Corticosteroids for treating Guillain-Barré syndrome.
BACKGROUND
The cause of Guillain-Barré syndrome (GBS) is inflammation of the peripheral nerves which corticosteroids would be expected to benefit.


OBJECTIVE
To examine the efficacy of corticosteroids in hastening recovery and reducing the long term morbidity from Guillain-Barré syndrome (GBS).


METHODS
Search of the Cochrane Neuromuscular Disease Group register for randomised trials and enquiry from authors of trials and other experts in the field.


METHODS
Types of studies: quasi-randomised or randomised controlled trials


METHODS
patients with GBS of all ages and all degrees of severity Types of interventions: any form of corticosteroid or adrenocorticotrophic hormone Types of outcome measures: Primary: improvement in disability grade on a commonly used seven point scale four weeks after randomisation Secondary: time from randomisation until recovery of unaided walking, time from randomisation until discontinuation of ventilation (for those ventilated), mortality, proportion of patients dead or disabled (unable to walk without aid) after 12 months, improvement in disability grade after six months, improvement in disability grade after 12 months, proportion of patients who relapse, and proportion of patients with adverse events related to corticosteroid treatment


METHODS
We identified six randomised trials. One author extracted the data and the other checked them. We obtained some missing data from investigators.


RESULTS
The six eligible trials included a total of 195 corticosteroid treated patients and 187 control subjects. One trial of intravenous methylprednisolone accounted for 243 of the total 382 subjects studied (63%). This trial did not show a significant difference in any disability related outcome between the corticosteroid and placebo groups. There was no significant difference between the corticosteroid and control groups for the primary outcome measure, improvement in disability grade four weeks after randomisation. The weighted mean difference of the three trials for which this outcome was available showed no difference. The actual figure was 0.01 (95% CI -0.27 to 0.29) grade in favour of the corticosteroid group. There was also no significant difference between the groups for most of the secondary outcome measures. However in the largest trial hypertension developed less often in the intravenous methylprednisolone group (2/124, 1.6%) than in the control group (12/118, 10.2%), a significant difference in favour of corticosteroid treatment (relative risk 0.20, 95% CI 0.04 to 0.66).


CONCLUSIONS
Corticosteroids should not be used in the treatment of Guillain-Barré syndrome. If a patient with Guillain-Barré syndrome needs corticosteroid treatment for some other reason its use will probably not do harm. The effect of intravenous methylprednisolone combined with intravenous immunoglobulin in Guillain-Barré syndrome is being tested with a randomised trial.
Hughes
R A
RA
Department of Neuroimmunology, Guy's, King's and St Thomas' School of Medicine, Guy's Hospital, London, UK, SE1 9RT. richard.a. hughes@kcl.ac.uk
van Der Meché
F G
FG
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D005938:Glucocorticoids / Q000627:therapeutic use*; D020275:Guillain-Barre Syndrome / Q000188:drug therapy*; D006801:Humans; D016032:Randomized Controlled Trials as Topic; D013256:Steroids
D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D013256:Steroids