It is genetically conditioned wrong answer to grain protein – gluten, which leads to the damage of intestinal villi. This leads to malabsorption of nutrients. When gluten is withdrawn from the diet, regeneration of intestinal mucosa takes place and symptoms recede. The celiac disease is present in countries where grains containing gluten, that is wheat, rye and barley, are basic part of diet.

The disease may assume various shapes.

1. Classic form – known the most, with full clinical symptoms and atrophic changes in mucous membrane. Typical symptoms include diarrhoea, weight loss in children, loss of appetite or stunted growth
2. Mute form – when the condition’s symptoms are very discreet, often outside the alimentary canal, for instance anaemia, tooth enamel problems and emotional disorders
3. Latent form – present in persons with genetic predisposition to the condition, who do not show any clinical symptoms at the time of examination, but the symptoms either were present in the past, or will be present in the future, along with changes in small intestine mucous membrane. Coeliac disease serologic markers are found to be present in such cases
4. Potential form – genetic predisposition to the condition

The classic form of the disease is observed in Poland on the average at the frequency of 1:1500 (in Europe 1:1000), and the mute form – 1:130-500. The clinical symptoms of Coeliac disease can occur at any age, after varied period of exposition to gluten. The occurrence of symptoms is delayed if the infant is breast-fed for a long time, whereas early introduction of gluten to diet may advance it. Nowadays the coeliac disease most often is diagnosed at the pre-school and school age, more seldom before the second birthday, as it happened in former times. Infection or another disease, such as diabetes, may be causative factors of the symptoms occurrence.

The coeliac disease can be diagnosed on the basis of clinical symptoms, blood tests – serologic coeliac disease markers, and biopsy of the small intestine mucous membrane.

The coeliac disease serologic markers, most often used in diagnostics, are as follows:

1. Anti-endomysium (EMA) antibodies – routinely denoted in class IgA, in persons with IgA deficiency in class IgG
2. Tissue transglutaminase (tTG) antibodies
3. Biopsy of small intestine and histopathology examination of specimen are NECESSARY for the diagnosis

Diet cannot be introduced if this examination has not been conducted.

Specimen are taken from duodenum, currently most often during endoscopy. The only effective treatment is a lifelong gluten-free diet (according to the present state of knowledge). This requires products containing wheat, barley, rye and oats to be excluded from the diet. Corn, rice, soybean, buckwheat, millet, potato flour, tapioca, amaranth and such products that contain not more than 20 mg gluten per kilogram, such as gluten-free wheat starch, are regarded to be naturally gluten-free products.

Gluten-free products are marked with a crossed out ear of corn.

EmA and tTG serological markers are used to monitor the adherence to gluten-free diet.

Complications resulting from non-adherence to diet:

1. Infertility
2. Osteoporosis and osteomalacia
3. Alimentary canal (small intestine and gullet) tumour