CD is an autoimmune-mediated inflammatory disorder of the small bowel; it is triggered by gliadin, which is a gluten protein found in wheat, barley, and rye.
Celiac's disease is also referred to as gluten-induced enteropathy, non-tropical sprue, and celiac sprue.
Celiac's disease affects 1% of US adults.
To screen for celiac's disease we can use serological markers: IgA anti-tissue transglutaminase (tTG-IgA, tTG-IgG), deamidated gliadin peptide antibodies, and anti-endomysial antibodies (EMA-IgA).
Serological screening can suggest, but not diagnose, celiac's disease.
Diagnosis requires endoscopy with small bowel biopsy.
We look for histologic changes concurrent with gluten-containing diet and clinically significant improvement when the gluten-containing diet is stopped.
On gross inspection, we see "scalloping" of the duodenal folds and increased vascularity.
Scalloping is not specific to celiac's disease, but reflects the villous atrophy and edema of duodenal injury.
Celiac's disease histopathology is characterized by increased lymphocytes, mucosal inflammation, villous atrophy, and crypt hyperplasia upon exposure to gluten, all of which diminish when gluten is removed from the diet.
Genetic markers include haplotypes HLA-DQ2 and HLA-DQ8 (which are common in the general population, so are only useful for ruling out Celiac's disease).
Other common associations include dermatitis herpetiformis (approximately 10% of patients with CD), reduced bone density due to calcium deficiency, and increased risk of malignancy.