Cholinesterase and Inflammation: Exploring Its Role and Associations with Inflammatory Markers in Patients with Lower

Maximilian Mitteregger1,2, Sabine Steiner1, Andrea Willfort-Ehringer1

  • 1Department of Internal Medicine II, Division of Angiology, Medical University of Vienna, 1090 Vienna, Austria.

Biomedicines
|April 29, 2025
PubMed

Insights

Serum cholinesterase (ChE) levels correlate with inflammation in lower extremity artery disease (LEAD). Lower ChE indicates higher inflammation, especially in critical ischemia, suggesting ChE as a potential biomarker for LEAD severity.

Area of Science:

  • Vascular Medicine
  • Inflammation Research
  • Biomarker Discovery

Background:

  • Inflammation is a key factor in atherosclerotic diseases like lower extremity artery disease (LEAD).
  • Serum cholinesterase (ChE) influences cardiovascular health and modulates inflammatory responses.

Purpose of the Study:

  • To examine the association between serum ChE levels and inflammatory markers in patients with hemodynamically significant iliac artery stenosis.
  • To assess the role of ChE in the inflammatory processes underlying LEAD.

Main Methods:

  • Retrospective analysis of 150 patients with iliac artery stenosis (δPSV ≥ 1.4 m/s).
  • Investigated ChE relationship with neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), hemoglobin-to-platelet ratio (HPR), and other parameters.

Main Results:

  • Significant difference in ChE levels between stable claudication and critical ischemia (7.76 mg/dL vs. 6.77 mg/dL, p = 0.004).
  • Inverse correlation between ChE and NLR (r = -0.303, p < 0.001) and PLR (r = -0.162, p = 0.049).
  • Positive correlation between ChE and body mass index (BMI) (r = 0.298, p < 0.001).

Conclusions:

  • Findings suggest active inflammation in LEAD, particularly in critical ischemia.
  • Serum ChE may serve as a potential biomarker for inflammation in LEAD, differentiating disease severity.
  • Further research is warranted to explore ChE's role in cholinergic regulation of inflammation in LEAD.

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