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Pathology of the intestinal mucosa



Celiac disease (celiac enteropathy, celiac disease, celiac disease, non-tropical sprue).

Causes of development: congenital chronic disease of the small intestine due to the absence or decrease in the activity of peptidases of the brush border of the small intestine that break down gliadins, a component of the protein of various cereals (wheat, rye, barley, oats).

Diagnosis of malabsorption: subtotal or total atrophy of the small intestine mucosa, clinical effect of a gluten-free diet, improved absorption and X-ray data when gluten is excluded from the diet, improvement of the small intestine morphology from the use of a gluten-free diet, relapse of morphological abnormalities after discontinuation of the gluten-free diet.

X-ray signs: dilatation of the intestine is the most constant and important symptom, it is especially pronounced in the middle and distal jejunum. Dilation of the intestine is explained by its hypotension. Colorectal expansion is absent in pancreatic steatorrhea and is not a consequence of the increased fat content in the intestine.

Serological diagnosis is possible: determination of serum antigliadin (AHA) antibodies, anti-endomysial (EMA) and antireticular (ARA) IgA antibodies. The presence of these antibodies is considered specific for the disease, and their study can be used to screen the closest relatives of patients, as well as to establish the frequency of celiac disease in the population.

In the expanded program - the presence of neutral fat and especially fatty acids and soaps, a flat sugar curve with a glucose load, indicating a violation of the absorption of di- and mono-substances.

The main treatment is a diet with the exception of all products containing gluten. Of cereals, only rice, buckwheat, corn, cakes, pastries, soy, rice flour, starch biscuits are allowed. The diet is prescribed even with an asymptomatic course of the disease and must be observed throughout the patient's life. It must be remembered that even 100 mg of wheat flour taken daily cause pronounced changes in the morphological picture during biopsy.

Lactase deficiency. Lactase deficiency in children and adults has a heterogeneous molecular genetic nature.

There are two varieties of the enzyme: infant lactase and more specific adult-type lactase. At the age of 3-5 years, the gene regulation of enzyme synthesis is switched from a child to an adult type.

There are 4 forms of lactase deficiency:

1) primary hereditary lactase deficiency: alactasia with an autosomal recessive (possibly dominant) type of inheritance;

2) transient lactase deficiency of premature infants;

3) adult type hypolactasia (persistence of the infant form of lactose);

4) secondary lactase deficiency (with enteritis, food allergies, celiac disease, immunodeficiency). Clinical manifestations in the form of diarrhea after milk intake. Diagnosis: diarrhea, in coprogram pH <5.0. If there is no violation of the cavity or membrane digestion, then other changes in the coprogram can not be found, the glycemic curves under the load of glucose, galactose, d-xylose are normal, and with a load of lactose - flat.

Small intestine biopsy - in individuals with a primary deficiency of morphological changes in the small intestine mucosa, usually they are not found, eunoscopy is more often without features, the visual endoscopic picture of the mucosa is a positive effect when milk products are canceled, and worsening of the condition (diarrhea) after milk intake.

Treatment, if lactase deficiency occurs in a child who is breastfeeding, has 2 options.

1. If the child has clinical and laboratory signs of lactase deficiency, but is gaining weight, breastfeeding should be continued, but milk and dairy products, as well as beef, should be excluded from the mother’s diet.

2. If, against the background of lactase deficiency, the body weight of the baby does not increase or decreases with a sufficient amount of breast milk, and therapeutic measures do not give a positive effect, it is necessary to stop breastfeeding and transfer to food without dairy or low-lactose mixtures. With the correct diagnosis, the clinical effect is observed already in the first 2-3 days.

Sugar and isomaltase deficiency. Diagnosis: recurrent diarrhea, vomiting after taking sucrose, delayed physical development, the onset of the disease after transferring the child to mixed or artificial feeding, improvement in general condition after exclusion of sucrose and starch from the diet, a flat glycemic curve after loading with sucrose, normal, usually a curve with glucose load, urinary sugar chromatography, coprogram, as in lactase deficiency.

