Malabsorption syndrome in newborns. Symptoms of chronic malabsorption in pediatrics. Special diet with mixtures

Malabsorption syndrome- a condition in which there is a violation of absorption nutrients V small intestine. Literally, the term "malabsorption" means "poor absorption." Malabsorption occurs at any age, but is especially common in children, due to the immaturity of the gastrointestinal tract, enzyme and immune systems.

Introduction to food absorption and malabsorption syndrome

Nutrients entering the gastrointestinal tract are affected by digestive enzymes(contained in the intestines, gastric juice, pancreatic juice, bile, etc.), as a result, they are split into components. Only in this form, nutrient substrates are absorbed into the blood - speaking in "medical terms", the small intestine, acting as a selective sieve, allows the absorption of only split products.

Based on this, the causes of malabsorption syndrome can be both diseases of the stomach, pancreas, liver, hereditary enzyme defects that lead to disruption of the digestive process, and diseases of the stomach itself. small intestine leading to a violation of the absorption process.

Causes leading to the development of malabsorption syndrome

Depending on the reasons causing the syndrome malabsorption, it is customary to divide it into primary (congenital, hereditary) and secondary (acquired).

Primary malabsorption syndrome

The cause of the primary malabsorption syndrome, as a rule, is a genetically determined deficiency of a digestive enzyme, or hereditary disorders in the structure of the mucous membrane of the intestinal wall.

The most common hereditary diseases that occur with the development of malabsorption syndrome are:

1. Deficiency of the digestive enzyme lactase (lactase deficiency). In this case, malabsorption syndrome is genetically determined low activity the enzyme lactase, which breaks down the milk sugar lactose. Great importance this disease has early childhood, since lactose is found in milk, which is the main food of the child.
2. cystic fibrosis- a common hereditary disease in which the glands of the body are affected. Malabsorption syndrome in intestinal form cystic fibrosis develops as a result of pancreatic insufficiency and a decrease in the activity of digestive enzymes secreted by it.
3. . The occurrence of celiac disease is due to intolerance to the components of the cereal protein - prolamine and glutenin (common name - gluten). In genetically predisposed people, under the influence of gluten, inflammation and subsequent atrophy of the intestinal mucosa develop, leading to the development of malabsorption syndrome.
4. Congenital hypoplasia of the pancreas- a malformation in which the pancreas is underdeveloped. Accordingly, the syndrome of malabsorption in this case is due to a lack of pancreatic juice. Manifestations of the disease appear in the first days or weeks of life and intensify when the child is transferred to artificial feeding.

Malabsorption syndrome: secondary forms

Secondary forms of malabsorption in children most often develop in acute intestinal infections and helminthiases (especially giardiasis), dysbacteriosis, allergic inflammation intestines. Rarer causes of secondary malabsorption syndrome in children are removal of the stomach or part of the intestine, diseases of the liver, pancreas, etc.

The main manifestations of malabsorption syndrome

Manifestations of malabsorption syndrome depend on the disease that caused it. The severity of each symptom depends on the degree of nutritional deficiency, as well as on which organ has experienced the greatest violations of biochemical processes.

Common manifestations of malabsorption syndrome include:

• weight loss of the patient or a weak rate of weight gain, growth retardation, poor development of subcutaneous adipose tissue;
• weakness, lack of appetite;
• edema (as a sign reduced content protein in the blood)
• manifestations associated with hypovitaminosis - dry skin, seizures, soreness of the tongue, stomatitis, increased bleeding, increased hair loss, brittle nails, etc .;
• anemia (as a result of insufficient absorption of iron and folic acid);
• with insufficient absorption of protein, there may be endocrine disorders(retarded sexual development, menstrual function and so on.)

On the part of the intestine, manifestations of the syndrome of malabsorption, in the first place, are stool disorders: frequent, profuse diarrhea is characteristic, in which impurities of mucus and foam can be detected. The color of feces changes (from yellow to green), the smell (from sour to fetid).

A manifestation of fat malabsorption is the so-called "fatty stool" - steatorrhea (pale-colored soft stool that sticks to the walls of the toilet or floats and is difficult to wash off). According to the analysis of feces, malabsorption syndrome also reveals creatorrhea (increased content of undigested muscle and connective tissue fibers in the feces), amylorrhea (excretion of an increased amount of undigested starch with feces).

In addition, the characteristic signs of malabsorption in children are anxiety during feeding (intestinal colic), an increase in the size of the abdomen, bloating, rumbling, there may be vomiting, and frequent regurgitation.

In case of any delay in growth and development, it is necessary to show the child to the doctor. Specific analyzes help determine which food products or nutrients are not absorbed by the body. In most cases of diseases accompanied by malabsorption syndrome, enzyme replacement therapy and diet provide positive effects.

Violation of the absorption function of the intestine, leading and accompanying severe pathologies, is called malabsorption syndrome. As a result of this disorder, the body does not receive the necessary elements required for normal functioning. The disease is especially dangerous for children, causing a serious delay in maturation and growth in the child.

The concept of "malabsorption" includes a whole group of pathologies that occur in the body due to a complete or partial inability to absorb necessary substances and elements. This is a condition in which the body is not able to fully develop and function.

The syndrome of malabsorption is closely related to the syndrome of insufficiency digestive function Gastrointestinal tract (), since in both of these cases a general digestive and absorption dysfunction of various parts of the gastrointestinal tract develops.

Types and forms

Varieties of malabsorption include 2 main groups (forms) according to the type of indigestibility of substances:

1. Selective view, when one element is not absorbed.
2. Total, arising from extensive lesions intestines, characterized by a complete lack of digestibility of all elements.

In turn, the forms of malabsorption syndrome (hereinafter referred to as SMA) are divided into varieties according to the type of rejected substance:

1. Protein indigestibility.
2. Disorder of digestion of carbohydrates.
3. Inability to absorb vitamins.
4. Fat intolerance.
5. Malabsorption associated with indigestibility of the mono- and disaccharide group or glucose-galactose. Most often occurs in newborns from the first days of life.
6. rejection of minerals.
7. Violation of the absorption of amino acids.

galactose malabsorption in running form cause severe consequences in children. up to coma and death. However, with timely diet and drug therapy the prognosis is quite favorable.

Origin of the syndrome

To provoke the occurrence of malabsorption syndrome in a child can:

Malabsorption is directly related to the nutrition of children. Only a highly qualified doctor can make a diet for your child. If after breastfeeding (milk formula) in an infant or whole milk in an older child observed general deterioration conditions, pain, bloating, rumbling, diarrhea - it is worth sounding the alarm. Even one of these symptoms can be an indicator of lactase deficiency.

If the same is observed after the consumption of sugar-containing foods and foods containing galactose and glucose (including sugar, milk, etc.), these may be manifestations of malabsorption of the glucose-galactose form. Is it possible to drink kefir with HB, read.

Malabsorption syndrome is serious illness, which can lead to severe consequences, up to disability, and in some cases even death!

Causes and diseases that provoke pathology

SMA is a multi-causal disease because it has many factors. The occurrence of malabsorption syndrome may be due to congenital and acquired nature:

• A hereditary disease is most often observed in children at the level prenatal development, in the event of genetic fermentopathy and congenital anomalies. Hereditary diseases include such severe pathologies as lactase, disaccharide deficiency, celiac disease.
• SMA provoked already an existing disease, against which there is an absorption dysfunction of the intestine (enteropathy, neoplasms in the small intestine, enteritis, intoxication, unbalanced, malnutrition, systemic diseases).

Diseases that cause malabsorption:

1. Cystic fibrosis (cystofibrosis).
2. Anomalies in development and functioning, neoplasms of the pancreas
3. Foci of inflammation and primary pathologies, allergic and infectious lesions intestines.
4. Diarrhea of ​​various nature.
5. Pancreatitis of any kind.
6. Acanthocytosis.
7. Sucrase-isomaltase deficiency.
8. Indigestibility of bile salts.
9. Crohn's disease.
10. Lactase deficiency.
11. rejection of monosaccharides.
12. Deficiency of trypsinogen, enterokinase, duodenase.
13. Cholestasis of any origin.
14. Enterocytic disorders.
15. celiac disease
16. Shwachman-Diamond syndrome.
17. Enteropathy due to immune damage
18. Reducing the suction area.
19. Congenital short intestine.
20. Protein-energy deficiency.
21. Invasive lesions.
22. Syndrome of congestive (blind) intestinal loop.
23. Pathology of the lymphatic and blood vessels.

We offer you to watch a video about the symptoms of one of the most common diseases that cause malabsorption - celiac disease:

Manifestations and degree of development of the disease

Common manifestations of malabsorption in childhood allocate:

• diarrhea of ​​an acute and chronic nature, often alternating with constipation (dominant, predominant sign);
• increased gas formation;
• severe symptoms of body dystrophy;
• abdominal pain;
• lag in development and growth;
• loss of appetite;
• manifestations of multivitamin deficiency, disturbances in water and electrolyte balance, are classified according to the type of substance intolerance:

What to do if vomiting occurs in a child, read.

Manifestations of the disease with certain rejected elements:

Depending on the underlying disease, variable symptoms are added to the general manifestations:

1. The syndrome of impaired absorption function against the background of celiac disease is characterized by copious sticky stools, vomiting, dysphagia (swallowing disorders), atopic dermatitis, and allergies.
2. Pancreatitis chronic type manifested by steatorrhea - fatty "soapy" feces with great content starch and muscle fibers.
3. Cholestasis (syndrome of violation of bile flow) is characterized by abundant fatty feces with a strong fetid odor.

I want to draw attention to one of the symptoms of malabsorption is diarrhea. No wonder experts around the world consider it dominant. Based on the manifestations of the diarrheal syndrome, it is possible to significantly narrow the parameters of the diagnostic search.

Foamy, acidic stools of a particularly thin consistency are characteristic of galactose malabsorption. Water is possible with protein intolerance to cow's milk, mastocytosis, hereditary adrenal hyperplasia, some types of hormone-producing tumors.

Fatty stool appears when intestinal pathologies, including celiac disease, dysbacteriosis, short intestine, cholepathies. The feces are especially fatty (with characteristic fatty secretions), characteristic of cystic acidosis. Polyfecalia - celiac disease, dermatitis.

alternation mushy stool and constipation against the background of neurosis - irritable bowel syndrome. The combination of diarrhea with abdominal pain signals infectious and invasive lesions.

And this is only a small list of varieties of diarrheal disorders. Attentive attitude to this symptom will greatly facilitate the diagnosis.

According to the severity of the severity of the lesion, the malabsorption syndrome is divided into degrees:
1
Light (1 degree of severity). It manifests itself in the form of symptoms of vitamin deficiency, the child has a slight decrease in body weight (does not exceed 10%), the syndrome chronic fatigue(astheno-neurotic), disharmony of general development.
2
Moderate (2 degree). Signs are more pronounced: weight loss reaches 20%, more pronounced symptoms of vitamin, water and electrolyte deficiency, anemic conditions.
3
Severe (3 degree). Weight deficit exceeds 20%, there is a pronounced delay psychophysical development, obvious symptoms of vitamin and water-electrolyte deficiency, anemic conditions.

Diagnostic measures

Malabsorption syndrome is initially diagnosed on the basis of identifying and summarizing the obvious signs. The clinical picture of the disease in children is specified when the following diagnostic studies are prescribed:

• testing for D-xylose;
• endoscopic and biopsy studies;
• detection of fat and its amount in feces;
• radiography of the small intestine (allowing from the very early age identify pathologies of the organ structure);
• additional testing to confirm the diagnosis.

You can find out what the presence of blood in the feces of a child indicates.

Treatment: methods, goals, principles

The main types of elimination of the malabsorption syndrome are therapeutic and dietary nutrition (the dominant type) and drug adjustment. Rare congenital species SMA in children may require surgery And specific therapy.

This takes into account:

• type of SMA (hereditary or acquired);
• the degree of violation of the absorption function;
• condition of the digestive tract;
• age, appetite, food preferences and habits;
• level of intestinal sensitivity to osmotic load.

• relief of manifestations of malabsorption;
• recovery normal weight body;
• elimination of the underlying disease that provoked SMA.

The main principles of treatment:

1. Elimination of the underlying disease that caused malabsorption.
2. Diet therapy.
3. Correction of vitamin-protein metabolism.
4. Correction of violations of water-electrolyte metabolism.
5. Restoration of normal motor function of the digestive tract.
6. Elimination of dysbacteriosis.

Rational nutrition of the newborn is essential condition which determines the state of health not only in infancy, but also in subsequent life stages. Monitoring the perception of nutrition, its adjustment is especially important in babies with absorptive dysfunction syndrome. So, with glucose-galactose malabsorption, the child needs intravenous administration of glucose along with formula feeding and the addition of a vitamin complex.

Preventive measures are aimed at preventing the disease that provoked the occurrence and development of malabsorption. With quality prevention and timely adequate treatment positive forecasts.

Conclusion

Sometimes, SMA is eliminated during dietary therapy and does not require medical adjustment. A huge role in the prevention and treatment of diseases that caused a disorder of the absorption function in a child (especially in the first year of life) is played by his mother. She should eat rationally and fully (when breastfeeding) and observe the reaction of the baby after feeding, inform the doctor about his condition.

In addition, we suggest watching a video on how digestion and absorption of nutrients in the intestine occurs:

Enteropathy - pathological condition, which leads to a lack or dysfunction of certain intestinal enzymes, due to the absence, deficiency or violation of the structure of certain intestinal enzymes that provide digestive processes.

Absorption of carbohydrates: food carbohydrates consist of disaccharides:

1) sucrose (regular sugar = fructose + glucose), lactose (milk sugar = galactose + glucose);

2) monosaccharides: glucose and fructose;

3) vegetable starches (a polysaccharide consisting of glucose molecules).

The enterocyte is unable to transport carbohydrates more than the monosaccharide. Therefore, carbohydrates must be broken down before absorption. Malabsorption syndrome is a syndrome of impaired intestinal absorption, malabsorption syndrome can lead to: lack of pancreatic enzymes - a violation of the abdominal phase of digestion; cholestasis, intestinal dysbiosis - a violation of the metabolism of bile acids, lipid transport to a violation of the biliary phase of digestion; deficiency of cavity enzymes (disaccharidases, peptidases, etc.) leads to disruption of membrane digestion; atrophy of the mucous membrane of the small intestine - to a violation of absorption, i.e., the cellular phase of digestion, while membrane digestion also suffers; pathology of the intestinal lymph flow, mesenteric circulation to - deterioration of the further transport of absorbed substances - the outflow phase suffers; accelerated passage of food through the intestines - to a violation of all types of digestion.

Enzymopathy is a pathological condition caused by the absence, deficiency or violation of the structure of certain cellular enzymes that provide digestive processes.

The clinical picture is due to impaired absorption through the mucous membrane of the small intestine of one or more nutrients. Clinical manifestations malabsorption syndrome in the form of diarrhea, weight loss, protein deficiency, signs of hypovitaminosis.

Malabsorption syndrome can be primary (hereditary) or secondary (acquired). Classification. pathogenic classification.

1. Exocrine pancreatic insufficiency:

1) cystic fibrosis of the pancreas;

2) chronic malnutrition with protein and calorie deficiency;

3) Shwachman-Diamond syndrome;

4) chronic pancreatitis with exocrine insufficiency;

5) specific enzyme defects (lipase, trypsinogen).

2. Insufficiency of bile acids:

1) obstruction of the biliary tract (atresia biliary tract, cholelithiasis, pancreatic head cancer);

2) resection of the ileum;

3) cirrhosis of the liver, chronic hepatitis (decreased secretion);

4) dysbacteriosis.

3. Violations of the functions of the stomach:

1) postgastrectomy syndrome;

2) vagotomy;

3) pernicious anemia caused by vitamin B deficiency 12

4. Dysmotility:

1) hyperthyroidism;

2) diabetes mellitus;

3) scleroderma; 4 amyloidosis.

5. Pathology of the intestinal mucosa:

1) celiac disease;

2) lactase deficiency;

3) sucrase and isomaltase deficiency (combined);

4) exudative enteropathy;

5) intolerance to cow's milk protein (and/or soy);

6) insufficiency of enterokinase;

7) abetalipoproteinemia (Bassen-Kornzweig syndrome);

8) impaired transport of amino acids (tryptophan, methionine, lysine, etc.);

9) vitamin B 12 malabsorption (transcobalamin-II deficiency);

10) congenital disorders of folic acid absorption processes;

11) chlorine-losing diarrhea;

12) vitamin D-dependent rickets;

13) enteropathic acrodermatitis;

14) Menkes syndrome (curly hair syndrome);

15) Crohn's disease;

16) malabsorption after suffering enteritis;

17) tropical sprue;

18) Whipple's disease;

19) chronic infections(immunodeficiency), in particular giardiasis;

20) primary immune deficiency (Wiskott-Aldrich syndrome);

21) congenital short intestine;

22) short bowel syndrome after resection (resection of the proximal portion of the small intestine, resection of the ileum, resection of the ileocecal region);

23) eosinophilic gastroenteritis.

Etiology. The etiology in each case is different (absence or reduced activity of lactase, a-glucosidase, enterokinase). Disaccharidase deficiency (sugarase, lactase, isomaltase), true celiac disease (gliadin intolerance), enterokinase deficiency, intolerance to monosaccharides (glucose, fructose, galactose), malabsorption of amino acids (cystinuria, Hartnup's disease, etc.) ), vitamin B malabsorption 12 and folic acid, etc. Secondary, or acquired, malabsorption occurs in many chronic diseases of the stomach and intestines (pancreatitis, hepatitis, dysbacteriosis, dyskinesia, Crohn's disease, etc.).

Clinic. The clinical picture in children is dominated by chronic diarrhea with a high content of lipids in the feces. Dystrophy gradually develops, children lag behind in growth. Clinical manifestations of vitamin deficiency, disturbances in water and electrolyte balance (dry skin, seizures, glossitis, hypokalemia, hyponatremia, hypocalcemia, etc.) are added. Pancreatic digestion deficiency syndrome is characterized (pancreatic steatorrhea): fat, amylorrhea (extracellular starch). For the syndrome, disturbances in the flow of bile are typical (hepatogenic steatorrhea): steatorrhea (with a predominance of fatty acids against the background of a smaller amount of neutral fat in the complete absence of soaps), creatorrhea is possible (altered muscle fibers prevail).

