Human Leukocyte Antigen DQB1 (HLA-DQB1) Polymorphisms and the Risk for Guillain-Barré Syndrome: A Systematic Review and Meta-Analysis.

Peng-Peng Jin,Li-Juan Liu,Gang Zhao,Bo-Jun Ding,Li-Li Sun,Xue-Dong Liu,Feng Xia,Bin Zhou,Li Li,Yan-Chun Deng,Wen Wang,Na Qin,Shuang-Xing Hou,Ralf Andreas Linker

doi:10.1371/journal.pone.0131374

Abstract

Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system. There is no consensus regarding reported associations between human leukocyte antigen DQB1 (HLA-DQB1) polymorphisms and the risk for developing GBS. Here, we evaluated possible associations between HLA-DQB1 polymorphisms and the risk for GBS using a meta-analysis. We searched PubMed for case-control genetic association studies for HLA-DQB1 polymorphisms (*020x, *030x, *040x, *050x, and *060x) and the risk for GBS. Fixed-effect meta-analytical methods were used for the outcome measure and subgroup analyses. Estimated odds ratios (ORs) and 95% confidence intervals (CIs) were used to investigate the associations between HLA-DQB1 polymorphisms and the risk for GBS. Nine case-control studies involving 780 cases of GBS and 1353 controls were identified in the current study. The meta-analysis demonstrated no significant associations between HLA-DQB1 polymorphisms and the risk for GBS in Asian and Caucasian populations. There were two associations that approached significance: HLA-DQB1*030x in Asian patients (P = 0.07; OR: 0.76, 95% CI: 0.57–1.03) and HLA-DQB1*060x in all patients (P = 0.08; OR: 1.48, 95% CI: 0.96–2.29). Additional studies with larger sample sizes are required to establish a definitive assessment of the contribution of HLA-DQB1 polymorphisms to GBS risk.

Highlights

Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system
GBS is a heterogeneous disorder with several subtypes, including acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [1]
We conducted a systematic search of PubMed (1950–December, 2014) using the following key words: “Human leukocyte antigenÃ” odds ratios (ORs) “HLAÃ” AND “allele” OR “polymorphism” OR “genotype” AND “Guillain-Barré syndrome” OR “acute infiammatory demyelinating polyneuropathy” OR “acute motor axonal neuropathy” OR “acute motor sensory axonal neuropathy.”

Summary

Introduction

Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system. GBS is initiated by an abnormal response to an infectious pathogen and is characterized by progressive flaccid paralysis and loss of reflexes. GBS is a heterogeneous disorder with several subtypes, including acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [1]. The prevalence of the subtypes varies regionally; AIDP is the most common subtype in the West, while AMAN and AMSAN are more common in Asia [2]. Infections including Cytomegalovirus, Epstein-Barr virus, and Campylobacter jejuni have all been linked to GBS [1,2]. C. jejuni infection is the most common infectious trigger and is present in 25–40% of GBS cases [2]. The rarity of GBS cases, even in patients with C. jejuni, suggests that other factors determine whether a patient will develop GBS following infection

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