| Name: | Description: | Size: | Format: | |
|---|---|---|---|---|
| 709.16 KB | Adobe PDF |
Advisor(s)
Abstract(s)
A Síndrome de Guillain-Barré (SGB) é uma polineuropatia desmielinizante aguda do Sistema Nervoso Periférico (SNP) mediada imunologicamente. Caracteriza-se pelo início agudo e rapidamente progressivo de uma tetraparésia ascendente, acompanhada frequentemente por arreflexia e, ocasionalmente, por anomalias sensoriais e do Sistema Nervoso Autónomo (SNA).
Esta doença divide-se em variantes clínicas, e, como tal, apresenta uma ampla diversidade de manifestações. Apesar destes subtipos diferirem na sua fisiopatologia, pensa-se que o “mimetismo molecular” possa constituir um dos mecanismos-chave envolvidos na patogénese desta doença. Através deste processo, os agentes agressores produzem autoanticorpos contra determinados componentes dos nervos periféricos do hospedeiro, levando à sua destruição e consequente aparecimento da clínica.
A resposta imune depende tanto de fatores do hospedeiro como de fatores relacionados com o agente agressor. Os eventos precedentes mais comuns são as infeções, principalmente as respiratórias e gastrointestinais. Atualmente investiga-se o papel de outros possíveis fatores menos comuns, como as imunizações e as cirurgias. No entanto, são ainda necessários mais estudos para comprovar totalmente estes fatores como causadores da doença. É ainda de realçar a existência de fatores genéticos que assumem um papel igualmente importante. Assim, há um conjunto de genes candidatos que têm vindo a ser estudados para a SGB.
Existem diversos mecanismos imunológicos subjacentes à SGB. A imunidade celular e a imunidade humoral, associadas respetivamente aos linfócitos T ativados e aos autoanticorpos, contribuem, em conjunto, para a doença. Como resultado final desta cascata inflamatória vamos ter, entre outros, desmielinização, lesão axonal e bloqueio da condução nervosa.
A SGB ainda é uma doença potencialmente fatal e que encerra um mau prognóstico em pelo menos 20% dos casos. Assim, é fundamental salientar a necessidade de melhores tratamentos para esta doença, com o objetivo de reduzir o número de pessoas que persistem com défices residuais. O conhecimento da sua fisiopatologia e dos processos imunes envolvidos assume repercussões terapêuticas relevantes, ao permitir a investigação de novos fármacos que vão atuar sobre as principais moléculas envolvidas na patogénese da SGB.
The Guillain-Barré Syndrome (GBS) is an acute demyelinating polyneuropathy of the Peripheral Nervous System (PNS) which is immunologically mediated. It is characterized by an acute and rapidly progressive onset of an upward tetraparesis, often accompanied by areflexia and occasionally by sensory and Autonomic Nervous System anomalies (ANS). This disease can be divided into clinical variants, and as such, has a wide variety of manifestations. Although these subtypes differ in their pathophysiology, it is believed that the "molecular mimicry" may be one of the key mechanisms involved in the pathogenesis of this disease. Through this process, the aggressors produce autoantibodies against certain components of the peripheral nerves of the host, leading to its destruction and the consequent presentation of the clinic. The immune response depends on both host factors as factors related to the offending agent. The most common previous events are infections, especially respiratory and gastrointestinal. The potential role of other less common factors, such as the immunizations or surgery is currently under investigation. However, more studies are still needed to fully verify these factors as causes of the disease. It is also worth noting the existence of genetic factors that assume an equally important role. Thus, there is a set of candidate genes that have been studied for GBS. There are several immunological mechanisms underlying the GBS. The cellular immunity and humoral immunity, respectively associated with activated T lymphocytes and autoantibodies, contribute altogether to the disease. As an end result of the inflammatory cascade we have, among others, demyelination, axonal damage and blockage of nerve conduction. GBS is still a life threatening condition and determines a poor prognosis by at least 20% of cases. Thus, it is essential to emphasize the need for better treatments for this disease, in order to reduce the number of people who persist with residual deficits. The knowledge of the pathophysiology and immune processes involved assumes relevant therapeutic effects, by allowing the development of new drugs which act on the key molecules involved in the pathogenesis of GBS.
The Guillain-Barré Syndrome (GBS) is an acute demyelinating polyneuropathy of the Peripheral Nervous System (PNS) which is immunologically mediated. It is characterized by an acute and rapidly progressive onset of an upward tetraparesis, often accompanied by areflexia and occasionally by sensory and Autonomic Nervous System anomalies (ANS). This disease can be divided into clinical variants, and as such, has a wide variety of manifestations. Although these subtypes differ in their pathophysiology, it is believed that the "molecular mimicry" may be one of the key mechanisms involved in the pathogenesis of this disease. Through this process, the aggressors produce autoantibodies against certain components of the peripheral nerves of the host, leading to its destruction and the consequent presentation of the clinic. The immune response depends on both host factors as factors related to the offending agent. The most common previous events are infections, especially respiratory and gastrointestinal. The potential role of other less common factors, such as the immunizations or surgery is currently under investigation. However, more studies are still needed to fully verify these factors as causes of the disease. It is also worth noting the existence of genetic factors that assume an equally important role. Thus, there is a set of candidate genes that have been studied for GBS. There are several immunological mechanisms underlying the GBS. The cellular immunity and humoral immunity, respectively associated with activated T lymphocytes and autoantibodies, contribute altogether to the disease. As an end result of the inflammatory cascade we have, among others, demyelination, axonal damage and blockage of nerve conduction. GBS is still a life threatening condition and determines a poor prognosis by at least 20% of cases. Thus, it is essential to emphasize the need for better treatments for this disease, in order to reduce the number of people who persist with residual deficits. The knowledge of the pathophysiology and immune processes involved assumes relevant therapeutic effects, by allowing the development of new drugs which act on the key molecules involved in the pathogenesis of GBS.
Description
Keywords
Autoimunidade Fisiopatologia Síndrome de Guillain-Barré Sistema Nervoso Periférico