Neurology 1999;52:1833
© 1999 American Academy of Neurology
Articles
IV immunoglobulin reduces circulating proinflammatory cytokines in Guillain-Barré syndrome
M. K. Sharief, MD, PhD, MRCP,
D. A. Ingram, MB,
M. Swash, MD, FRCP and
E. J. Thompson, DSc, FRCPath
From the Department of Neurology (Dr. Sharief), United Medical and Dental School, Guy’s Hospital; Departments of Clinical Neurophysiology (Dr. Ingram) and Neurology (Dr. Swash), The Royal London Hospital; and Department of Neuroimmunology (Dr. Thompson), Institute of Neurology, London, England.
Address correspondence and reprint requests to Dr. M.K. Sharief, Department of Neurology, Guy’s Hospital, London SE1 9RT, England.
BACKGROUND: Treatment with human IV immunoglobulin (IVIg) modifies the course of Guillain-Barré syndrome (GBS), but its specific mode of action is unknown. Cellular interactions mediated through the release of cytokines play a role in the pathogenesis of GBS and may be regulated by IVIg therapy.
OBJECTIVE: To delineate possible immunoregulatory mechanisms of IVIg in patients with GBS.
METHODS: Circulating levels of the proinflammatory cytokines, tumor necrosis factor (TNF)- and interleukin (IL)-1ß, were assayed in 21 patients with GBS before and serially after IVIg therapy. Comparisons were made with serum concentration of the anti-inflammatory cytokines, soluble TNF- receptor and IL-10. Serial measurements were also performed in 12 untreated patients with relatively mild disease and 7 patients treated by plasma exchange.
RESULTS: Circulating levels of TNF- and IL-1ß decreased after treatment with IVIg but remained relatively high in untreated patients and in those treated by plasma exchange. Clinical improvement in patients treated with IVIg was associated with a reduction in unbound TNF- during the acute phase of the illness. Circulating levels of anti-inflammatory cytokines were not affected by IVIg treatment.
CONCLUSION: Data presented here suggest a novel mechanism of action of IVIg that involves selective modulation of circulating proinflammatory cytokines.
This article has been cited by other articles:
|
|
|
|
 
M. Ballow
Clinical and investigational considerations for the use of IGIV therapy
Am. J. Health Syst. Pharm.,
August 15, 2005;
62(16_Supplement_3):
S12 - S18.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G Triolo, A Ferrante, A Accardo-Palumbo, F Ciccia, M Cadelo, A Castelli, A Perino, and G Licata
IVIG in APS pregnancy
Lupus,
September 1, 2004;
13(9):
731 - 735.
[Abstract]
[PDF]
|
|
|
|
|
|
|
N. Yuki, K. Susuki, M. Koga, Y. Nishimoto, M. Odaka, K. Hirata, K. Taguchi, T. Miyatake, K. Furukawa, T. Kobata, et al.
Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain-Barre syndrome
PNAS,
August 3, 2004;
101(31):
11404 - 11409.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Nishimoto, M. Koga, M. Kamijo, K. Hirata, and N. Yuki
Immunoglobulin improves a model of acute motor axonal neuropathy by preventing axonal degeneration
Neurology,
June 8, 2004;
62(11):
1939 - 1944.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H F Petereit, H Lindemann, and S Schoppe
Effect of immunomodulatory drugs on in vitro production of brain-derived neurotrophic factor
Multiple Sclerosis,
February 1, 2003;
9(1):
16 - 20.
[Abstract]
[PDF]
|
|
|
|
|
|
|
M. C. Dalakas
Mechanisms of action of IVIg and therapeutic considerations in the treatment of acute and chronic demyelinating neuropathies
Neurology,
December 24, 2002;
59(90126):
S13 - 21.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
M. D. Kazatchkine and S. V. Kaveri
Immunomodulation of Autoimmune and Inflammatory Diseases with Intravenous Immune Globulin
N. Engl. J. Med.,
September 6, 2001;
345(10):
747 - 755.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. K. Asbury
New Concepts of Guillain-Barre Syndrome
J Child Neurol,
March 1, 2000;
15(3):
183 - 191.
[Abstract]
[PDF]
|
|
|
|
|
|
|
Possible Mechanism of Action of IV Immunoglobulin in GBS
Journal Watch Neurology,
October 1, 1999;
1999(1001):
14 - 14.
[Full Text]
|
|
|
|
