Duodenal secretomotor function in untreated coeliac disease

Area of Science:

• Gastroenterology
• Epithelial Physiology
• Coeliac Disease Pathophysiology

Background:

• Coeliac disease is an autoimmune disorder triggered by gluten ingestion.
• It primarily affects the small intestine, leading to villous atrophy and crypt hyperplasia.
• Epithelial transport alterations in the distal duodenum are not well-characterized in untreated coeliac disease.

Purpose of the Study:

• To investigate the epithelial transport properties of the distal duodenal mucosa in individuals with untreated coeliac disease.
• To compare fluid and bicarbonate transport, and electrogenic anion secretion between coeliac patients and healthy controls.
• To explore the relationship between epithelial transport and interdigestive motility.

Main Methods:

• Utilized a triple-lumen perfusion technique to measure net fluid and bicarbonate transport in 20 coeliac patients and 22 healthy controls.
• Recorded interdigestive motility using manometry.
• Measured transmural potential difference (PD) as an indicator of electrogenic anion secretion.

Main Results:

• Patients with untreated coeliac disease exhibited net fluid secretion (-1.04 mL/min x 10 cm) compared to controls (0.12 mL/min x 10 cm; p < 0.01).
• No significant net bicarbonate absorption was observed in coeliac patients (5.6 mumol/min x 10 cm) versus controls (27.5 mumol/min x 10 cm; p < 0.001).
• Epithelial transport varied with motility; a secretory shift occurred during phase II of the migrating motor complex (MMC), with a significantly lumen-negative PD (p < 0.001).

Conclusions:

• Untreated coeliac disease is associated with enhanced active chloride secretion and reduced Na+/H+ exchange in the distal duodenum.
• The remodelled duodenal mucosa retains responsiveness to neurogenic stimuli, evidenced by MMC-related changes in secretion.
• These findings suggest potential therapeutic targets related to ion transport and neurogenic regulation in coeliac disease.