Intestinal diarrhea is characterized by steatorrhea, which is predominantly soaps and fatty acids. Diagnostics. Methods of paraclinical examination.

1. General analysis blood.

2. General analysis of urine.

3. Feces for Giardia, helminth eggs, scraping for enterobiasis.

4. Coprogram (extended, expanded): starch, neutral fat, fatty acid, connective tissue, iodine-philic microflora in normal feces are absent.

5. Biochemical research blood serum: proteinogram, liver function tests (ALT, AST, alkaline phosphatase, bilirubin, cholesterol), K, Fe, Ca, P, folic acid, vitamin B 12 , carotene).

6. Sugar curve - A flat sugar curve indicates diffuse mucosal damage. It should be noted that the study of glucose is carried out on an empty stomach, after 15-30, 60-120 minutes.

7. d-xylose test. d-xylose is a pentose absorbed passively through intact mucosa. Excreted by the kidneys. In malabsorption, most of the xylose is lost in the stool and does not reach the circulatory system. At least 30% is excreted in the urine, i.e. more than 1.25 g of the administered per os (5 g), (P. S. According to studies, this test has a direct correlation with glucose load test. Given the complexity of the d-xylose test).

8. Load tests with lactose, maltose, sucrose, starch. With a lactose load, an increase in the blood lactose cleavage product after oral administration of 50 g of lactose by less than 20% indicates lactase deficiency.

9. Chromatographic identification of carbohydrates, amino acids contained in urine.

10. Hydrogen breath test: Determination of the amount of hydrogen in the exhaled air after loading with sugars at a dose of 2 g/kg (up to a maximum of 50 g). The test is based on the fact that if sugar is not adsorbed in upper divisions small intestine, then it reaches the distal sections, in which intestinal bacteria act on it with the formation of hydrogen. The latter is rapidly absorbed and exhaled in measurable amounts. An increased amount of exhaled hydrogen (more than 20 g/million during the first 2 hours) is considered a pathology. (P.S. In patients taking ABs, and in about 2% of healthy individuals, hydrogen-producing intestinal flora is absent).

11. Sowing feces for dysbacteriosis.

12. Research of pancreatic enzymes in blood and urine.

13. Ultrasound of the pancreas, liver, gallbladder.

14. Determination of chlorine (Cl) in sweat fluid. If necessary, molecular genetic testing for cystic fibrosis.

15. X-ray of the gastrointestinal tract - information about the time of passage of barium through the intestines, damage to the mucous membrane, the presence of a stricture or tumor.

16. Gastroduodenoscopy with biopsy. A biopsy of the small intestine helps in the diagnosis of celiac disease, but it is not indicative of many other diseases.

17. Colonoileoscopy with biopsy.

Cystofibrosis of the pancreas (cystic fibrosis) is a hereditary disease with a recessive type of inheritance. Frequency in population 2–8: 100,000 population. In patients with cystic fibrosis, the chloride channel on the apical part of the cell membrane “does not work”, leading to disruption of the release of chlorine from the cell, which contributes to an increased escape from the lumen into the cell of sodium ions, followed by the water component intercellular space. The consequence is a thickening of the secretions of the glands of external secretion ( bronchopulmonary system, pancreas, salivary glands, sex glands). The respiratory system and pancreas are most commonly affected. The disease is manifested by respiratory and intestinal syndromes already in the first year of life. The degree of interest of systems and organs is different. Paraclinical markers are: coprogram - the presence of a large amount of neutral fat and almost always its predominance over muscle fibers and polysaccharides.

Ultrasound of the pancreas - diffuse compaction of the parenchyma, and with age, a decrease in the size of the pancreas.

High sweat chlorides (60.0 mmol/l or more), repeatedly positive (at least 3 times).

Molecular genetic testing. But it should be noted that negative results these studies do not rule out a diagnosis of cystic fibrosis.

Shwachman-Diamond syndrome (congenital hypoplasia of the pancreas, combined with neutropenia, short stature and anomaly of the bones).

Diagnosis based on the syndrome of pancreatic insufficiency in the first year of life, neutropenia, normal sweat chlorides.

Chronic pancreatitis with exocrine insufficiency - causes may be past diseases, including parotitis, injuries, drugs, toxins, diseases and anomalies of the bile and pancreatic ducts, systemic diseases.

Specific enzyme defects (lipase, trypsinogen).

1. Isolated deficiency of pancreatic lipase (Shedon-Rey syndrome) is manifested by fatty diarrhea due to neutral fats. Children have a good appetite, adequately develop physically and mentally.

Diagnosis: based on fatty stools, neutral fat in feces, normal sugar curve, d-xylose test, sharp decrease or absence of lipase in pancreatic juice, no morphological changes in the pancreas, normal sweat chlorides.

