# Glycolipid Antibodies in Patients With Chronic Idiopathic Axonal Polyneuropathy and Gluten Neuropathy

## TL;DR

This study found that patients with chronic idiopathic axonal polyneuropathy and gluten neuropathy have higher levels of antibodies against nerve glycolipids, suggesting an autoimmune cause.

## Contribution

The first study to report increased antibody detection rates against peripheral nerve glycolipids in these patient groups using a new microarray technique.

## Key findings

- CIAP and GN patients showed higher IgM antibody positivity against glycolipid complexes compared to controls.
- GN patients had higher IgM positivity against the GM2:GT1b complex than CIAP patients.
- IgG antibodies against specific glycolipid complexes were more prevalent in both patient groups than in controls.

## Abstract

To evaluate the presence of IgM and IgG antibodies in the serum of patients with chronic idiopathic axonal polyneuropathy (CIAP) and gluten neuropathy (GN) using a newly developed microarray technique.

Sera from 42 CIAP patients, 32 GN patients, and 79 healthy controls were tested for IgM and IgG antibodies against 16 single glycolipids and their 120 heteromeric complexes. Positivity rates were analyzed using the 95th percentile from controls.

IgM positivity against 8 heteromeric complexes was more frequent in CIAP patients (16.7% to 28.6%) compared to controls, while GN patients showed higher rates (18.8% to 46.9%) across 15 complexes. GN patients had a higher rate of IgM positivity against the GM2:GT1b complex than CIAP patients (46.9% vs. 21.4%). IgG antibodies against seven antigens were also more prevalent in CIAP (16.7% to 26.2%) and GN patients (18.8% to 28.1%) than controls. GN patients showed a higher rate of IgG positivity against the GM1:Sulfatide complex than CIAP patients (15.6% vs. 0%).

This is the first study to report increased antibody detection rates against peripheral nerve glycolipids, both individually and in complexes. The findings suggest that a significant proportion of CIAP and GN patients may have an autoimmune pathogenesis, potentially targetable by immunotherapy.