Coeliac disease is an autoimmune condition where exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel.

Gluten is the entire protein content of the cereals wheat, barley and rye.

Epidemiology:

• Affects up to 1% of the general population, though most have clinicaly silent disease
• It usually develops in early childhood but can start at any age.

Pathophysiology

Gliadin (in gluten) normally bound to IgA in muscularis mucosae layer of GI tract, allowing it to be eliminated - in coeliac disease it resides in Lamina Propria(more superficial).

Autoantibodies are created in response to exposure to gluten, these cause inflammation of the epithelum of the small intestine:

• anti-tissue transglutaminase (anti-TTG)
• anti-endomysial (anti-EMA)

These antibodies relate to disease activity and will rise with more active disease and may disappear with effective treatment.

The mucosa of the proximal small bowel is predominantly affected, the mucosal damage decreasing in severity towards the ileum as gluten is digested into smaller ‘non-toxic’ fragments.

Upon repair ➡️  Villous trophy and flatten ➡️  decreased surface area for digestion = malabsorption

Genetic Associations:

• HLA-DQ2 gene (90%)
• HLA-DQ8 gene

Autoimmune Associations: