Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Eur J Neurol. 2005 Feb;12(2):139-43.

Association between Helicobacter pylori infection and acute inflammatory demyelinating polyradiculoneuropathy.

Author information

  • 1Department of Gastroenterology, Second Medical Clinic, Aristotle University of Thessaloniki, 8 Fanariou Street, Byzantio, 551 33 Thessaloniki, Macedonia, Greece. jannis@med.auth.gr

Abstract

The aim of this study was to investigate a possible association between Helicobacter pylori infection and acute inflammatory demyelinating polyradiculoneuropathy (AIDP). Of 17 consecutive patients with Guillain-Barre syndrome (GBS), 13 patients (six females; mean age 50 +/- 24 years) with AIDP were investigated. Clinical status was evaluated according to Hughes' score, and electrophysiological tests were performed within 2 weeks from disease onset. Helicobacter pylori infection was detected histologically and serum H. pylori-specific IgG antibodies were analysed by ELISA. Twenty asymptomatic patients (12 females; mean age 63 +/- 8 years), undergoing upper gastrointestinal endoscopy for investigation of mild iron deficiency anaemia, served as controls. Helicobacter pylori was found in 12 of 13 AIDP patients (92%), and in 10 of 20 controls (50%), (P = 0.02). Electrophysiological studies showed demyelination in all AIDP patients. High levels of anti-H. pylori IgG antibodies correlated with advanced clinical status. Five of seven AIDP patients with high levels of anti-H. pylori IgG antibodies had delayed F-wave latencies, indicating affection of proximal segments of peripheral nerves. Helicobacter pylori infection seems to be more frequent in AIDP patients. Anti-H. pylori titre might reflect advanced clinical status. Anti-H. pylori IgG antibodies are also associated with involvement of the proximal parts of peripheral nerves in AIDP.

PMID:
15679702
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk