Plasma Exchange for Guillain-Barré Syndrome

Hôpital Raymond Poincaré, Garches, France.
Cochrane database of systematic reviews (Online) (Impact Factor: 6.03). 07/2012; 7(7):CD001798. DOI: 10.1002/14651858.CD001798.pub2
Source: PubMed


Guillain-Barré syndrome is a rare but serious disease of the peripheral nerves (nerves outside the central nervous system) that causes paralysis. Many patients have had a recent chest or stomach infection that may cause an allergic response in the nerves. Autoimmune factors such as antibodies are thought to cause the disease, so plasma exchange is used to treat Guillain-Barré syndrome. Plasma exchange aims to remove these antibodies from the blood stream and replace them with artificial plasma, usually albumin. This review of six randomised controlled trials involving 649 participants found that plasma exchange helps speed recovery from Guillain-Barré syndrome. It is more beneficial when started within seven days of the disease onset. No new trials have been done since the first publication of this review.

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    • "Conflicting results were obtained in the studies that compares PE and IVIG in terms of cost-effectiveness[9]. But there is lack of randomized, controlled studies of IVIG in children with GBS to show efficacy; however, most experts consider it a reasonable treatment option in children on the basis of its effectiveness in adults with GBS, although there are no reliable data suggesting that one or the other is su- perior8910. Although PE has been performed in an 8-month-old child with a diagnosis of GBS, experience in infants younger than 12 months is very limited[11]. "
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    ABSTRACT: Despite being the most common cause of acute flaccid paralysis in children Guillain-Barre Syndrome has a low incidence under 18 years old and it is even rarer under the age of 2. Established treatment regimens include intravenous immunoglobulin and plasma exchange in older children and adults. However very limited data are available for the efficacy and safety of plasma exchange in infants younger than 12 month-old. This article presents the experience of plasma exchange in the case of 7-month-old boy diagnosed with Guillain-Barre Syndrome.
    Full-text · Article · Jan 2016 · Transfusion and Apheresis Science
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    • "Active immune modulation with IvIg [61] or plasma exchange [62] is the mainstay of treatment with IvIg being preferred in most circumstances due to ease of availability and greater safety in patients with unstable blood pressure and pulse. IvIg is usually given at a dose of 0.4 gm/kg for 5 days although the optimum dose has never been established. "
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    ABSTRACT: Guillain-Barré syndrome (GBS) was first described in 1916 (Guillain G, 1916) and is approaching its 100th anniversary. Our knowledge of the syndrome has hugely expanded since that time. Once originally considered to be only demyelinating in pathology we now recognise both axonal and demyelinating subtypes. Numerous triggering or antecedent events including infections are recognised and GBS is considered an immunological response to these. GBS is now considered to be a clinical syndrome of an acute inflammatory neuropathy encompassing a number of subtypes with evidence of different immunological mechanisms. Some of these are clearly understood while others remain to be fully elucidated. Complement fixing antibodies against peripheral nerve gangliosides alone and in combination are increasingly recognised as an important mechanism of nerve damage. New antibodies against other nerve antigens such as neurofascin have been recently described. Research databases have been set up to look at factors associated with prognosis and the influence of intravenous immunoglobulin (IvIg) pharmacokinetics in therapy. Exciting new studies are in progress to examine a possible role for complement inhibition in the treatment of the syndrome.
    Full-text · Article · Jan 2014
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    • "Meanwhile, the cerebrospinal fluid (CSF) of GBS patients usually shows characteristic albumin-cytological dissociation, that is, elevated protein levels and approximately normal cell counts, from two weeks after the disease onset [2]. There is strong evidence proving that both humoral and cellular immune mechanisms are involved in the pathogenesis of GBS: (i) serum antibodies to various gangliosides in human peripheral nerves have been found in about half of GBS patients [3]; (ii) pathological findings in GBS include lymphocytic infiltration in spinal roots and peripheral nerves, followed by macrophage-mediated, multifocal stripping of myelin [4]; (iii) plasma exchange (PE) and intravenous immunoglobulin (IVIg) therapies are effective in the treatment of GBS patients [5] [6]. However, the exact immunological mechanism of GBS remains not understood. "
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    ABSTRACT: Guillain-Barré syndrome (GBS) is an acute autoimmune-mediated inflammatory demyelinating disease that causes rapidly progressing paralysis and occasionally respiratory failure. We hypothesized that interleukin (IL)-17 and IL-22 are elevated in GBS and participate in the autoimmune inflammatory response of GBS. We used sandwich enzyme-linked immunosorbent assay (ELISA) to measure the IL-17 and IL-22 levels in the CSF, and plasma from 22 GBS patients at the acute phase and 18 healthy controls (HC). The results show that CSF and plasma levels of IL-17 and IL-22 are elevated in GBS patients compared with HC. IL-17 and IL-22 levels in CSF, respectively, are correlated with GBS disability scale scores (GDSs). Meanwhile, IL-17 and IL-22 levels in CSF, IL-22 in CSF, and plasma of GBS patients have positive correlation, respectively. The increased levels of IL-17 and IL-22 in CSF may be explained by the disruption of blood-brain barrier (BBB) and peripheral nervous system (PNS) local inflammation in GBS. Meanwhile, the elevated levels of these two cytokines in plasma suggest the activation of Th17 and Th22 cells in the systemic immune response of GBS. Our data provide preliminary evidence that GBS is associated with high levels of IL-17 and IL-22 in CSF and plasma. These cytokines display pathogenic potential and may serve as useful biomarkers for GBS.
    Full-text · Article · Oct 2012 · Mediators of Inflammation
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