Malabsorption

MALABSORPTION SYNDROME

(French mal disease + absorption; synonym:
malabsorption syndrome, impaired intestinal absorption syndrome
) - a clinical symptom complex caused by impaired absorption through the mucous membrane of the small intestine of one or more nutrients. The syndrome of impaired intestinal absorption can be primary (hereditarily caused) and secondary (acquired).

The absorption of monomers (monoglycerides, fatty acids, amino acids, monosaccharides) is preceded by hydrolysis (breakdown) of food polymers (proteins, fats, carbohydrates) under the influence of digestive enzymes. Violation of the breakdown of proteins, fats and carbohydrates due to insufficiency of digestive enzymes (digestive enzymes) is called digestive insufficiency syndrome (maldigestion). The combination of both types of disorders (splitting and absorption) was proposed to be designated as malassimilation. However, the tradition of M. s. has taken root in the literature. include malabsorption caused by both disorders of transport mechanisms and insufficiency of digestive enzymes.

Etiology and pathogenesis

The direct cause of the disorder in the absorption of food ingredients may be the reduced activity of digestion enzymes and transport carriers of the final products of digestion through the intestinal wall. Another reason for M. s. is an insufficient supply of enzymes to the intestines with digestive juices due to blockage of the ducts of the glands of the mucous membrane of the small intestine with a viscous secretion, as is observed, for example, in cystic fibrosis. What matters is the lack of formation of enzymes that break down, for example, proteins, which leads to a deficiency of amino acids and protein starvation of the body.

Inactivation of cleavage enzymes and transport carriers also causes the development of M. s. Thus, some antibiotics (chlortetracycline, neomycin) can suppress lipid breakdown processes and increase steatorrhea (see).

2. Causes and factors of malabsorption syndrome

The development of malabsorption syndrome can be caused by congenital anomalies, functional failure, or disorders at different stages of the digestive process.

The most common underlying conditions that carry a potential risk for developing SMA include:

lack of enzyme production;
pathology of the walls of the small intestine;
intestinal circulatory disorders;
weakened peristalsis;
intestinal dysbiosis;
reduction in the length of the small intestine;
damage to the absorbable surface of the intestine due to irradiation, taking certain medications, chemical burns;
disruption of the process of mixing food with gastric secretions and other digestive juices;
altered composition of bile;
lack of enzymes produced by the pancreas;
parasitic and bacterial infections;
insufficient absorption of folic acid, vitamins and microelements, impaired absorption of monosaccharides, electrolytes, lipids, bile acids, etc.;
diseases of the digestive organs (stomach, liver, pancreas).

In addition, SMA can result from problems with the motor-evacuation function of the small intestine, tumor processes in the intestine and neoplasms in the pancreas, atrophic diseases of the digestive system, neuropathies of autonomic origin, and portal hypertension.

Visit our Gastroenterology page

Classification

There are several classifications of M. s. The following classification testifies to the multiplicity of etiological and pathogenetic factors underlying the occurrence of MS. 1. Primary M. s. (hereditarily determined): intolerance to disaccharides (lactose, sucrose, isomaltose, trehalose) - disaccharidase deficiency; peptidase deficiency (celiac disease); enterokinase deficiency; intolerance to monosaccharides (glucose, galactose, fructose); impaired absorption of amino acids (Hartnup disease, Cystinuria, tryptophan malabsorption, methionine malabsorption); impaired absorption of vitamins - cyanocobalamin (B12), folic acid. 2. Secondary M. s. (acquired): gastrogenic, observed after gastrectomy, with gastritis, stomach cancer; pancreatogenic, caused by various diseases of the pancreas (pancreatitis, cystic fibrosis, cancer, tumors of the islet apparatus, etc.); hepatogenic, observed in acute and chronic liver diseases, intra- and extrahepatic cholestasis; enterogenous, caused by various intestinal diseases (enterocolitis, celiac disease, Crohn's disease, diverticulitis, blind loop syndrome, infectious, parasitic, vascular intestinal diseases), as well as postoperative (resection of the small intestine); endocrine, observed in diabetes mellitus, hyper- and hypothyroidism; so-called Iatrogenic, caused by long-term use of antibiotics, laxatives, cytostatics and other drugs, as well as radiation therapy.

There are other classifications, for example, according to Polonovsky (C. Polonovski, J. Polonovski), the cut is based on the division of M. s. according to the type of its origin (impaired absorption of gastric and intestinal origin, due to bile deficiency, due to pathology of the pancreas).

With primary M. s. Most often, there is a selective deficiency of enzymes or transport carriers and, as a result, the absorption of one food substance or several substances similar in structure suffers.

With secondary M. s. Usually there is a deficiency of many enzymes and transporters, various mechanisms of malabsorption are realized, which leads to impaired absorption of a number of nutrients. Of the primary malabsorption disorders in adults, hl occurs. arr. intolerance to disaccharides (disaccharidase deficiency), mainly lactose, other forms of primary M. s. quite rare, most of them are observed in children. Secondary M. s., especially in an erased form, is relatively often noted in the clinic of gastroenterological diseases of adults.

