Association of mannose-binding lectin 2 gene polymorphisms with Guillain-Barré syndrome

Abstract

Complement activation plays a critical role in the pathogenesis of Guillain-Barré syndrome (GBS), a debilitating immune-mediated neuropathy. Mannose-binding lectin (MBL) is a complement activation factor of lectin pathway which as genetic host factor may influence the susceptibility or severity of GBS. We investigated the frequency of MBL2 promoter (− 550H/L and − 221X/Y) and functional region (exon 1 A/O) polymorphisms and their association with disease susceptibility, clinical features and serum MBL among GBS patients (n = 300) and healthy controls (n = 300) in Bangladesh. The median patient age was 30 years (IQR: 18–42; males, 68%). MBL2 polymorphisms were not significantly associated with GBS susceptibility compared to healthy controls. HL heterozygosity in GBS patients was significantly associated with mild functional disability at enrolment (P = 0.0145, OR, 95% CI 2.1, 1.17–3.82). The HY, YA, HA and HYA heterozygous haplotypes were more common among mildly affected (P = 0.0067, P = 0.0086, P = 0.0075, P = 0.0032, respectively) than severely affected patients with GBS. Reduced serum MBL was significantly associated with the LL, OO and no HYA variants and GBS disease severity. No significant association was observed between MBL2 polymorphisms and electrophysiological variants, recent Campylobacter jejuni infection or anti-ganglioside (GM1) antibody responses in GBS. In conclusion, MBL2 gene polymorphisms are related to reduced serum MBL and associated with the severity of GBS.

Neutrophil‐lymphocyte ratio in Guillain‐Barré syndrome: A prognostic biomarker of severe disease and mechanical ventilation in Bangladesh

“…Disease severity was assessed using the GBS‐DS at enrolment; patients able to walk independently with a GBS‐DS < 3 were considered mildly affected and patients unable to walk independently with a GBS‐DS of ≥ 3, severely affected 25 . Short‐term disease outcome was assessed using the GBS‐DS at 4 weeks and long‐term disease outcomes were assessed using the GBS‐DS at 13 weeks and 26 weeks 22 ; a GBS‐DS ≥3 at follow‐up was defined as poor prognosis 25 .…”

“…Disease severity was assessed using the GBS‐DS at enrolment; patients able to walk independently with a GBS‐DS < 3 were considered mildly affected and patients unable to walk independently with a GBS‐DS of ≥ 3, severely affected 25 . Short‐term disease outcome was assessed using the GBS‐DS at 4 weeks and long‐term disease outcomes were assessed using the GBS‐DS at 13 weeks and 26 weeks 22 ; a GBS‐DS ≥3 at follow‐up was defined as poor prognosis 25 . Patients with respiratory distress and other minor complications including atelectasis, severe bulbar dysfunction, unable to clear bronchial secretions or unable to cough received MV at the discretion of the consultant/neurologist at the hospital in charge of the patient 26 .…”

“…25 Short-term disease outcome was assessed using the GBS-DS at 4 weeks and long-term disease outcomes were assessed using the GBS-DS at 13 weeks and 26 weeks 22 ; a GBS-DS ≥3 at follow-up was defined as poor prognosis. 25 Patients with respiratory distress and other minor complications including atelectasis, severe bulbar dysfunction, unable to clear bronchial secretions or unable to cough received MV at the discretion of the consultant/neurologist at the hospital in charge of the patient. 26 A GBS-DS of 5 during or within 7 days of enrolment to the study was classified as MV.…”

Interleukin‐10 promoter polymorphisms and haplotypes in patients with Guillain–Barré syndrome

“…Strain properties and host properties are both crucial in determining the risk of developing GBS 8 . Host factors and their genetic predisposition to GBS is very important to decipher their role in GBS pathogenesis as well as disease progression and severity 9–11 . Therefore, the serum IL‐10 level and polymorphisms in it may be potential decider here.…”