GLUTEN DISEASE (synonym: disease of gluten insufficiency, gluten enteropathy, glyutenchuvstvitelny Gee's disease, idiopathic Gee's disease) — the disease caused by intolerance of one of the main parts of protein of cereals — gluten, and caused by the inborn or acquired deficit of one of enzymes of intestinal juice.
it is allocated in an independent disease from big group patol. the states combined under the term «Gee's disease» and representing manifestation of fermental insufficiency. Unlike other forms Gee's diseases (see), observed preferential at children, G. occurs often at adults, being sometimes combined with disakharidazny insufficiency, the shown intolerance of milk (see. Malabsorption syndrome ).
For the first time harmful effect of gluten is established Dick, Veyersy, Wang-de-Kamerom (W. Dicke, H. Weijers, J. Van de Kamer) in 1950. Gluten consists of two fractions — glyuteninovy and gliadinovy from which only the last would promote G.'s manifestation. The reason of the damaging action of this fraction of protein and the mechanism of development of G. still are completely not clear. The disturbing factor is purely not allocated.
the Pathogeny of a disease is difficult. Various reasons promoting a course of a disease are discussed, but the role them remains hypothetical. The leading pathogenetic value has deficit of specific enzyme from the group of peptidases-aminopeptidases which is contained in intestinal juice and splitting gliadine to water-soluble peptide fraction (fraction 3). This peptide fraction, keeping the damaging effect of gliadine, G. would cause. It is proved that patol, effect of gliadine and peptide fraction disappears at their incubation with extract of a mucous membrane of a small bowel of a pig. The neutralizing action is attributed to the enzyme which is contained in a mucous membrane of a small bowel of a pig a gliadinamidaza. It is known that the mucous membrane of a small bowel of the healthy person also has ability to split peptide fraction to the making amino acids; mucous membrane of sick G. it is deprived of this ability. At deficit of specific enzymes products of incomplete splitting of gluten are soaked up, as defines toxic effect.
In G.'s development. the large role is played by the condition of a hyper sensitization coming in response to introduction to an organism of gluten and some of its fractions. Extreme extent of allergic reactions of such patients is so-called gliadinovy shock. Confirmation immunol, theories of a pathogeny of G. decrease in a caption of komplementfiksiruyushchy antibodies to proteins of rye and wheat in response to the gluten food test (the gliadinotolerantny test) and existence in serum of the sick antibodies to peptide fraction decreasing at observance of an aglyutenovy diet serves. Also accumulation at G. would testify to a hyper sensitization. a large number of plasmocytes in contents of a small bowel and reduction of their quantity against the background of an aglyutenovy diet. The role immunol, a factor is confirmed by emergence in Calais of sick specific antibodies — koproantitet, immunological competent cells which formation is connected with products of antibodies in the most small bowel in response to administration of gluten. Identification in a secret of proximal department of a jejunum of immunoglobulins is of great importance. In plasmocytes of a gut concentration of IgA is very high, it is much less than IgM and very few IgG.
Pathoanatomical changes at G. differ from changes at other forms of a Gee's disease a little and consist in an atrophy of fibers of the small bowel which is followed by decrease of the activity of specific peptidases in membranes of a brush border. Infiltration of a mucous membrane of a gut is expressed by plasmocytes. Patol, process is more intensively shown in a proximal part of a small bowel that is connected, obviously, with immediate effect of the damaging agent — digestion and absorption of gluten in this department of guts.
A clinical picture
persistent ponosa with polyexcrements Are characteristic, steatorrhea (see), meteorism (see); during the progressing of a disease — the disorder of exchange processes (exhaustion, a hypoproteinemia, hypovitaminoses, anemia, disturbances mineral and a water salt metabolism) caused by disturbance of absorption in a gut. In far come cases there are changes of mentality, at children lag in development is observed.
Exact and direct diagnostic methods of G. no. The gliadinotolerantny test — test with loading gliadine belongs to indirect methods (350 mg of gliadine on 1 kg of weight): reception of gliadine causes in patients substantial increase of level of a glutamine in blood. However this test cannot be recognized as rather reliable.
The most convincing diagnostic character of G. — disappearance of all symptoms at observance of an aglyutenovy diet and emergence of a recurrence at the use of the products containing gluten.
the Only thing efficiently of treatment is purpose of an aglyutenovy diet to long terms (months, years). Bread and grain products are recommended made of wheat starch, free of gluten. The diet shall be full on structure, mechanically and chemically sparing.
At development of a syndrome of the broken absorption increase amount of animal protein in a diet, according to indications administer parenterally proteinaceous drugs, vitamins.
Full treatment is possible, apparently, only in cases of enzymopathies when use of an aglyutenovy diet promotes recovery of very tectonics of the small bowel and its fermental activity acquired gluten.
Bibliography: Beyul E. A. and Ekisenin N. I. Chronic enterita and colitis (Questions of a pathogeny, clinic and treatment), page 164, M., 1975; The Reference book on gastroenterology, under the editorship of V. of X. Vasilenko, page 95, M., 1976; Tashev T. A. and d river. Stomach diseases, intestines and a peritoneum, the lane with bolg., page 461, Sofia, 1964; Frolkis A. V. Functional diagnosis of diseases of intestines, page 28, M., 1973; D i s s a n and at a k e A. S. and. lake of Identifyng toxic fractions of wheat gluten and their effect on the jejunal mucosa in coeliac disease, Gut, v. 15, p. 931, 1974, bibliogr.; F a 1 with h u k Z. M and. S t r o-b e r W. Gluten-sensitive enteropathy, ibid., p. 947, bibliogr.; K a m e r J. H. a., W e i] e r s H. A, Malabsorption syndrome. Fed. Proc., v. 20, p. 335, 1961.
E. A. Beyul.