Clinical picture

One of the most important wedge, symptoms of M. s. in children it is chronic, diarrhea, and a unique indicator of insufficient absorption is steatorrhea - increased excretion of lipids in feces. The child stops gaining weight, malnutrition develops, and then exhaustion, and growth retardation (hypostature) is observed. Depending on the duration and nature of the process, changes in other organs and systems increase: the skin becomes dry, with a pellagroid coloration; glossitis is pronounced, the tongue is red without papillae; swelling appears due to disturbances in protein and water-electrolyte metabolism; hypochromic anemia, hypokalemia, hyponatremia, hypocalcemia are noted. In some forms of M. s. changes in the urine are observed, for example, with milk intolerance associated with lactose deficiency; in some cases, lactosuria is noted in the urine (see). There may be seizures, osteoporosis or osteomalacia due to calcium deficiency in the body; bloating, intestinal colic due to hypokalemia and increased fermentation processes in the intestines. However, M. s. can proceed without any sharp disturbances from the gastrointestinal tract. tract.

In adults, wedge, picture of M. s. largely due to the nature of the underlying disease. The intensity of intestinal symptoms (stool upset, rumbling, etc.) depends on the degree of intestinal damage, on the involvement of the colon in the patol process, often there are no intestinal symptoms at all. General manifestations predominate, indicating violations of the basic metabolic processes and functions of a number of organs and systems, which is associated with insufficient supply of nutrients to organs and tissues.

Patients complain of increased fatigue, decreased performance, weakness, decreased appetite, weight loss, sometimes exhaustion up to cachexia (see). They experience dry skin, hair loss, and increased brittleness of nails. There may be diarrhea, steatorrhea, creatorrhea. In the blood - hypoproteinemia, dysproteinemia, changes in the composition of blood amino acids, in the urine - hyperaminoaciduria (see Aminoaciduria). The concentration of cholesterol, total lipids and their fractions in the blood serum decreases. Wedges and signs of thiamine deficiency (paresthesia in the limbs, pain in the legs, sleep disorders), riboflavin (cheilitis, angular stomatitis), nicotinic acid (glossitis, pellagroid skin changes), ascorbic acid (bleeding gums) and others are often observed vitamins (see Vitamin deficiency). A number of wedges, symptoms are caused by impaired electrolyte metabolism: hyponatremia (arterial hypotension, tachycardia, dry skin and tongue, thirst), hypokalemia (muscle weakness, muscle pain, weakened tendon reflexes, decreased intestinal motility, extrasystole, etc.), hypocalcemia (numbness of lips and fingers, increased neuromuscular excitability, osteoporosis), manganese deficiency (decreased sexual function). In severe cases, osteomalacia with bone fractures and tetany may occur. Iron deficiency and B12-folate deficiency anemia often occur. In the oral cavity there are atrophic processes, desquamative changes in the tongue, and sometimes periodontopathy. The skin becomes atrophic, dry, folded, acquires a dirty gray color, and pigmentation appears. Cracks appear around the mouth, eyes, and anus; in severe cases, the disease is complicated by eczema and neurodermatitis. Changes in the endocrine system are noted (hypocortisolism, sexual function disorders, etc.); in severe cases, pluriglandular insufficiency syndrome may develop with damage to the pituitary gland, adrenal glands, gonads, and thyroid gland (see Polyglandular insufficiency). Neurotic disorders and hypochondriacal conditions are often observed.

Klin, painting by M. s. to a certain extent depends on the localization patol. process in the small intestine. For example, when its proximal parts are predominantly affected, the absorption of calcium, iron, folic acid, and B vitamins is affected. When the middle parts are affected, the absorption of fatty acids and amino acids is impaired. Absorption of monosaccharides is impaired when the proximal and middle parts of the intestine are affected. When the distal parts of the small intestine are affected, there is insufficient absorption of vitamin B12 and bile cells, therefore, in the case of resection of the ileum, in some forms of Crohn's disease, the enterohepatic circulation of bile cells is disrupted.

With M., especially when the distal ileum is affected, the excretion of oxalates in the urine often increases - enteral oxaluria, which can lead to the formation of oxalate stones.

Malabsorption (malabsorption syndrome) is characterized by a disorder of absorption in the small intestine of one or more nutrients and the occurrence of metabolic disorders.
There are hereditary and acquired malabsorption syndromes.
Intestinal manifestations of malabsorption: diarrhea, polyfecalia, steatorrhea, creatorrhea, amilorrhea.
Malabsorption syndrome is manifested by disturbances in protein, carbohydrate, fat, vitamin, mineral and water-salt metabolism.

In
the intestine, as is known, the final stage of the process of digestion and absorption of food occurs, as well as the release of a number of substances. When one or another part of the intestine is damaged, a group of signs characterizing its disease appears. Thus, when the small intestine is damaged, the syndrome of insufficiency of digestion and the syndrome of insufficiency of intestinal absorption are most often observed. These two syndromes are closely related; more precisely, insufficiency of digestion is an integral part of the malabsorption syndrome. Digestive insufficiency syndrome is a manifestation of disturbances in the digestion of nutrients due to a deficiency of digestive enzymes. The occurrence of digestive disorders is based on genetically determined or acquired insufficient production of digestive enzymes in the small intestine. Moreover, there is either a lack of synthesis of one or more enzymes, or a decrease in their activity, or a change in biochemical reactions affecting enzymatic activity. Among congenital enzymopathies, the most common is deficiency of disaccharidases (lactase, sucrase, isomaltase, etc.), peptidases (gluten enteropathy), and enterokinase. Acquired enzymopathies are observed in diseases (chronic enteritis, Crohn's disease, diverticulosis with diverticulitis, etc.) and resection of the small intestine, diseases of other digestive organs (pancreatitis, hepatitis, cirrhosis of the liver) and endocrine system organs (diabetes, hyperthyroidism), as well as when taking some medications (antibiotics, cytostatics, etc.) and radiation. Of the acquired enzymopathies, the most common is nutritional, in which disturbances in the production and activity of enzymes are associated with the nature of nutrition. Thus, a deficiency of protein, vitamins, microelements in the diet, unbalanced nutrition (amino acid imbalance, imbalance between fatty acids, water- and fat-soluble vitamins, mineral salts) can lead to persistent disorders of the digestive process. Inhibition of the activity and biosynthesis of enzymes and proteins may also be due to the toxic effects of some natural food components or foreign impurities contaminating them. In a number of foods (legumes, cereals, rice, eggs, etc.) thermostable specific protein inhibitors have been found that form stable complexes with proteinases of the gastrointestinal tract (GIT), causing inhibition of their activity and, as a result, disruption of the digestion and assimilation of food protein. The biosynthesis of some enzymes is disrupted by a deficiency of coenzymes - water-soluble vitamins. This is due to the presence of antivitamins in food products, which destroy or replace vitamins in the structure of the enzyme molecule, significantly reducing or completely suppressing the specific effect of vitamins. Antagonists of nicotinic acid are low-molecular compounds - niacitin and niacinogen, isolated from corn, pyridoxine - linatine, contained in flax seeds. Freshwater fish contain thiaminase, which catalyzes the hydrolytic breakdown of thiamine. The protein avidin, found in raw eggs, forms a stable complex with biotin in the gastrointestinal tract. Contamination of food products with salts of heavy metals (mercury, arsenic), pesticides, mycotoxins (aflatoxins, trichothecene mycotoxins, etc.), which react with sulfhydryl groups of protein molecules, suppress protein biosynthesis, and cause inhibition of enzymatic activity. There are several forms of digestive insufficiency syndrome:

disturbance of predominantly cavity digestion,
disruption of predominantly parietal (membrane) digestion,
disruption of predominantly intracellular digestion,
mixed forms.

All these disorders are accompanied by diarrhea, flatulence and other dyspeptic disorders. At the same time, each of the forms has its own pathogenetic characteristics. Disorders of predominantly cavity digestion (dyspepsia)

occurs due to an uncompensated decrease in the secretory function of the stomach, intestines, pancreas, and bile secretion.
A significant role in its occurrence is played by a violation of the motor function of the gastrointestinal tract: stagnation of contents due to spasm, stenosis or compression of the intestine, or accelerated passage of food chyme due to accelerated peristalsis. The appearance of dyspepsia is facilitated by previous intestinal infections, changes in the intestinal microflora, when the number of bifidumbacteria and E. coli decreases, the upper parts of the small intestine are colonized by microorganisms, and pathogenic flora is activated, causing fermentation and putrefaction processes in the large intestine. Dyspepsia is caused by nutritional disorders: overeating, unbalanced nutrition and consumption of excessive amounts of either carbohydrates, proteins, or fats; eating food devoid of vitamins. Excessive food load in combination with mental and physical overstrain, overheating, hypothermia, i.e., with factors leading to inhibition of the secretory function of the digestive glands, is especially dangerous. In the pathogenesis of dyspepsia, an important role is played by insufficiently complete breakdown of nutrients by digestive enzymes located in the intestinal cavity. Insufficiency of parietal digestion
develops in chronic diseases of the small intestine, the morphological substrate of which is inflammatory, dystrophic and sclerotic changes in the mucous membrane, changes in the structure of villi and microvilli and a decrease in their number per unit surface.
The occurrence of insufficiency of parietal digestion is facilitated by changes in the enzymatic layer of the intestinal surface and disorders of intestinal motility, in which the transfer of nutrients from the intestinal cavity to the surface of enterocytes is disrupted. Insufficiency of intracellular digestion
is associated with primary or secondary fermentopathy, which is based on genetically determined or acquired intolerance to disaccharides and certain proteins.
Primary insufficiency of intracellular digestion, as a rule, develops in young children when an intolerable disaccharide is introduced into food. Acquired insufficiency is often a consequence of diseases of the small intestine. In the pathogenesis of the syndrome, the intensification of fermentation processes due to the entry of unsplit disaccharides into the large intestine and activation of microbial flora, the toxic effect of fractions of certain proteins (gliadin) is of significant importance. Malabsorption syndrome (malabsorption)
is characterized by impaired absorption of one or more nutrients in the small intestine and metabolic disorders.
The development of this syndrome is based on a number of factors:

morphological changes in the mucous membrane of the small intestine,
changes in enzyme systems, impaired digestion of nutrients,
disorder of specific transport mechanisms,
intestinal dysbiosis,
violation of intestinal motor function.

There are primary (hereditarily caused) and secondary (acquired) malabsorption syndrome. Primary syndrome develops with hereditary changes in the structure of the mucous membrane of the small intestine and genetically determined enzyme Topathies. This group includes a relatively rare congenital malabsorption of the small intestine, caused by a deficiency of specific transport enzymes in the mucous membrane of the small intestine. This disrupts the absorption of monosaccharides and amino acids (for example, tryptophan). This group also includes impaired absorption of the protein of cereals (wheat, barley, rye, oats) - gluten, leading to the occurrence of celiac disease. Of the primary malabsorption disorders in adults, disaccharide intolerance is the most common. Secondary malabsorption syndrome is associated with acquired changes in the structure of the mucous membrane of the small intestine that occur as a result of certain diseases, as well as diseases of other abdominal organs involving the small intestine in the pathological process. Among the diseases of the small intestine characterized by disruption of the intestinal absorption process are chronic enteritis, Crohn's disease, Whipple's disease, exudative enteropathy, diverticulosis with diverticulitis, extensive (more than 1 m) resection and tumors of the small intestine. The malabsorption syndrome can be aggravated by concomitant diseases of the pancreas that occur with a violation of its exocrine function and the hepatobiliary system. It is observed in diseases involving the small intestine in the pathological process, in particular in amyloidosis, scleroderma, agammaglobulinemia, abetalipoproteinemia, lymphoma, heart failure, arterio-mesenteric circulation disorders, thyrotoxicosis and hypopituitarism. Absorption is also impaired by poisoning, blood loss, vitamin deficiency, and radiation damage. The small intestine is very sensitive to the action of ionizing radiation, in which neurohumoral regulation is disrupted, cytochemical and morphological changes in its mucous membrane occur, degeneration and shortening of the villi, disruption of the ultrastructure of the epithelium and its desquamation, microvilli are reduced and deformed, their total number decreases, and the structure of the mitochondria is damaged. As a result of these changes, the absorption process during irradiation, especially its parietal phase, is disrupted. The occurrence of malabsorption syndrome in acute and subacute conditions is associated with various factors:

acute and subacute conditions - impaired intestinal digestion of nutrients, accelerated passage of contents through the intestines,
chronic conditions - dystrophic, atrophic, sclerotic changes in the mucous membrane of the small intestine.

In acute and subacute conditions, malabsorption is caused primarily by a disorder of the digestive process and motor function, and in chronic conditions - by a change in the structure of the mucous membrane of the small intestine. At the same time, villi and crypts are shortened and flattened, the number of microvilli decreases, fibrous tissue grows in the intestinal wall, and blood and lymph circulation is disrupted. A decrease in the total absorption surface and absorption capacity leads to disruption of intestinal absorption processes. As a result, the body receives insufficient quantities of hydrolysis products of proteins, fats, carbohydrates, as well as mineral salts and vitamins. Metabolic processes are disrupted, a picture reminiscent of alimentary dystrophy develops. The pathological process in the small intestine, which occurs with protein deficiency, resembles that of intestinal diseases. It is characterized by thinning of the mucous membrane, loss of brush border disaccharidases, impaired absorption of mono- and disaccharides, decreased digestion and absorption of proteins, increased time of transport of contents through the intestine, and colonization of the upper parts of the small intestine by bacteria. Due to disruption of the structure of the mucous membrane of the small intestine, its passive permeability changes, due to which large macromolecules can penetrate the subepithelial tissues, increasing the likelihood of functional damage to intercellular connections. Insufficient formation of enzymes that break down proteins, transport carriers of the final products of digestion through the intestinal wall, leads to a deficiency of amino acids and protein starvation of the body. Defects in the hydrolysis process, impaired absorption and utilization of carbohydrates lead to a deficiency of mono- and disaccharides. Disorder of the processes of breakdown and absorption of lipids increases steatorrhea. In the malabsorption of fats, which has been studied most fully, a significant pathogenetic role is played, in addition to changes in the mucous membrane and intestinal dysbiosis, decreased secretion of pancreatic lipase and impaired emulsification of fats by bile acids. Impaired fat absorption also occurs with excess intake of calcium and magnesium salts from food. Patients with intestinal diseases develop a deficiency of water- and fat-soluble vitamins, iron, and microelements due to impaired absorption of these substances. The influence of some nutrients on the absorption of others was noted. Thus, in patients with impaired absorption of nicotinic acid, protein deficiency, in particular tryptophan deficiency, is detected. There is information about the dependence of the absorption of various substances on the localization of the process in the small intestine. Damage to the predominantly proximal parts of the small intestine is accompanied by impaired absorption of B vitamins, folic acid, iron, calcium, monosaccharides, the middle parts - impaired absorption of amino acids and fatty acids, and the distal parts - vitamin B12 and bile acids. Selective deficiency of only one nutrient is extremely rare; absorption of a number of ingredients is more often affected, which causes a variety of clinical manifestations of malabsorption syndrome. The clinical picture of this syndrome is quite characteristic: a combination of diarrhea and other intestinal manifestations (polyfecalia, steatorrhea, creatorrhoea, amilorrhea) with a disorder of all types of metabolism. The patient's exhaustion increases to the point of cachexia; general weakness, decreased performance; sometimes mental disorders and acidosis occur. Frequent signs are: polyhypovitaminosis, osteoporosis and even osteomalacia, B12-folate and iron deficiency anemia, trophic changes in the skin, nails, hypoproteinemic edema, muscle atrophy, polyglandular insufficiency. The skin becomes dry, often hyperpigmented in places, swelling occurs due to disturbances in protein and water-electrolyte metabolism, subcutaneous tissue is poorly developed, hair falls out, and nails become brittle. Due to vitamin deficiency, the following appear: with thiamine deficiency - paresthesia of the skin of the hands and feet, pain in the legs, insomnia; nicotinic acid - glossitis, pellagroid skin changes; riboflavin cheilitis, angular stomatitis; ascorbic acid - bleeding gums, hemorrhages on the skin; vitamin A - twilight vision disorder; vitamin B12, folic acid, iron-anemia. Clinical signs associated with impaired electrolyte metabolism include tachycardia, arterial hypotension, thirst, dry skin and tongue with sodium deficiency; muscle pain and weakness, weakened tendon reflexes, heart rhythm disturbances, often in the form of extrasystoles - with potassium deficiency - a positive symptom of a muscle roll due to increased neuromuscular excitability, a feeling of numbness of the lips and fingers, osteoporosis, sometimes osteomalacia, bone fractures, muscle cramps - with calcium deficiency. Changes in the endocrine organs are manifested by menstrual irregularities, the occurrence of impotence, and signs of hypocortisolism. The diagnosis of malabsorption syndrome is made on the basis of the clinical picture of the disease, determination of the content of total protein, protein fractions, immunoglobulins, total lipids, cholesterol, potassium, calcium, sodium, iron in the blood serum. Blood tests reveal, in addition to anemia, hypoproteinemia, hypocholesterolemia, hypocalcemia, hypoferremia, and moderate hypoglycemia. A scatological examination reveals steatorrhea, creatorrhoea, amilorrhea (extracellular starch is detected), and increased excretion of undigested nutrients in the feces. With disaccharidase deficiency, the pH of the stool decreases to 5.0 or lower; as a result, the test for sugar in milk in the stool and urine is positive. With lactase deficiency and intolerance to milk as a result, lactosuria can sometimes be detected. Tests with a load of mono- and disaccharides (glucose, D-xylose, sucrose, lactose) with their subsequent determination in the blood, feces, and urine help in diagnosing disaccharide intolerance. In the diagnosis of celiac disease, first of all, the effectiveness of a gluten-free diet (not containing products from wheat, rye, oats, barley) and the detection of antibodies to gluten in the blood serum are taken into account, and in the diagnosis of exudative hypoproteinemic enteropathy - daily protein excretion in feces and urine. Valuable information can be obtained by x-ray examination of the small intestine, paying attention to the passage of barium, the relief of the mucous membrane, the level of liquid and gas. Histological examination of a biopsy of the mucous membrane of the jejunum or distal duodenum allows us to characterize the morphological substrate of the malabsorption syndrome and, in some cases (for example, with Whipple's disease), determine its cause. Absorption tests help in diagnosis and allow you to get an idea of the degree of malabsorption of various products of intestinal hydrolysis: in addition to tests with D-xylose, galactose and other saccharides, iodine-potassium test, studies with loading of iron, carotene are used. For this purpose, methods based on the use of substances labeled with radioactive isotopes are also used: albumin, casein, methionine, glycine, oleic acid, vitamin B12, folic acid and others, as well as the jeunoperfusion method. Treatment for malabsorption syndrome includes:

a diet with limitation (exclusion) of intolerable, indigestible and intestinal irritating foods,
agents that stimulate membrane hydrolysis processes in the small intestine,
correction of metabolic disorders,
enzyme preparations,
antidiarrheals,
agents that normalize intestinal flora,
symptomatic remedies.

Treatment of primary (hereditarily caused) malabsorption syndrome consists primarily of prescribing a diet with the exclusion or limitation of intolerable foods and dishes that cause a pathological process in the small intestine. Thus, in case of intolerance to mono- and disaccharides, a diet that does not contain them or contains them in small quantities is recommended; In case of gluten intolerance (celiac disease), a gluten-free diet is prescribed. In case of secondary (acquired) syndrome of impaired intestinal absorption, the underlying disease should be treated first. Due to the insufficient activity of membrane digestive enzymes, anabolic steroids (retabolil, nerobol), a phosphodiesterase inhibitor - aminophylline, and an inducer of lysosomal enzymes - phenobarbital are prescribed, which stimulate the processes of membrane hydrolysis in the small intestine. They normalize the absorption of monosaccharides, increasing it at low rates and decreasing it at high rates, kinin inhibitors (parmidine), anticholinergic (atropine) and ganglion-blocking (benzohexonium) agents. In order to correct metabolic disorders, parenteral administration of protein hydrolysates, intralipid, glucose, electrolytes, iron is prescribed , vitamins. Good results in osteoporosis have been obtained from the use of drugs that affect bone tissue remodeling (2% xydiphone solution - 5 mg/kg/day in combination with oxydevit - 0.0005 - 0.001 mg/day). Pancreatic enzymes (Pancreatin, Mesimforte, Trienzyme, Panzinorm, etc.) are used as replacement therapy. The antidiarrheal effect, in addition to astringents and antibacterial drugs, including intetrix and smecta, is provided by enterosorbents - polyphepan, bilignin, etc. For malabsorption syndrome associated with intestinal dysbiosis, antibacterial drugs are recommended (short courses of broad-spectrum antibiotics, dental antibiotics - bactrim, naphthyridine derivatives - nevigramon, as well as intetrix with the subsequent use of biological drugs such as bifidumbacterin, colibacterin, bificol, lactobacterin. In case of impaired intestinal absorption caused by a disorder of the ileum (with terminal ileitis, resection of this part of the small intestine), drugs are prescribed that adsorb unabsorbed bile acids, promoting their excretion with feces (lignin) or form non-absorbable complexes with them in the intestine (cholestyramine), which also leads to increased excretion from the body. Among the symptomatic drugs used for malabsorption syndrome are cardiovascular, antispasmodic, carminative, astringents, etc. The prognosis for impaired intestinal absorption syndrome, as with any suffering, depends on timely diagnosis and early prescription of targeted therapy. These circumstances are also associated with the prevention of secondary malabsorption in the small intestine.

Diagnosis

The diagnosis of malabsorption syndrome should be made as early as possible in order to avoid worsening metabolic changes and disruption of various organs and systems.

V. A. Tabolin, E. I. Shcherbatova, T. I. Korneva, V. P. Lebedev, E. K. Kurgasheva (1973) proposed a multi-stage system for clinical and biochemical diagnosis of intestinal malabsorption syndromes in children. The research begins with an assessment of anamnestic data and genealogical analysis (see Genealogical method). At the same time, pay attention to the presence of diseases in relatives. tract (gastritis, peptic ulcer, cholecystitis, enterocolitis, pancreatitis), respiratory system (chronic, bronchitis), metabolic disorders (diabetes mellitus, hyperthyroidism). Along with genealogical analysis, screening tests are envisaged, such as tests for various sugars in feces and urine; scatological examination, determination of stool pH, reaction of stool filtrate with trichloroacetic acid, boiling test. The following tests are used: Benedict's test for sugars, Welk's test for lactose and maltose, Helman's test for sucrose, determination of carbohydrate content in feces using Clinitest tablets using the Anderson method. These tests allow us to identify changes characteristic of individual syndromes.

If celiac disease is suspected (see), the greatest value is the study of the content of total protein, protein fractions, immunoglobulins, total lipids, cholesterol and phosphorus, potassium and sodium in the blood serum, rentgenol. research went.-kish. tract with a suspension of barium sulfate, radiography of long bones, as well as assessment of the effectiveness of the ongoing gluten-free elimination diet - exclusion from the diet of products from rye, wheat, barley and oatmeal (see Celiac disease).

To confirm the diagnosis of M. s. in case of cystic fibrosis (see), it is necessary, along with the determination of sodium and chlorine in sweat fluid, nail plates, and testing with DOX, to study the immune status, the functional state of the liver, as well as the proximal parts of the nephron.

In patients with exudative enteropathy (see Exudative enteropathy), muscle fibers are revealed during scatological examination; qualitative reactions indicate the presence of plasma proteins in the stool. With disaccharidase deficiency, a decrease in stool pH to 5.0 or lower is detected; extracellular starch is found in the coprogram; tests for sugar in urine and stool are positive. Of great importance in the diagnosis of disaccharide intolerance are stress tests with mono- and disaccharides (glucose, D-xylose, lactose, sucrose, etc.) followed by blood tests and their chromatographic identification in feces and urine, as well as the study of daily urinary excretion of carbohydrates and proteins.

If Hartnup's disease is suspected (see Hartnup's disease), along with the characteristic wedge symptoms, the determination of the content of indican, amino acids proline and argine in the urine is of great importance for the diagnosis. Positive tests of verification studies make it possible to conduct more in-depth studies using quantitative analytical methods: blood, daily urine, feces are examined; using an x-ray film test and a test with iodolipol, the activity of trypsin and lipase is assessed; identification of proteins in blood serum and feces is carried out. A study of the daily excretion of carbohydrates in urine reveals melituria (see) in the intestinal form of cystic fibrosis, disaccharidase deficiency, glucose and galactose intolerance. Identification of proteins in blood serum and feces using immunoelectrophoresis (see) makes it possible to diagnose exudative enteropathy. After conducting clinical biochem. By comparing the results obtained, the presumptive diagnosis is confirmed by targeted clinical, radiological and gastroduodenoscopic studies, which are carried out taking into account the data obtained earlier.

All of the listed methods are used in practice to establish the diagnosis of M. s. in adults. Methods for recognizing disorders of the absorption function of the small intestine - see Intestines.

