Celiac disease (from the Classical Greek: koiliakòs - who has got a stomachache) also known as gluten-sensitive enteropathy or celiac sprue, is defined as a permanent intolerance to ingested gluten (storage protein component of gluten contained especially in wheat flour, barley and rye).

The intolerance to gluten results in immune-mediated damage to the mucosa of the small intestine characteristically inducing villous atrophy and crypt hyperplasia that can be solved with the removal of gluten from the diet.

Although celiac disease is defined by the small intestine injury and resulting malabsorption, more recently it has been recognized to be a multisystem disorder that may affect other organs, such as the nervous system, bones, skin, heart, and the liver.

Celiac disease is now known to affect about 1% of the population.

The clinical presentation of celiac disease can vary from a classical malabsorption syndrome to more subtle atypical gastrointestinal manifestations or extraintestinal presentations (infertility, osteoporosis, and iron-deficiency anaemia).

Celiac disease can be clinically silent, often detected by serologic screening of those subjects at risk, with villous atrophy in the intestine.

Finally, an individual may have a latent predisposition to celiac disease, which is defined by a positive serology in the absence of villous atrophy on the small intestine.

There isn’t a therapy for celiac patients.
Celiac disease requires an appropriate approach to manage a permanent gluten-free diet and to cope the psychological and social consequences that this diet comports.