Coeliac disease (CD)
Coeliac disease is an autoimmune disease triggered by an abnormal immune response to gluten. Gliadin, one of the two proteins which form gluten, is the toxic component in coeliac disease initiating immune activation. The inflammatory damage primarily affects the small intestine, with intra-epithelial lymphocytosis, crypt hyperplasia and villous atrophy. Systemic manifestations of coeliac disease include fatigue, weight loss, diarrhoea, anaemia, osteoporosis and depression. Pathological changes are ultimately reversed after gluten withdrawal from the diet. However, complete recovery of structure and function may take several years after gluten withdrawal. An estimated 1% of Western populations are affected by CD.
Non-coeliac gluten sensitivity (NCGS)
Non- coeliac gluten sensitivity has more recently been recognised as a clinical entity, occurring in 6% of the population. NCGS is a condition that is neither autoimmune nor allergic, yet leads to subjective symptoms similar to those seen in coeliac disease when gluten is consumed. The condition is characterised by negative antibodies (except, perhaps to gliadin) and normal intestinal mucosal histology. The cardinal sign is the clinical improvement of symptoms on a gluten-free diet in the absence of antibodies and intestinal mucosal abnormalities.
Wheat allergy is a less common condition than CD and NCGS, affecting around 0.1% of the population. It is characterised by an IgE-mediated reaction to gliadins. Unlike CD, patients with wheat allergy usually do not need to restrict other gluten-containing grains, such as rye, barley, and oats from their diet. The symptoms of wheat allergy are typical of those of an IgE-mediated reaction, with more immediate reactions than CD and NCGS of acute swelling of the face,skin, respiratory and gastrointestinal tract.