Glucose-galactose malabsorption: causes, symptoms, treatment, prognosis

Here are the main points you need to know:

Glucose-galactose malabsorption (GGM) is a rare metabolic disorder in which the cells lining the intestines are unable to metabolize two specific sugars, glucose and galactose. This disease appears after the birth of the child.
Sahara . A person with HGM who consumes these sugars has trouble digesting them because they cannot be absorbed by the body. This causes water to remain outside the body's cells, causing diarrhea and dehydration.
Risk factors for the development of glucose-galactose malabsorption have not been found, since this disease is hereditary, i.e. it is passed down from generation to generation from parents to children. HGM is caused by the inheritance of two copies of a specific gene that are essentially defective.
Heredity . If it is known that the child's parents or grandparents suffered from glucose-galactose malabsorption, then most likely this child will have this disease. If there is constant, watery diarrhea in the first few days of his life, then the child has HGM. However, the severity of symptoms may vary from one child to another.
The diagnosis of glucose-galactose malabsorption is usually made early in a child's life. There are also special diagnostic procedures that can be performed with the help of medical personnel to make a physical diagnosis of this metabolic disorder.
Complications . Complications of glucose-galactose malabsorption include: dehydration during the first few days of an infant's life. Severe diarrhea and loss of large amounts of water from the body. Adults with HGM often experience abdominal discomfort (bloating, diarrhea, nausea, and cramps) after eating foods that contain certain sugars (milk sugar and table sugar).
Treatment . To treat glucose-galactose malabsorption, it is necessary to avoid consuming sugars found in certain foods. These sugars are replaced with fructose (fruit sugar).
The prognosis for HGM is positive. As long as you avoid these sugars and foods containing them, symptoms will not be felt. However, the disease is incurable and is present throughout a person's life.

Who suffers from glucose-galactose malabsorption (gender and age)

Glucose-galactose malabsorption is diagnosed during the first few weeks of an infant's life. Both men and women suffer from this disease.

But about two-thirds of cases (or about 67%) occur in women. There is no geographic localization of glucose-galactose malabsorption.

In addition, no ethnic group or race is more susceptible to developing HGM than one another.

Risk factors (predisposing factors)

Glucose-galactose malabsorption is a hereditary disease passed from generation to generation. Heredity is the main risk factor. There are no other known risk factors that predispose to the development of this disease.

It is important to note that the presence of a risk factor does not mean that a person will necessarily suffer from HGM. A risk factor increases the likelihood of developing this disease compared to a person without risk factors. Additionally, the absence of risk factors does not mean that a person cannot be born with the disease.

Causes of occurrence (etiology)

HGM occurs due to a genetic abnormality:

Glucose-galactose malabsorption is a disease that is caused by the inheritance of a certain gene that is responsible for the production of a protein involved in the transport of sodium and glucose. This protein is found primarily in the gastrointestinal tract.
A mutation that occurs in this gene changes its sequence, resulting in the inability of cells in the intestines to absorb glucose and galactose.
This gene (known as the SLC5A1 gene) depends on sodium to transport glucose and galactose. HGM occurs when two mutant copies of this gene are inherited. This is called an autosomal recessive mechanism of inheritance of the disease.

Autosomal recessive diseases occur when two copies of an abnormal gene have been inherited on a non-sex chromosome. If both parents have an autosomal recessive disorder, the chance of passing on the mutated genes to their child is 100%.

If only one mutant copy of the gene is inherited, the individual will be a carrier of the disease but will not experience any of its symptoms.

Children born to two carriers have a 25% chance of being homozygous dominant (without symptoms of the disease), a 50% chance of being heterozygous (carrier), and a 25% chance of being homozygous recessive (with symptoms of the disease).

Signs and symptoms of glucose-galactose malabsorption

Signs and symptoms of glucose-galactose malabsorption include:

A severe form of diarrhea and dehydration that occurs during the first few days (or even on the very first day) of the baby's life.
Adults with HGM often experience bloating and discomfort, nausea, diarrhea, and abdominal pain.

Malabsorption syndrome in children may vary in severity of signs and symptoms. Some may experience mild signs and symptoms, while others may have severe symptoms.

Diagnosis of glucose-galactose malabsorption

To diagnose glucose-galactose malabsorption, the following tests and analyzes are used:

A thorough assessment of family medical history and a complete physical examination.
The presence of persistent, watery diarrhea during the first few days of an infant's life causes the attending physician to suspect HGM.

If the doctor suspects the presence of glucose-galactose malabsorption syndrome, he may refer for the following diagnostic procedures:

Hydrogen breath test. This test is used to detect lactose (milk sugar) intolerance. To do this, you need to exhale into a special bag that looks like a balloon. The purpose of this test is to detect hydrogen in the exhaled air, the presence of which indicates malabsorption (malabsorption syndrome).
As a rule, the level of hydrogen in the air exhaled by a person is very low. Elevated hydrogen levels indicate lactose intolerance, which is a sugar containing glucose and galactose.

Many clinical conditions may have similar signs and symptoms. Your doctor may perform additional tests to rule out other conditions to help make a definitive diagnosis.

Complications of glucose-galactose malabsorption

Glucose-galactose malabsorption can cause the following complications:

Severe dehydration as a result of severe diarrhea early in the infant's life.
Nutrient deficiencies can occur due to severe diarrhea and dehydration.
In adults with glucose-galactose malabsorption, abdominal complications may occur when consuming certain sugars.
Osteopenia is a decrease in bone mineral density.
Osteoporosis is thinning of bone tissue, weakening of bones and increasing the risk of fractures.

