Controlled Trial of Plasma Exchange in Acute Inflammatory Polyradiculoneuropathy

Greenwood, R; Hughes, Richard A.; Bowden, Alexandra; Gordon, N.; Millac, Paul; Newsom‐Davis, John; Aslan, Sina; Chadwick, David; McLellan, D. L.; Stott, R.B.; Armitage, P.

doi:10.1016/s0140-6736(84)91341-2

Cited by 164 publications

(49 citation statements)

References 19 publications

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“…15,16 One trial involving 29 participants showed a trend toward more improvement in disability after 4 weeks with PE. 17 The other five trials showed significantly more improvement in disability grade or more patients improved in disability grade after 4 weeks. 15,16,[18][19][20][21] In a metaanalysis of all six studies, the proportion of patients on the ventilator 4 weeks after randomization was reduced to 48 of 321 in the PE group compared with 106 of 325 in the control group (relative risk [RR], 0.56; 95% CI, 0.41 to 0.76; p ϭ 0.0003).…”

Section: Plasma Exchangementioning

confidence: 94%

Practice parameter: Immunotherapy for Guillain–Barré syndrome

et al. 2003

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Abstract-Objective:To provide an evidence-based statement to guide physicians in the management of Guillain-Barré syndrome (GBS). Methods: Literature search and derivation of evidence-based statements concerning the use of immunotherapy were performed. Results: Treatment with plasma exchange (PE) or IV immunoglobulin (IVIg) hastens recovery from GBS. Combining the two treatments is not beneficial. Steroid treatment given alone is not beneficial. Recommendations: 1) PE is recommended for nonambulant adult patients with GBS who seek treatment within 4 weeks of the onset of neuropathic symptoms. PE should also be considered for ambulant patients examined within 2 weeks of the onset of neuropathic symptoms; 2) IVIg is recommended for nonambulant adult patients with GBS within 2 or possibly 4 weeks of the onset of neuropathic symptoms. The effects of PE and IVIg are equivalent; 3) Corticosteroids are not recommended for the management of GBS; 4) Sequential treatment with PE followed by IVIg, or immunoabsorption followed by IVIg is not recommended for patients with GBS; and 5) PE and IVIg are treatment options for children with severe GBS. NEUROLOGY 2003;61:736 -740 Guillain-Barré syndrome (GBS) affects between 1 and 4 per 100,000 of the population annually throughout the world, 1 causing respiratory failure requiring ventilation in approximately 25%, death in 4 to 15%, 2-6 persistent disability in approximately 20%, 7 and persistent fatigue in 67%. 8 The costs in the United States have been estimated as $110,000 for direct health care and $360,000 in lost productivity per patient. 9 This practice parameter classifies the relevant evidence on immunotherapy to provide evidence-based recommendations for the management of GBS. 10Evidence review. A search of MEDLINE from 1966 and of the Cochrane library was performed in March 2002. "Polyradiculoneuritis" was limited by "human" and cross-referenced with "therapy." The search results were reviewed for each question by at least two members of the practice parameter group and supplemented from the reference lists in the articles retrieved and the personal reference lists of the members of the practice parameter group. Those titles representing relevant randomized controlled trials (RCTs) are included in the tables on the Neurology Web site for this article (www.neurology.org). Recommendations were graded according to the levels established by the AAN Quality Standards Subcommittee at the inception of this project (table).

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Section: Plasma Exchangementioning

confidence: 94%

Practice parameter: Immunotherapy for Guillain–Barré syndrome

et al. 2003

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“…In 1984, two small clinical trials showed some positive effects of plasma exchange in GBS 79,80 , and in 1985, a larger study confirmed the effect and demonstrated that plasma exchange in patients who were unable to walk hastened recovery, especially when started within 2 weeks of GBS onset 81 .A subsequent study obtained similar results 82 . Plasma exchange consequently became the first proven therapy for GBS, but the treatment is not always straightforward and carries particular risks for patients with autonomic disturbance, which is common in GBS.…”

Section: [H1] Therapymentioning

confidence: 95%

Guillain–Barré syndrome: a century of progress

2016

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In 1916, Guillain, Barré and Strohl reported on two cases of acute flaccid paralysis with high cerebrospinal fluid protein levels and normal cell counts -novel findings that identified the disease we now know as Guillain-Barré syndrome (GBS).100 years on, we have made great progress with the clinical and pathological characterization of GBS. Early clinicopathological and animal studies indicated that GBS was an immune-mediated demyelinating disorder with secondary axonal injury if severe; the current treatments of plasma exchange and intravenous immunoglobulin, which were developed in the 1980s, are based on this premise. Subsequent work has, however, shown that the underlying disease can be an axonal injury. The association of Campylobacter jejuni strains has led to confirmation that anti-ganglioside antibodies are pathogenic and that axonal GBS involves an antibody and complement-mediated disruption of nodes of Ranvier, neuromuscular junctions and other neuronal and glial membranes. Now, ongoing clinical trials of the complement inhibitor eculizumab are the first of targeted immunotherapy in GBS.Guillain-Barré syndrome (GBS) is the commonest cause of acute flaccid paralysis and manifests as rapidly evolving weakness and sensory disturbance in arms, legs and in some patients, facial, bulbar and respiratory muscles. Many patients will make a good recovery over many months but in severe cases patients can require months of intensive care support and be left with permanent severe weakness, sensory disturbance and pain. Furthermore, around 5% die from complications including respiratory failure, pneumonia and arrhythmias, making it a medical emergency with a high morbidity and significant mortality.Descriptions of clinical cases that closely resemble the condition we now know as GBS were made at least as early as 1859, when Jean Baptiste Octave Landry reported on "acute ascending paralysis". His report led to use of the term "Landry's ascending paralysis" to describe subacute ascending peripheral sensory and motor dysfunction. He observed that:

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“…Similar protocols have been shown to be safe in other neurologic disorders, including MS, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and myasthenia gravis. 35,[37][38][39][40] Thus, using the protocol suggested by the model, the 1-g/mL threshold can be reached approximately 15 days after natalizumab dosing. In the absence of PLEX, historic pharmacokinetic data indicate that the same threshold would take approximately 82 days longer.…”

Section: Figure 1 Effects Of Plasma Exchange On Serum Concentration Omentioning

confidence: 99%