Our pooled data indicated that TNF-α 308G/A polymorphism was significantly associated with GBS, AMAN, and AMSAN but not with AIDP; TNF-α857C/T polymorphism was significantly associated with AMAN but not with GBS or AIDP.
Variant genotype T/T of TNF-alpha -857 C>T polymorphism was also significantly associated with acute motor axonal neuropathy (p = 0.034; OR = 3.93, 95% CI = 1.11-13.91).
The serum levels of CXCL13 were also higher in inflammatory demyelinating neuropathic patients but not in acute motor axonal neuropathy or a hereditary demyelinating neuropathy, Charcot-Marie-Tooth disease type 1a.
Three differentially expressed proteins were identified, including the upregulated haptoglobin (Hp) and heat shock protein 70 (Hsp70), and downregulated cystatin C. There were no significant differences between the AIDP and AMAN patients in the positive rates and quantitative expression levels of the three differentially expressed proteins.
Three differentially expressed proteins were identified, including the upregulated haptoglobin (Hp) and heat shock protein 70 (Hsp70), and downregulated cystatin C. There were no significant differences between the AIDP and AMAN patients in the positive rates and quantitative expression levels of the three differentially expressed proteins.
Hp and Hsp70 are significantly increased, and cystatin C is downregulated in CSF of GBS patients, which provides important biomarkers for early GBS diagnosis, although these proteins cannot distinguish AIDP and AMAN.
Serum IL-27 concentrations were elevated (p=0.002) whereas serum IL-35 concentrations were decreased (p=0.031) in patients with GBS comparing with healthy controls, particularly in patients exhibiting AMAN (p=0.012).
Serum IL-27 concentrations were elevated (p=0.002) whereas serum IL-35 concentrations were decreased (p=0.031) in patients with GBS comparing with healthy controls, particularly in patients exhibiting AMAN (p=0.012).
Serum IL-27 concentrations were elevated (p=0.002) whereas serum IL-35 concentrations were decreased (p=0.031) in patients with GBS comparing with healthy controls, particularly in patients exhibiting AMAN (p=0.012).
Homozygous genotype (Lys/Lys) of NOD1 was significantly associated with GBS (p=0.013); and its subtypes viz. acute motor axonal neuropathy (AMAN) and acute inflammatory demyelinating polyneuropathy (AIDP) (p=0.008 and p=0.024 respectively) than controls.
In NOD2 (Arg702Trp and Gly908Arg) polymorphisms, only heterozygous genotype (Arg/Trp and Gly/Arg) showed significant association with GBS (p=0.001 and p=0.01 respectively); subtypes AMAN, acute motor-sensory axonal neuropathy (AMSAN) and AIDP showed association with heterozygote Arg702Trp (p=0.001; p=0.029 and p=0.001 respectively) whereas only AIDP was associated with heterozygote genotype Gly908Arg (p=0.003).
The results showed enhanced IL-12, IL-12R1 in AIDP and TNF-alpha in AMAN during the acute phase, as well as increased TNF-alpha and TNFR1 during the plateau phase of AIDP.