intestinal malabsorption

Intestinal malabsorption - general name of chronic non-inflammatory bowel disease, which are based on or fermentopathy congenital intestinal wall structure.

Enteropathy celiac (sprue European, sprue nontropical, celiac adults steatorrhea idiopathic) - a rare hereditary disease (fermentopathy) intestines, characterized by the absence or reduced output of the intestinal wall of the enzymes that break down gluten (gluten) - polypeptide contained in some cereals (wheat, rye, barley, oats). The absence of (or relative lack of) development of this peptidase is particularly evident when eating disorders, the prevalence of food cereals containing gluten, the intestinal infections. incomplete digestion of gluten-free products (gliadin and others.) toxic effects on the intestinal wall.

Characteristic of diarrhea that occurs by eating food made from wheat, rye and barley. With the progression of the disease are joining polyhypovitaminosis, electrolyte imbalance, exhaustion. In advanced cases develop chronic enteritis syndrome suction failure. A known aid in differential diagnosis may provide samples to the load gliadin (rapid elevation of glutamine blood after oral administration of gliadin in a dose of 350 mg / kg), signs of early childhood diseases, aggravation of symptoms of the disease with a significant addition to a food diet products of wheat, rye, barley, oats, as well as regression of disease symptoms when transferring the patient on a gluten-free diet (gluten is absent in all foods of animal origin, in corn, rice, soybeans, potatoes, vegetables, fruits, berries, and other products).

Treatment in severe cases is carried out in a hospital. Translations patient completely on a gluten-free diet with a high content of vitamins, orally administered cathartic and binding affinity. With the improvement of the diet are expanding, but the content in the daily diet, gluten-free, leave limited.

Malabsorption disaharidazodefitsitnye - hereditary diseases caused by the lack or insufficiency of developing mucous membrane of the small intestine disaccharidases (. Lactase, maltase, invertase, etc.), resulting in impaired parietal hydrolysis in the intestine corresponding disaharoz-lactose, maltose, sucrose. Inheritance is not set accurately.

Clinically manifested intolerance to one (or more) disaccharides and increased fermentation processes when administered in usual and especially in high doses; there are symptoms of fermentation dyspepsia, rumbling in the abdomen, bloating, diarrhea, polifekaliya with acidic feces.

Diagnosis and differential diagnosis with other chronic diseases of the small intestine are based on a number of specific tests: 1) improvement of the clinical picture of the disease after exclusion from the diet of relevant disaccharides; 2) study of the glycemic curve after oral administration to patients of various disaccharide, sucrose, lactose, maltose (no rise in blood sugar after taking one of the disaccharides and increase it after receiving monosaccharides, within them, is a sign of violation of splitting a disaccharide). Congenital disaharidoa intolerance is usually manifested since childhood. However, the violation fermentoproduktsii may be acquired due to severe enteritis. In the latter case, the breach disaccharidases products usually associated with impaired development of the intestinal epithelium and other enzymes.

The flow in most cases, not heavy, but over time, with a large content in the diet of sugary substances, and other adverse conditions due to prolonged secondary irritation of the intestinal mucosa enhanced fermentation products may develop chronic enteritis, accompanied by a deficiency syndrome suction.

Treatment. Strict adherence to a diet with the exception of the diet (or severely restricting content) corresponding to the disaccharide; in more severe cases - the appointment of an enzyme replacement therapy.

Exudative enteropathy (exudative gipoproteinemicheskaya lymphangiectasia) -rare disease occurs mainly in young adults.

The etiology and pathogenesis are not clear. It is characterized by abnormal enlargement of the lymph vessels and increased permeability of the intestinal wall, diarrhea, significant loss of protein through the gastrointestinal tract, gipoproteinemicheskimi edema. In severe cases, it develops cachexia. Frequent hypochromic anemia, leukocytosis with a slight tendency to lymphopenia. Hypoproteinemia celebrated mainly by reducing the content of albumin and gamma tobulinov; hypocholesterolemia; hypocalcemia. In the faeces increased content of neutral fat, fatty acids and soaps. Special laboratory methods show increased protein content in GJ secret and increased release it with feces. Radioisotope study of the excretory function of the small intestine to determine the increase in fecal radioactivity and the rapid decline of blood radioactivity after intravenous administration of albumin serum labeled with 1131 or 51Sg, t. E. Confirms the increased loss of protein from the body through the intestines. In biopsies of the mucosa of the intestinal wall is observed expansion of lymphatic vessels, inflammatory tissue infiltration. The expanded lymphatic vessels and sinuses mesenteric lymph nodes - lipofagi containing protoplasm oil microdroplets.

The differential diagnosis is carried out with enteritis, enterocolitis, as well as non-inflammatory disaharidazodefitsitnymi enteropathy, sprue, celiac disease. With certainty the diagnosis of exudative enteropathy allows enterobiopsiya. The disease is chronic and slowly progressing. Patients susceptible to intercurrent infections (pneumonia, purulent infection, sore throat and so on. D.) That can cause death. In severe cases, the prognosis is poor.

Treatment is carried out in the period of acute hospital. Prescribe a diet high in protein, vitamins, and fluid restriction salt. Intravenous plasma transfusions. Enter vitamins, while hypocalcemia - calcium supplements. When edema along with transfusions of plasma and different protein drugs prescribed diuretics.