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Volume 112, Issue 3, Pages 193-198 (April 2010)


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Could Helicobacter pylori play an important role in axonal type of Guillain-Barré Syndrome pathogenesis?

Mojdeh Ghabaeea, Davod GhanbarianaCorresponding Author Informationemail address, Gholamreza Nikbakht Brujenib, Saeed Bokaeic, Farideh Siavoshid, Shahriar Gharibzadehe

Received 15 March 2009; received in revised form 7 November 2009; accepted 13 November 2009.

Abstract 

In this case-control study, ELISA and Western blot with whole bacterial protein lysate were performed on serum and cerebrospinal fluid (CSF) of 15 controls and 15 patients. According to Griffin subtypes, 10 of our patients were in acute inflammatory demyelinating polyradiculoneuropathy (AIDP) group, 3 in acute motor axonal neuropathy (AMAN) group, and 2 in acute motor sensory axonal neuropathy (AMSAN) subtype. 86.6% of patients were positive for Helicobacter pylori (H. pylori) IgG. Serum anti-H. pylori IgG of patients and controls were significantly different. CSF anti-H. pylori IgG was significantly higher in patients than controls. In patients, the titer of anti-H. pylori IgG in serum was significantly higher than CSF, which may indicate extra-neural antibody synthesis. CSF IgG titer was higher in patients having axonal pattern. Western blot was positive in CSF of 13 patients and negative in all controls. There was a correlation between the number of antibody types against H. pylori particles and the titer of anti-H. pylori IgG in CSF and serum. Also, antibody against cytotoxin associated protein (CagA) was associated with primary axonal pattern.

The association between the presence of anti-CagA and primary axonal pattern, is in favor of the relation between axonal neuropathy and H. pylori infection.

a Iranian Center of Neurological Research, Neurology Department, Tehran University of Medical Sciences, Iran

b Department of Microbiology and Immunology, Faculty of Veterinary Medicine, University of Tehran, Iran

c Division of Epidemiology, Department of Food Hygiene, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran

d Department of Microbiology, Faculty of Sciences, University of Tehran, Iran

e Neuromuscular Systems Laboratory, Faculty of Biomedical Engineering, Amirkabir University of Technology, Iran

Corresponding Author InformationCorresponding author. Tel.: +98 21 6690 4777; fax: +98 21 6649 5655.

PII: S0303-8467(09)00305-9

doi:10.1016/j.clineuro.2009.11.008


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