Treatment: elimination diet.

Exudative enteropathy. Exudative enteropathy (protein-losing enteropathy) is characterized by increased secretion due to increased permeability of the intestine of the protein into the intestinal lumen from the blood and loss of protein with feces.

Primary and secondary forms of exudative enteropathy are distinguished.

Primary - a congenital generalized disease of the lymphatic system, selectively localized in the intestine. In foreign literature they are characterized as an independent nosological unit.

Pathogenesis: increased protein extravasation occurs with an increase in pressure in the lymphatic vessels of the intestine.

Secondary causes of the development of exudative enteropathy are celiac disease, gastroenteritis, intolerance to protein of cow's milk and many other diseases.

Pathogenesis: increased permeability of intestinal membranes for macromolecules.

Clinic and diagnosis: edematous syndrome; blood serum: a decrease in the total level of protein, y-globulins, cholesterol; in the coprogram: as in celiac disease due to impaired absorption of fat and its transport (neutral fat, fatty acids, soaps); intestinal fluoroscopy: radiological changes are associated with swelling of the intestinal wall. The passage of contrast medium is timely. With lymphangiectasia, the intestinal wall may have a cone-shaped thickening of circular folds in the form of a garland. In more pronounced cases, pseudopolyposis manifestations can be detected. The endoscopic picture is diverse: with intact folding of the jejunum mucosa, its pale pink or pink color with a pronounced vascular pattern, sometimes combined with point hemorrhages, lymphofollicular hyperplasia, free mucosal hyperplasia in the form of numerous bulges is also observed.

Biopsy: according to Waldmann, with exudative enteropathy revealed changes in the lymphatic system of the mucous membrane and mesentery of the small intestine, which are called intestinal lymphangiectasia - expansion of the lymphatic vessels, interstitial edema.

Treatment.

1.
A low-fat diet, it is recommended that triglycerides containing medium-chain fatty acids be prescribed, since they are absorbed without the participation of the intestinal lymphatic system and can reduce pressure in the intestinal lymphatic vessels. Limit salt.

2. In / in the introduction of protein preparations.

3. Symptomatic therapy.

Intolerance to cow's milk protein. Protein intolerance to cow's milk occurs most often in children mainly under the age of 2 years, about 1 in 200 young children.

Pathogenesis: an immune response to proteins, mainly β-lactoglobulin (this protein is not found in human milk). Clinical manifestations in the form of diarrhea.

Diagnosis: acute symptoms should be stopped within 48 hours, and chronic - within 1 week after stopping milk feeding. With endoscopy and biopsy of the jejunum: changes develop that resemble cases of untreated celiac disease, although not so pronounced, an increased titer of antibodies to cow's milk protein.

Treatment: elimination of cow's milk, and if necessary, soy.

Enterokinase deficiency. Enterokinase activates pancreatic trypsinogen, converting it into the active enzyme trypsin. Due to enterokinase deficiency, protein digestion in the intestine is impaired. It is found only in children.

Clinical manifestations: diarrhea, edema, hypoproteinemia, the activity of enterokinase is practically absent in the duodenal contents, while the activity of amylase and lipase is not changed.

Treatment: pancreatic enzyme replacement therapy.

Abetolipoproteinemia. Abetolipoproteinemia (Bassen-Kornzweig syndrome) is a condition in which the apo-B protein necessary for the formation of chylomicrons and lipoproteins of very low density is absent, which leads to overflow of enterocytes with fats, fat absorption is impaired.

Clinical manifestations in the first year of life, a developmental delay is detected. Fecal masses are plentiful and discolored, the stomach is stretched. Mental development is somewhat behind. Characteristically, after 10 years, the appearance of cerebellar symptoms. In adolescence, atypical retinitis pigmentosa develops. Diagnosis: detection of acanthocides in peripheral blood, hypocholesterolemia (200-800 mg / l), absence or minimal amount of a-, b-lipoproteins (a- or b-lipoproteinemia), pronounced fasting lipid accumulation in villi of the duodenal mucosa enterocytes.

