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Our project is about celiac disease, this is a enteropathy, autoimmune affecting individuals who possess genes HLA-DQ8 or HLA-DQ2, where T cells attack the body when the gliadins and glutenins are absorbed by the small intestine, in others words, celiac patients have a permanent intolerance to gluten-containing foods.

A strict diet throughout life gluten-free allows to the small intestine get health. Obvious sources of gluten are bread, many cereals for breakfast, pasta, pizza, cakes and biscuits. The gluten can also be used to give structure to the food products, such as sausages, stock cubes, soups and sauces. Naturally the gluten-free foods include meat, fish, eggs, fruits, vegetables, dairy products, beans, potatoes, rice, corn, quinoa and buckwheat. Food substitutes as the especially gluten-free bread, flour, pasta and biscuits, have increased in recent years in variety and are available by prescription in some countries.

But what makes this a problem?, well the problem is the cost of this diet, which often are priced high in gluten-free foods, besides the clear deprivation the patient celiac without meals as common as pizza, and even drinks such as beer. So we think of a way to solve the gap between celiac patients and those persons without eating disorders, but without forgetting the price, therefore, we also consider the low cost of production and, like that, was born the idea of creating a pill that is able to degrade gluten before its contact with the enterocytes.

When the gluten enter in contact with the villi of the small intestine (enterocytes) the helper T cells (type of reporter) detects the gluten as a toxic substance and leaves a chemical trail, which is followed by antibodies, among the more important the Transglutaminase and the Antigliadin (in this case); In addition to the lymphocytes T and B. The first ( lymphocytes T) would be the natural killers and an army of these cells will attack to the infected cells, which could cause a cancerous effect, in this case the dangerous cells are the enterocytes, and after of the atack they could causing inflammation, poor absorption, and other symptoms. But does not stop there the auto-immune action, also the B cells serves as a kind of memory which is used to the next time that the threat enter in the body, the reply will be more quickly and efficiently.

The damage caused by the autoimmune reaction can cause histological damage in the villi, and a biopsy of these is the means of diagnosis of this pathology. The only current treatment is a diet without gluten, which is expensive and difficult to follow.

This is the tip of the iceberg of celiac disease, the symptoms as are easy to diagnose, but there are other four ways where the symptoms are not so clear. These forms are:

Silent Celiac Disease: Patients have no symptoms but if damage histological.
Latent Celiac Disease: There are not symptoms and stunted villi. Individuals tend to develop the disease suddenly.
Potential Celiac Disease: Are subjects with high genetic risk that could have the disease.
Refractory Celiac Disease: Those patients diagnosted celiac and despite follow a diet without gluten doesn't improve and can get diseases even more serious.

The celiac disease are associated with many diseases, these can also be complications of refractory patients. But is important know the variety of diseases that can produces by de celiac disease:

- Food intolerance problems.
- Variety of cancers.
- Diseases related to the nervous system.
- Diseases related to the circulatory system.
- Skin-related illnesses.

Statistics

In our country Chile, the statistics are the following:

The probability of having celiac disease is 1 each 265.
The celiac patients represent 15% of the Chilean population.
Most die by cancer without really knowing their status.

But Europe have the contries with more celiacs internationally, also they are the places with more deaths by this pathology and the regions than more consuming wheat in the world. In Europe it is estimated that the 1% of adults and children have the disease. The prevalence varies widely; for ages 30 to 64 years, that is eight times higher in Finland (2.4%) than in Germany (0.3%), perhaps relating both to genetic and environmental factors. In Finland, the prevalence has doubled in 20 years.

Since the main gene pool of people with this mutation originated in Northern Europe, all of their descendents throughout North America, Australia, South Africa, etc. are at a higher risk for inheriting this genetic predisposition to the disease. For example in the United States, the prevalence of celiac disease by ethnic race is:

Team:San Andres/Software

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Statistics