# Blood Lipid Levels and the Severity of Guillain–Barré Syndrome: A Single-Center Retrospective Cohort Study

## TL;DR

This study found that high LDL cholesterol and low ApoA levels are linked to more severe Guillain–Barré syndrome and cranial nerve involvement.

## Contribution

The study identifies LDL and ApoA as independent predictors of GBS severity and cranial nerve involvement.

## Key findings

- Each 1 mmol/L increase in LDL raises severe GBS risk by 2.5-fold.
- ApoA levels below 1.071 g/L are associated with milder disease.
- LDL ≥ 2.355 mmol/L increases cranial nerve involvement risk.

## Abstract

Objective: To investigate the association between lipid profiles and disease severity/cranial nerve involvement in Guillain–Barré syndrome (GBS), providing evidence for early clinical intervention.

Methods: This retrospective study enrolled 182 GBS patients (148 males and 34 females) admitted to the First Affiliated Hospital of Shihezi University from December 2019 to April 2024. Patients were stratified into mild (Hughes Functional Disability Scale [HFDS] 1–3) and severe (HFDS 4–6) groups. Multivariate logistic regression (adjusted for age, sex, and antecedent infections) was used to analyze independent associations of low-density lipoprotein cholesterol (LDL-C) and apolipoprotein A (ApoA) with disease severity and cranial nerve involvement. ROC curve analysis determined predictive thresholds.

Results: Disease severity: each 1 mmol/L increase in LDL elevated severe disease risk by 2.5-fold (OR = 2.503, p=0.009) and each 0.1 g/L decrease in ApoA reduced severe disease risk by 99.6% (OR = 0.004, p < 0.001). Cranial nerve involvement: LDL ≥ 2.355 mmol/L significantly increased cranial nerve involvement risk (OR = 1.925, p=0.018). Predictive thresholds: LDL ≥ 2.215 mmol/L optimally predicted severe disease and ApoA ≤ 1.071 g/L indicated higher probability of mild disease.

Conclusion: Elevated LDL and reduced ApoA are independent risk factors for GBS progression and cranial nerve involvement. Combined detection may aid early identification of high-risk patients. Dyslipidemia likely exacerbates GBS pathology through neuroinflammatory mechanisms, suggesting targeted lipid regulation as a potential therapeutic strategy.