Treatment: replacement therapy.

2. Isolated trypsin deficiency occurs with a frequency of 1: 10,000; the type of inheritance is autosomal recessive.

Clinically manifests shortly after birth with mushy or watery, fetid stools against the background of breastfeeding, poor development and increasing malnutrition. A large amount of protein and fats is found in the feces. Treatment: replacement therapy.

3. Amylase deficiency - diagnosis based on clinical manifestations, watery, sour-smelling stools. Coprogram (starch). Decreased or absent amylase activity. Effect on the background of an elimination (starch-free) diet.

Obstruction of the biliary tract (atresia of the biliary tract, cholelithiasis, cancer of the head of the pancreas), resection of the ileum, dysbacteriosis, cirrhosis of the liver, chronic hepatitis (decrease in secretion). In a coprological study, the predominance of fatty acids against the background of a smaller amount of neutral fat in the complete absence of soaps; Creatorrhoea is possible - altered muscle fibers predominate.

Post-gastrectomy syndrome, vagotomy, pernicious anemia caused by vitamin B deficiency 12 .

Hyperthyroidism, increased thyroid hormone levels, increased motility, reduced food transit time, decreased digestion and absorption of fats, diarrhea and steatorrhea. Diabetes Mellitus: Diarrhea is secondary and is associated with diabetic neuropathy.

Syndrome mechanisms:

1) violation of the exocrine function of the pancreas, steatorrhea;

2) decreased motility of the antrum of the stomach, impaired emulsification of fats, steatorrhea;

3) violation of the autonomic vegetative regulation of the intestine, intestinal stasis, increased reproduction of bacteria, deconjugation of bile acids, malabsorption of fats. Scleroderma, decreased motility of the small intestine associated with a decrease in the number of smooth muscle cells of the intestinal wall, increased reproduction of bacteria, deconjugation of bile acids, malabsorption of fats. Amyloidosis, deposition of amyloid protein in many organs, including the smooth muscle tissue of the intestinal wall, decreased motility, increased multiplication of bacteria, deconjugation of bile acids, malabsorption of fats.

Celiac disease (gluten enteropathy, celiac disease, celiac sprue, 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, which break down gliadin, constituent part protein of various cereals (wheat, rye, barley, oats).

Diagnosis of malabsorption: subtotal or total atrophy of the mucous membrane of the small intestine, clinical effect from a gluten-free diet, improvement in absorption and x-ray data with the exclusion of gluten from the diet, improvement in the morphology of the small intestine from the use of a gluten-free diet, recurrence of morphological disorders after stopping the gluten-free diet.

X-ray signs: dilatation of the intestine - the most permanent and important symptom, it is especially pronounced in the middle and distal jejunum. Dilatation of the intestine is explained by its hypotension. Expansion of the intestine is absent in pancreatic steatorrhea and is not due to increased fat content in the intestine.

Possible serological diagnosis: determination of the content of anti-gliadin (AGA) antibodies, anti-endomysial (EMA) and anti-reticular (ARA) IgA antibodies in the blood serum. The presence of these antibodies is considered specific for the disease, and their study can be used to screen the next of kin of patients, as well as for determining the frequency of celiac disease in the population.

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

The main method of treatment is a diet with the exclusion of all foods containing gluten. Of the cereals, only rice, buckwheat, corn, the preparation of cakes, pastries, cookies from soy, rice flour, and starch are allowed. The diet is prescribed even in the asymptomatic course of the disease and must be observed throughout the life of the patient. It must be remembered that even 100 mg of wheat flour taken daily causes pronounced changes. morphological picture with a 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 the more specific adult-type lactase. At the age of 3–5 years, the gene regulation of enzyme synthesis switches from the child to the 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 in preterm infants;

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

4) secondary lactase deficiency (with enteritis, food allergies, celiac disease, immunodeficiency states). Clinical manifestations in the form of diarrhea after taking milk. Diagnosis: diarrhea, pH coprogram< 5,0. Если нет нарушения полостного или мембранного пищеварения, то других изменений в копрограмме можно не найти, гликемические кривые при нагрузке глюкозой, галактозой, d-ксилозой нормальные, а при нагрузке лактозой – плоская.

Biopsy of the small intestine - in individuals with a primary deficiency of morphological changes in the mucous membrane of the small intestine is usually not found, jejunoscopy - more often without features, visual endoscopic picture of the mucosa - a positive effect on the abolition of dairy products, deterioration (diarrhea) after taking milk.

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

1. If the child has clinical and laboratory signs lactase deficiency, but 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 child's body weight does not increase or decreases with a sufficient amount breast milk, A therapeutic measures do not give positive effect, it is necessary to stop breastfeeding and switch to a diet of dairy-free or low-lactose mixtures. With a correct diagnosis, the clinical effect is noted already in the first 2-3 days.

