Assessment of Endothelial Dysfunction With Adhesion Molecules in Patients With Celiac Disease

Atakan Comba1, Gönül Çaltepe, Keramettin Yank

  • 1*Department of Pediatric Gastroenterology, Hepatology and Nutrition †Department of Microbiology and Parasitology ‡Department of Biochemistry, Ondokuz Mayıs University Faculty of Medicine, Samsun, Turkey.

Insights

Elevated adhesion molecules in celiac disease (CD) indicate endothelial dysfunction. A strict gluten-free diet significantly lowers these markers, suggesting dietary management can mitigate CD-related risks.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Gastroenterology

Background:

  • Celiac disease (CD) is a systemic immune disorder with potential links to endothelial dysfunction.
  • Adhesion molecules are key indicators of endothelial health and inflammation.

Purpose of the Study:

  • To evaluate serum levels of adhesion molecules as markers of endothelial dysfunction in newly diagnosed CD patients and those adhering to a gluten-free diet.
  • To investigate the impact of a gluten-free diet on these markers.

Main Methods:

  • A prospective, case-controlled study involving 65 newly diagnosed CD patients and 51 controls.
  • Measurement of serum levels for vascular adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, vascular endothelial cadherin, high-sensitivity C-reactive protein, and homocysteine.

Main Results:

  • Newly diagnosed CD patients exhibited significantly higher levels of soluble vascular adhesion molecule-1, soluble intercellular adhesion molecule-1, and soluble endothelial selectin compared to controls.
  • Patients with CD fully compliant with a gluten-free diet showed significantly lower levels of soluble vascular adhesion molecule-1 and soluble endothelial selectin compared to newly diagnosed patients.

Conclusions:

  • Elevated serum adhesion molecule levels are associated with celiac disease, indicating endothelial dysfunction.
  • Adherence to a gluten-free diet can reduce the risks associated with endothelial dysfunction in CD patients.
Abstract