RT Journal Article
SR Electronic
T1 Diabetes Mellitus Is a Possible Risk Factor for Nodo-paranodopathy With Antiparanodal Autoantibodies
JF Neurology - Neuroimmunology Neuroinflammation
JO Neurol Neuroimmunol Neuroinflamm
FD Lippincott Williams & Wilkins
SP e1163
DO 10.1212/NXI.0000000000001163
VO 9
IS 3
A1 Luise Appeltshauser
A1 Julia Messinger
A1 Katharina Starz
A1 David Heinrich
A1 Anna-Michelle Brunder
A1 Helena Stengel
A1 Bianca Fiebig
A1 Ilya Ayzenberg
A1 Frank Birklein
A1 Christian Dresel
A1 Johannes Dorst
A1 Florian Dvorak
A1 Alexander Grimm
A1 Alexander Joerk
A1 Frank Leypoldt
A1 Mathias Mäurer
A1 Patrick Merl
A1 Sebastian Michels
A1 Kalliopi Pitarokoili
A1 Mathias Rosenfeldt
A1 Anne-Dorte Sperfeld
A1 Marc Weihrauch
A1 Gabriel Simon Welte
A1 Claudia Sommer
A1 Kathrin Doppler
YR 2022
UL http://nn.neurology.org/content/9/3/e1163.abstract
AB Background and Objectives Nodo-paranodopathies are peripheral neuropathies with dysfunction of the node of Ranvier. Affected patients who are seropositive for antibodies against adhesion molecules like contactin-1 and neurofascin show distinct clinical features and a disruption of the paranodal complex. An axoglial dysjunction is also a characteristic finding of diabetic neuropathy. Here, we aim to investigate a possible association of antibody-mediated nodo-paranodopathy and diabetes mellitus (DM).Methods We retrospectively analyzed clinical data of 227 patients with chronic inflammatory demyelinating polyradiculoneuropathy and Guillain-Barré syndrome from multiple centers in Germany who had undergone diagnostic testing for antiparanodal antibodies targeting neurofascin-155, pan-neurofascin, contactin-1–associated protein 1, and contactin-1. To study possible direct pathogenic effects of antiparanodal antibodies, we performed immunofluorescence binding assays on human pancreatic tissue sections.Results The frequency of DM was 33.3% in seropositive patients and thus higher compared with seronegative patients (14.1%, OR = 3.04, 95% CI = 1.31–6.80). The relative risk of DM in seropositive patients was 3.4-fold higher compared with the general German population. Seropositive patients with DM most frequently harbored anti–contactin-1 antibodies and had higher antibody titers than seropositive patients without DM. The diagnosis of DM preceded the onset of neuropathy in seropositive patients. No immunoreactivity of antiparanodal antibodies against pancreatic tissue was detected.Discussion We report an association of nodo-paranodopathy and DM. Our results suggest that DM may be a potential risk factor for predisposing to developing nodo-paranodopathy and argue against DM being induced by the autoantibodies. Our findings set the basis for further research investigating underlying immunopathogenetic connections.Caspr-1=contactin-1–associated protein 1; CIDP=chronic inflammatory demyelinating polyradiculoneuropathy; DM=diabetes mellitus; GAD=glutamate decarboxylase; GBS=Guillain-Barré syndrome; HbA1c=hemoglobin A1c; Ig=immunoglobulin; PE=plasma exchange