The dynamics of changes of villiferous structures in the small bowel during the progression of gluten enteropathy desease

SUMMARY

The aim of research is the Identification of possible interrelation between changes of Z fibers and patogistological changes according with Marsh classification.

There is the following dynamics of changes of villiferous structures in the GEP disease.

The Z-2 (Marsh– I) stage: fibers have normal sizes, located horizontally, tops are increased.

The Z - 2 (Marsh II) stage: the size of fibers is reduced, the improper form expansions of tops, local villiferous hyperplasia. The mobility of fibers is reduced, horizontally location.

The Z-3 (Marsh - III) stage: fibers are considerably reduced, deformed, inactive, placed diffusively horizontally.

According to these researches it is possible to make the following division of Z-2 into Z - 2a and Z - 2b which is the confidant to the histological picture Marsh – I and Marsh – II. There are no inflammatory changes in a stage Z – 2 one year later of a non-gluten diet. There is no atrophy progress in Z-3 stage (non-gluten diet), but poorly expressed inflammation remains still.

Keywords: gluten enteropathy, diagnostics, high-resolution endoscopy.

Gluten enteropathy is an inflammatory disease of a small bowel, which is characterized with the development of an atrophy of its mucous caused by intolerance of protein - gluten and a gliadine. The disease has genetic predisposition. Gluten enteropathy is inherited on autosomally -dominant type, with inexact penetration [1].

According to the results of serological tests of patohistological material (received with the help of white-light conventional endoscopy) the abundance of GEP hesitates over a wide range - from 1:500 to 1:3000 with an average value 1:1000 [2]:

In Estonia the incidence of GEP is - 1:2700 (in 1990-1992) [3], in Ireland-1:555,

in Italy - 4,6:1000, in Austria - 1:476, in Paris, among the European population 1:2000, in Sweden - 1-3,7:1000 [4] in Sahara 1: 18 [5].

Clinical picture of GEP is diverse. Typical symptoms are: (the beginning in children's age after the end of breast feeding), chronic diarrhea , delay in physical development, an abdominal distention, anorexia exhaustion, atrophy of muscles, anemia, irritability, GEP disease crises, delay of sexual development, osteoporosis. Atypical symptoms: (the beginning in average age) arthritis, aphthous stomatitis, lock, repeat relapsing abdominal pain, vomiting, defects of tooth enamel, dermatitis, hepatitis.

There are following diseases, which are probably associated with GEP pathogenetically: diabetes of 1st type, autoimmune thyreoiditis, autoimmune hepatitis, Shagren's syndrome,

ataxia, autism, depression, epilepsy, IgA - neuropathy. Diseases which are genetically associated with GEP: Down’s syndrome, Turner's syndrome, Williams's syndrome, deficiency of IgA [6].

According to our observations clinical picture of GEP can be similar to symptoms of acid-dependent diseases.

Complications of GEP disease are: 1. Systemic metabolic violations. 2. Erosive- ulcer duodenuitis. 3. Malignant defeats of a small bowel [6].

Clinical symptoms and complications of GEP generally are registered at the expressed atrophic changes of mucous of a small bowel. Well-timed diagnostics of GEP and well-timed gluten-free diet prescription can be not only the basic treatment, but also be as a preventive action of oncological diseases of the digestive path.

Despite the development of serological and genetic tests for GEP diagnostic , the "gold" standard of histological researches of small bowel remains still and bases on principles offered by Marsh M.N. in 1992 [10]. For the first time the histological research of a mucosa of a small bowel was made by Paulley J. W. in 1954, The material for researches was taken in laparotomiy at the patient with GEP [11]