Neuropediatrics 2016; 47(03): 151-156
DOI: 10.1055/s-0036-1579633
Original Article
Georg Thieme Verlag KG Stuttgart · New York

Polymorphisms of Immunoglobulin G Fc Receptors in Pediatric Guillain–Barré Syndrome

Authors

  • Lobna A. Mansour

    1   Department of Pediatrics, Faculty of Medicine, Cairo University, Cairo, Egypt
  • Marian Y. Girgis

    1   Department of Pediatrics, Faculty of Medicine, Cairo University, Cairo, Egypt
  • Mohamed Abdulhay

    2   Egypt Children Hospital, Cairo, Egypt
  • Ehab I. Abou ElEinein

    3   Department of Rheumatology and Rehabilitation, Faculty of Medicine, Cairo University, Cairo, Egypt
  • Rabab ElHawary

    4   Department of Clinical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt
  • Mariam Onsy F. Hanna

    4   Department of Clinical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt
Further Information

Publication History

10 October 2015

27 January 2016

Publication Date:
11 April 2016 (online)

Abstract

Introduction Guillain–Barré syndrome (GBS) is an autoimmune peripheral neuropathy characterized by demyelination and axonal damage. Biallelic functional polymorphisms in the immunoglobulin G Fc receptors (FcγR)–FcγRIIA: H131/R131, FcγRIIIA: V158/F158, and FcγRIIIB: NA1/NA2 affect the affinity of the IgG–FcγR interaction, therefore, diseases such as GBS in which this interaction plays a critical role might be influenced by the polymorphisms.

Methods We evaluated the role of FcγR polymorphisms in susceptibility to GBS in Egyptian pediatric patients and the association of the variant alleles with neurophysiological types, severity, and outcome of the disease. A total of 50 patients with GBS and 50 controls were examined for FcγR polymorphisms by allele-specific polymerase chain reaction.

Results FcγRIIA H131 allele (p = < 0.0001; odds ratio [OR] = 4.78; 95% confidence interval [CI], 2.62–8.70) and FcγRIIA H/H131 genotype (p = < 0.0001 ; OR = 10.56; 95% CI, 3.59–31.06) were significantly increased in GBS patients while FcγRIIIA and FcγRIIIB allelic distributions were similar among patients and controls. The FcγR genotypes showed no association with neurophysiological types of GBS, severity or outcome of the disease.

Conclusions These findings reflect that FcγRIIA H131 allele may represent a risk marker for susceptibility to GBS.