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

Treatment: elimination diet.

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

There are primary and secondary forms of exudative enteropathy.

Primary - congenital generalized disease 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 lymphatic vessels intestines.

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

Pathogenesis: increased permeability of intestinal membranes for macromolecules.

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

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

1. Low-fat diet, medium chain triglycerides are recommended because they are absorbed without the involvement of the intestinal lymphatic system and they can reduce pressure in the intestinal lymphatic vessels. Limit salt.

2. In / in the introduction of protein drugs.

3. Symptomatic therapy.

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

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

Diagnostics: acute symptoms should stop within 48 hours, and chronic - within 1 week after the cessation of feeding milk. 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 to the active enzyme trypsin. Due to the deficiency of enterokinase, the digestion of proteins in the intestine is disturbed. Occurs only in children.

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

Treatment: replacement therapy with pancreatic enzymes.

Abetolipoproteinemia. Abetolipoproteinemia (Bassen-Kornzweig syndrome) is a condition in which there is no apo-B protein necessary for the formation of chylomicrons and very low density lipoproteins, which leads to overflow of enterocytes with fats, and absorption of fats is impaired.

Clinical manifestations in the first year of life, developmental delay is detected. The feces are copious and discolored, the abdomen is distended. Mental development is somewhat behind. Typically after the age of 10 years, the appearance cerebellar symptoms IN adolescence develops atypical retinitis pigmentosa. Diagnosis: detection of acanthocides in peripheral blood, hypocholesterolemia (200–800 mg/l), absence or minimal amount b-, c-lipoproteins (b- or c-lipoproteinemia), pronounced accumulation of fasting lipids in the villi of enterocytes of the duodenal mucosa.

Treatment: restriction of long chain fats, vitamins A, D, E, K, consumption of medium chain triglycerides, Violation of amino acid transport.

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

Vitamin B 12 malabsorption (transcobalamin-P deficiency). Deficiency of transcobalamin-II, a protein essential for intestinal transport, vitamin B 12 leads to severe megaloblastic anemia, diarrhea, and vomiting.

Treatment: Vitamin B 12 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 Chlorine-wasting diarrhea is a rare specific congenital disease, caused by a defect in the transport of chlorides in ileum. Clinical manifestations: debilitating diarrhea from the moment of birth as a result of the accumulation of chloride ions in the intestinal lumen.

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

Enteropathic acrodermatitis is caused by malabsorption of Zn.

Clinic: dermatitis (rash at the transition of the skin into the mucous membrane), there may be alopecia, diarrhea, developmental delay, a decrease in Zn in the blood serum, alkaline phosphatase activity.

Treatment: zinc sulfate 150 mg/day.

Menkes syndrome. Menkes syndrome (curly hair syndrome) is caused by impaired transport of Cu (copper). It is inherited in an autosomal recessive manner.

Clinic: growth retardation, hair anomaly, cerebellar degeneration.

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

The prognosis is unfavorable.

Whipple syndrome. It almost never occurs in children.

Etiology: believe that rod-shaped microorganisms are affected, including the small intestine.

Clinic: fever, diarrhea, arthralgia, polyserositis.

Diagnosis: biopsy in duodenum, PAS-positive macrophages are detected, and bacteria can be detected in the mucosa.

Diagnosis methods.

I stage. Identification of the syndrome of malabsorption.

According to clinical signs:

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

2) plentiful fetid stools - reduced absorption of fat;

3) muscle weakness, edema - reduced absorption of proteins;

4) flatulence, rumbling in the abdomen, copious discharge of gases - the digestion of carbohydrates by the 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 - vitamin B deficiency 12 , folic acid and other B vitamins;

9) acrodermatitis - Zn deficiency.

II stage. Exclusion of infectious genesis of enteropathy.

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

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

2) in violation of parietal digestion (enteral mechanisms), you can use the following tricks: the timing (age of the patient) of the manifestation of the disease, the relationship of the manifestation of the disease with the characteristics of the child's nutrition, the relationship of deterioration of the stool with the characteristics of the child's nutrition. Forecast at timely diagnosis and favorable treatment.

Prevention consists in diet therapy with the exclusion of intolerable foods.

Malabsorption syndrome is common in children different ages. The cause of its occurrence is a violation of the digestion of food, as well as poor absorption into the small intestine of various useful substances(vitamins, proteins, carbohydrates). This syndrome can be both primary and secondary. Primary occurs as a result of hereditary ailments, and secondary malabsorption syndrome can be acquired.

