ETIOPATHOGENESIS

Officially the “discoverer” of celiac disease is considered to be an English doctor at the Bartolomeyev Hospital in London, Samuel G. (1888), who first described its classic symptoms in children – diarrhoea, exhaustion, anaemia and retardation, says Dr. Denis Slinkin.

The cause of celiac disease was established in the mid-20th century. (1954) by the Dutch pediatrician W.K. Dicke, who found a decrease in celiac symptoms in children against the background of starvation during the Second World War and a relapse of disease in the post-war period with the restoration of traditional diets and the consumption of flour products from cereals plants (wheat, rye).

Dr. Denis Slinkin

Dr. Denis Slinkin states: In the last decade, celiac disease has tended to be seen as a systemic autoimmune disease. It is well known that individuals with celiac disease are ten times more likely to develop autoimmune disease than the general population, and many studies have focused on the various ways in which this association can be created.

Gluten is a collective name for protein fractions, namely, prolamins and glutenins of cereals – wheat gliadins, barley glyadins, rye secalins and oat sheep, which, affecting the mucous membrane of the small intestine, cause the mobilization of elements of the immune system. 

The damaging effect of gliadin is realized through interepithelial T-lymphocytes and protective cells of the own plate of the small intestine mucosa. 

T-lymphocytes of the mucous membrane recognize only those gliadin peptides that have antigen properties (33-dimensional gliadin peptide), says Dr. Denis Slinkin.