Treatment: restriction of long chain fats, vitamins A, D, E, K, the use of medium chain triglycerides. Disruption of amino acid transport.

Diagnosis: based on thin-layer chromatography of amino acids of urine, blood serum.

Vitamin B12 malabsorption (transcobalamin-II deficiency). Deficiency of transcobalamin-II, a protein necessary for intestinal transport, vitamin B12, leads to severe megaloblastic anemia, diarrhea, and vomiting.

Treatment: Vitamin B12 at 1000 mcg / week for transcobalamin-II deficiency and 100 mcg / month for other diseases. Congenital disorders of folic acid absorption.

Clinic - megaloblastic anemia, decreased intelligence. Chloretic diarrhea is a rare specific congenital disease caused by a defect in the transport of chlorides in the ileum. Clinical manifestations: debilitating diarrhea from birth as a result of the accumulation of chlorine ions in the intestinal lumen.

Diagnosis: diarrhea, hypokalemia, hypochloremia, alkalosis. In other respects, the intestinal absorption function is not impaired. Treatment: additionally add potassium to the diet, limit the consumption of chlorides.

Enteropathic acrodermatitis is caused by impaired absorption of Zn.

Clinic: dermatitis (rash at the places where the skin passes into the mucous membrane), there may be alopecia, diarrhea, developmental delay, decreased Zn in blood serum, alkaline phosphatase activity. Treatment: zinc sulfate 150 mg / day.

Menkes syndrome. Menkes syndrome (curly hair syndrome) is caused by a violation of the transport of Cu (copper). Inherited by an autosomal recessive type.

Clinic: growth retardation, hair anomaly, cerebellar degeneration.

Diagnosis: based on the clinic and a decrease in Cu in blood serum.

The forecast is unfavorable.

Whipple's syndrome. In children, almost never occurs. Etiology: consider that rod-shaped microorganisms with damage including the small intestine.

Clinic: fever, diarrhea, arthralgia, polyserositis. Diagnosis: a biopsy in the duodenum, PAS-positive macrophages are detected, and bacteria can be detected in the mucous membrane.

Methods of diagnosis.

I stage. Identification of malabsorption syndrome.

According to clinical signs:

1) loss of body weight with normal or increased appetite - reduced absorption of fat, protein, carbohydrates;

2) profuse fetid stool - a decrease in fat absorption;

3) muscle weakness, swelling - decreased protein absorption;

4) flatulence, rumbling in the abdomen, copious exhaustion of gases - digestion of carbohydrates by intestinal microflora;

5) parasthesia, bone pain, tetany - decreased absorption of Ca and vitamin D;

6) muscle cramps - excessive loss of K and Mg;

7) hemorrhagic syndrome - decreased absorption of vitamin K;

8) glossitis, stomatitis, cheilitis - a deficiency of vitamin B12, folic acid and other B vitamins;

9) acrodermatitis - Zn deficiency.

II stage. Exclusion of the infectious genesis of enteropathy.

III stage. Establishment of the type (phase) of digestive disorders (abdominal, parietal-membrane):

1) in case of violation of abdominal digestion (preenteral mechanisms), identify its causes: violation of the functions of the stomach, excretory insufficiency of the pancreas, bile deficiency (decreased formation, impaired excretion or reabsorption in the intestine);

2) in case of parietal digestion disturbance (enteral mechanisms), the following methods can be used: timing (patient age) of the manifestation of the disease, the relationship of the manifestation of the disease with the nutritional characteristics of the child, the relationship of stool deterioration with the nutritional characteristics of the child. The prognosis for timely diagnosis and treatment is favorable.

Prevention consists in diet therapy with the exception of intolerable products.

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Pathology of the intestinal mucosa

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