The main signs of the disease

Another feature is weight loss. This phenomenon occurs as a result of the fact that the body of a little man does not receive as many nutrients as it needs. This negatively affects the metabolic processes, slows them down. Less often, it can be observed that the peanut with this ailment, on the contrary, is gaining excess weight.

Doctors call anemia a secondary sign of malabsorption syndrome. Due to the fact that iron enters the baby's body in insufficient quantities, anemia occurs.

Other symptoms of this disease include:

Vomiting and weakness;
bloating and pain in it;
growth retardation;
the baby gets tired quickly;
hypovitaminosis and the appearance of edema.

In addition, some sick children with malabsorption syndrome may develop a rash on different areas of the body, fever, cramps and muscle pain. Vitamin D deficiency leads to skeletal disorders and growth retardation.

Treatment of malabsorption syndrome in children

In order to find out exactly whether your little one has this ailment, you will have to take tests. The first of them is a blood test, you will also need to pass the baby's feces. In some cases, it is recommended to undergo a special Schilling test or to do an ultrasound of the organs. abdominal cavity. To diagnose malabsorption syndrome in children, a D-xylose test is also performed.

Before starting treatment, it is very important to determine the cause of this disease. When choosing treatment methods, a professional should take into account: the age of your baby, his appetite, the condition of the liver, the degree of malnutrition. It must be said that malabsorption syndrome in children responds well to treatment, but you should not let everything take its course.

The main methods of treatment are proper nutrition and diet. To restore normal work intestines little patient, you will need to exclude some food from his diet. The quantity and type of products depends primarily on the origin and intensity of absorption in the intestine. If the baby is lactose intolerant, then cow's milk and other products that are made on its basis should not be on its menu.

In the event that sucrose is not absorbed, the doctor will recommend to refrain from eating sugar, sweets and starchy foods (potatoes, semolina and others). If the food contains an enzyme that is poorly absorbed, it must be completely excluded from the menu. As soon as the bowel function returns to normal, under the supervision of a doctor, you can introduce those foods that were banned into the diet of the little one.

The duration, as well as the type of diet, should be determined only by a doctor. Sometimes a long-term observation of a small patient in a hospital may be required, and in some cases, enzyme replacement therapy is performed. One way or another, the doctor should prescribe the method of treatment, because he will be able to choose the right nutrition for your baby with malabsorption syndrome.

Causes of the syndrome

If the little man has congenital hypoplasia pancreas, then this, most likely, will also provoke the development of a primary malabsorption syndrome. Its manifestations can be noticeable from the first days of a baby's life, gradually they will intensify.

Secondary malabsorption syndrome in children has completely different causes. It can develop with dysbacteriosis, helminthiases, acute intestinal infections. Rarely, but still there are secondary forms of this syndrome - with diseases of the liver or pancreas.

If parents notice that their child is stunted or is constantly suffering from diarrhea, then this may be the first signs of malabsorption syndrome. It is better to go to the pediatrician once again and make sure that the baby is healthy. If the doctor suspects this disease, he will prescribe tests. Treating malabsorption syndrome in children is always easier and faster in the initial stages.

What is Malabsorption Syndrome? This is a pathological condition that occurs due to malabsorption of any nutrients, trace elements and vitamins directly in the small intestine.

The malabsorption syndrome that occurs in children can be primary and secondary.

1. Primary malabsorption syndrome. This syndrome is exclusively hereditary. In this case, the syndrome of malabsorption manifests itself from the first months of life.
2. Secondary malabsorption syndrome. IN this case syndrome occurs due to a variety of reasons. But the first reason why this disease occurs is a violation of the gastrointestinal tract.

Causes

First of all, the causes of the appearance and development of this syndrome are genetic disorders. In the primary syndrome, malabsorption leads to a violation in the production of one or more enzymes that are involved in the process of digestion of products in the small intestine. Because of this, metabolic disorders appear.

With the development secondary syndrome malabsorption, a complication of the course of enteritis appears, chronic diseases pancreas, liver, may also appear malignant formations in the small intestine.

These reasons can lead to one or more processes that actually contribute to the development of malabsorption syndrome in children:

1. Reduced enzyme activity thin department intestines;
2. Violation of abdominal digestion;
3. Violation of parietal digestion;
4. Violation of food hydrolysis and absorption of products.

As a result, undigested foods contribute to sharp decline weight and vitamin deficiencies also cause diarrhea.

Symptoms of malabsorption syndrome in children

main symptom this disease is dyspeptic, with the appearance of a child's appetite disorders, nausea, bloating, rumbling and abdominal pain, vomiting and stool disorders, mainly in the direction of diarrhea.

All of these symptoms are due to the fact that food is not digested. gastrointestinal tract. Therefore, children have a deficiency of vitamins and minerals. This deficiency is manifested by dry skin, glossitis, brittle hair and nails,