Anti-GM1, anti-central myelin proteins, and anti-cardiolipin autoantibodies during plasma-exchange in Guillain-Barre syndrome (GBS)

Citation
S. Mata et al., Anti-GM1, anti-central myelin proteins, and anti-cardiolipin autoantibodies during plasma-exchange in Guillain-Barre syndrome (GBS), J CLIN APH, 13(4), 1998, pp. 155-162
Citations number
43
Categorie Soggetti
Hematology
Journal title
JOURNAL OF CLINICAL APHERESIS
ISSN journal
07332459 → ACNP
Volume
13
Issue
4
Year of publication
1998
Pages
155 - 162
Database
ISI
SICI code
0733-2459(1998)13:4<155:AAMPAA>2.0.ZU;2-P
Abstract
We measured the autoantibodies to GM1, central myelin proteins, and cardiol ipin in 30 GBS patients using sensitive ELISA and Western blot techniques. The sequential modifications of titers during plasma-exchange (PE) and at f ollow-up were investigated in 15 patients. In pretreatment sera, we found s ignificantly increased antibody titers to GM1 (37% of the patients), centra l myelin proteins (28%), and cardiolipin (21%). Seventeen patients out of 2 9 (58%) presented increased IgG or IgM antibody to at least one of the anti gens considered as compared to 10 out of 70 controls (14%, P = 0.00001). By Western blot, IgG or IgM antibodies reactive with the triton insoluble fra ction of central myelin were observed in 19 out of 28 GBS patients (67%). T he follow-up measurements during and after PE showed a declining autoantibo dy titer in 10 out of 15 patients. However, in the remaining 5 GBS patients , we observed a persistently elevated titer or an increase from baseline va lues occurring during or after PE and reaching a peak. In 2 of the 5 patien ts, the titer peak preceded a clinical re-exacerbation. The presence of a p ersistently elevated or an increasing autoantibody titer during treatment w ith PE merits further investigation and may help to clarify the pathogenesi s of GBS and improve its treatment. J. Clin. Apheresis 13:155-162, 1998. (C ) 1998 Wiley-Liss,Inc.