Preceding infections, immune factors, and outcome in Guillain-Barré syndrome.
OBJECTIVE
To test the hypothesis that different preceding infections influence the neurophysiologic classification and clinical features of Guillain-Barré syndrome (GBS).


METHODS
We tested pretreatment sera, 7 +/- 3 (mean +/- SD) days from onset, from 229 patients with GBS in a multicenter trial of plasma exchange and immunoglobulin, for serological markers of infection, adhesion molecules, and cytokine receptors, and compared these with neurophysiologic and clinical features.


RESULTS
Recent infection by Campylobacter jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Epstein-Barr virus in four (2%). Patients with C. jejuni infection were more likely than others to have neurophysiologic criteria of axonal neuropathy or inexcitable nerves, antiganglioside GM(1) antibodies, pure motor GBS, lower CSF protein, and worse outcome. Patients with cytomegalovirus infection were younger and more likely than others to have raised serum concentrations of molecules important in T lymphocyte activation and migration, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2 receptor (sIL-2R). Concentrations of sICAM-1 and soluble tumor necrosis factor receptor were higher in patients with inexcitable nerves than those with demyelinating neurophysiology. Logistic regression analysis showed death or inability to walk unaided at 48 weeks were associated with diarrhea, inexcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentration and absence of immunoglobulin (Ig) M antiganglioside GM(1) antibodies.


CONCLUSIONS
Subtypes of GBS defined by preceding infections were only approximately associated with different patterns of clinical, neurophysiologic, and immunologic features. A single infectious agent caused more than one type of pathology in GBS, implying interaction with additional host factors. Most patients had no identified infection.
Department of Neuroimmunology, Guy's, King's and St. Thomas' School of Medicine, Swan), London, UK. rob.hadden@doctors.org.uk
R D
RD
Hadden
H
H
Karch
H P
HP
Hartung
J
J
Zielasek
B
B
Weissbrich
J
J
Schubert
A
A
Weishaupt
D R
DR
Cornblath
A V
AV
Swan
R A
RA
Hughes
K V
KV
Toyka
D000906:Antibodies / Q000276:immunology*; D001424:Bacterial Infections / Q000276:immunology*; D015815:Cell Adhesion Molecules / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005677:G(M1) Ganglioside / Q000276:immunology*; D020275:Guillain-Barre Syndrome / Q000276:immunology* / Q000382:microbiology; D004854:Herpesvirus 4, Human / Q000302:isolation & purification; D006801:Humans; D011379:Prognosis; D018121:Receptors, Cytokine / Q000276:immunology*; D012044:Regression Analysis
D000906:Antibodies; D015815:Cell Adhesion Molecules; D018121:Receptors, Cytokine; D005677:G(M1) Ganglioside