linfócitos B/efeitos dos fármacos , Linfócitos B/imunologia , Quimiotaxia de Leucócito/efeitos dos fármacos , Quimiotaxia de Leucócito/imunologia , Modelos Animais de Doenças , Síndrome de Guillain-Barré/imunologia , Síndrome de Guillain-Barré/metabolismo , Fatores Imunológicos/farmacologia , Fatores Imunológicos/uso terapêutico , Interleucina-17/metabolismo , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Masculino , Metaloproteinase 9 da Matriz/metabolismo , Neurite Autoimune Experimental/imunologia , Neurite Autoimune Experimental/metabolismo , Paraparesia/tratamento farmacológico , Paraparesia/imunologia , Paraparesia/prevenção & controle , Ratos , Ratos Endogâmicos Lew , Receptores de Lisoesfingolipídeo/metabolismo , Nervo Isquiático/efeitos dos fármacos , Nervo Isquiático/imunologia , Nervo Isquiático/metabolismo , Linfócitos T/efeitos dos fármacos , Linfócitos T/imunologia , Tiofenos/uso terapêutico , Resultado do Tratamento , beta-Alanina/farmacologia , beta-Alanina/uso terapêuticoRESUMO
Multiple sclerosis (MS) is the most common demyelinating disease caused by an autoimmune inflammatory process in the central nervous system (CNS) and is associated with aberrant immune response to myelin selfantigens. Coexistence of MS with other autoimmune disorders, including connective tissue disorders including systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome and scleroderma have been reported previously. In the present article we report the coexistence of MS, familial mediterranean fever and ankylosing spondylitis in a patient and review the clinical presentation, neurologic findings, cerebrospinal fluid and radiologic characteristics and treatment options. We further discuss the immunopathogenetic mechanisms for a possible association between MS and autoimmune disorders.