• J Pritchard.
• Department of Neuroimmunology, Guy's, King's and St Thomas' School of Medicine, Hodgkin Building, Guy's Hospital, London, SE1 9RT, UK. Jane.Pritchard@kcl.ac.uk
• Expert Opin Investig Drugs. 2000 Oct 1; 9 (10): 2307-18.

AbstractGuillain-Barré syndrome is an autoimmune disease which occurs throughout the world. Whilst the majority of patients can expect a reasonable recovery, about 10% die and 10% are left disabled with current therapy. The standard treatment is a five day course of iv. immunoglobulin, given at a dose of 0.4 g/kg/day, with plasma exchange as an equally efficacious alternative. Steroids are ineffective in Guillain-Barré syndrome. All new potential therapeutic agents need to be tested in addition to the standard agents available. Future potential therapies are suggested by the study of the animal model experimental autoimmune neuritis in the Lewis rat. Whilst in theory it is possible to target the different stages of the immune response, in practice not all of the steps at which experimental autoimmune neuritis can be prevented will be translatable to human Guillain-Barré syndrome. This is because Guillain-Barré syndrome probably presents after the immune reaction has been ongoing for some time and therefore early aspects of the immune response cannot be prevented. Many of the possible measures would have widespread immunosuppressive effects which would be unacceptable to patients. Interfering with the immune response by attempting to block antigen binding or inducing tolerance may not be practical, owing to the possibility of exacerbating disease. Once we have a more thorough understanding of the pathogenesis of Guillain-Barré syndrome, then immune-specific therapy for Guillain-Barré syndrome may become a possibility, rather than general immunosuppressive measures. Trials of beta-interferon and of a combination of steroid and i.v. immunoglobulin are underway. A trial of a second course of i.v. immunoglobulin is planned.

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