Dysimmune Neuropathy: An Underinvestigated Cause of Dry Eye Disease?

Abstract

Purpose : The role of inflammation and neurosensory abnormalities in dry eye disease (DED) has been defined by dry eye workshop II report. The etiologic role of autoimmune diseases, such as Sjögren’s syndrome, mixed connective tissue diseases, sarcoidosis, and related nerve loss has been established in DED. However, dysimmune neuropathies, which are caused by specific autoantibodies (Abs) against peripheral nerve axons and myelin have not been investigated. Therefore, our purpose was to evaluate the potential systemic etiologies in DED, by assessing serological Abs used for dysimmune neuropathies as well as autoimmune diseases.

Methods : Patients with moderate to severe DED (n=37) underwent serological testing for inflammatory (ESR, CRP), autoimmune, and dysimmune neuropathy Abs (anti-TSHDS, anti-FGFR3, anti-sulfatide IgM, anti-Histone H3, Anti-GD1a).

Results : At least one abnormal result was detected in 24 patients (64.8%) with 54.0% showing at least one positive dysimmune neuropathy Ab. Anti-TS-HDS and anti-FGFR3 were positive in 48.6% and 21.6% of patients, respectively. Acute inflammation markers ESR and CRP were positive in 24.3% and 16.2%, respectively. ANA was positive in 32.4% of patients. SS-A (13.5%) and SS-B (13.5%) were the most common disease specific autoimmune Abs followed by RF (5.4%). At least one positive Celiac Ab (anti-gliadin IgA, IgG, tissue transglutaminase IgA, IgG) was detected in 2.7% of patients.

Conclusions : Our findings suggest that dysimmune neuropathy may play a crucial role in DED etiology. Detailed serological evaluation detects higher positivity rates for dysimmune neuropathy Abs compared to well-known systemic etiologies, such as Sjögren’s syndrome and rheumatoid arthritis Abs, suggesting that neurosensorial abnormalities need further investigation in the course of DED.

This is a 2021 ARVO Annual Meeting abstract.