Treatment

In case of primary (hereditarily caused) syndrome of intestinal malabsorption, an important component of complex therapy is treatment. nutrition, which provides for the limitation or exclusion of foods that lead to the development of patol, symptoms. Thus, in the treatment of celiac disease, the main thing is to use a gluten-free diet. A high-calorie diet with sufficient protein, vegetables, and fruits is prescribed; products made from rye, wheat, and oats are completely excluded.

In case of intolerance to disaccharides and monosaccharides, a diet with restrictions is necessary, and in some cases with the exclusion of those sugars that the patient cannot tolerate.

Treatment of lactose intolerance in infants is a difficult task, since in severe forms of deficiency it is necessary to exclude milk from the diet. In these cases, lactose-free milk formulas (galantamine, soyaval) are used. If there is a lack of sucrose, the child should not be transferred to mixed and artificial feeding early. Nutrition of children with intestinal and mixed forms of cystic fibrosis with a predominance of disorders from the gastrointestinal tract. tract, is based on compliance with the standards of products and menus accepted under normal conditions, but with a high content of proteins and carbohydrates, some limitation of fats, and a sufficient content of vitamins and mineral salts.

In case of intolerance to sucrose and isomaltose, sucrose is excluded and starch is limited; in case of intolerance to glucose and galactose, these monosaccharides are sharply limited, fructose is prescribed in increased quantities; in case of celiac enteropathy and other forms of severe enterocolitis, a gluten-free diet is recommended. In case of severe malabsorption of fats (for example, with cystic fibrosis), it is recommended to limit regular fats and prescribe triglycerides containing fatty acids obtained from coconut oil, which are easily hydrolyzed and absorbed in the intestines. In patients with severe forms of M. s. the so-called has a good therapeutic effect. nutritional diet, which is a mixture of amino acids, dextrin, trace elements, vitamins with the addition of small amounts of fat. This diet does not contain lactose, whole protein, is extremely low in waste and fat, and does not contain allergens.

Therapy for secondary (acquired) intestinal malabsorption syndrome involves treating the underlying disease. In severe cases M. s. Parenteral nutrition courses (glucose, protein hydrolysates, basic electrolytes, vitamins) are very effective. With M. s. due to intestinal dysbiosis, short courses of broad-spectrum antibiotics or eubiotics (8-hydroxyquinoline derivatives, Bactrim, etc.) are indicated; biol drugs (colibacterin, bificol, bifidumbacterin, etc.) are also recommended.

An essential role among to lay down. measures are played by means of replacement therapy. Preparations of pancreatic enzymes (Pancreatin, Panzinorm Forte, etc.), Abomin and a number of other enzyme preparations are prescribed; Only large dosages of these drugs are effective. The administration of enzyme preparations together with antacids, which significantly inhibit gastric secretion, helps to enhance the therapeutic effect of enzyme preparations for M. s. due to pancreatic insufficiency. Vitamins (A, D, K, C, folic acid, complex B, B12), calcium, magnesium, iron, cobalt are prescribed in pharmacodynamic doses. The administration of protein preparations (plasma, protein hydrolysates, protein, etc.) is indicated. With M. s. Cholestyramine is recommended due to dysfunction of the ileum (after its resection, in Crohn's disease, etc.), lignin (polyphepan) can be used for the same purpose, adsorbing unabsorbed bile cells and promoting their excretion in feces.

In cases of secondary M. s., caused by hl. arr. insufficient activity of membrane digestion enzymes, Difril (Corontin) in sufficient doses (at least 180 mg per day), as well as anabolic steroids (Nerobol, etc.), which stimulate the processes of membrane hydrolysis in the small intestine, are indicated. The phosphodiesterase inhibitor aminophylline and the inducer of lysosomal enzymes phenobarbital also increase the activity of membrane digestive enzymes. Some adrenomimetic drugs stimulate the absorption of monosaccharides in the small intestine - ephedrine, L-dopa, beta-blocker propranolol (obzidan, anaprilin), deoxycorticosterone acetate, aminophylline. The kinin inhibitor prodectin (parmidine), anticholinergic (atropine) and ganglion-blocking (benzohexonium) drugs have a normalizing effect on the absorption of monosaccharides - and at low initial rates they stimulate it, at high levels they inhibit it. For diseases where M. s. is secondary, when malabsorption is not associated with a deficiency of digestive enzymes or transport carriers, correction of intestinal absorption processes with the help of medications can be effective.

What is malabsorption syndrome: glucose-galactose form

The glucose-galactose form of malabsorption has a hereditary predisposition. The pathology is characterized by a change in the gene responsible for the formation of the transport protein. This component takes part in the movement of galactose and glucose, so the disease often occurs against the background of diabetes mellitus. As a result of the violation:

the concentration of glucose in the blood decreases;
oxygen transport by red blood cells deteriorates;
symptoms of mental and mental disorders are formed.

The manifestation of the syndrome is influenced by the following factors:

allergy to a certain product;
foods with sugar can trigger glucose deficiency;
infant formula and cow's milk - for lactase deficiency and protein intolerance;
cereal food - for celiac disease (damage to the villi of the small intestine due to exposure to certain foods with proteins).

Statistics: the congenital form of malabsorption is most often detected immediately after birth or in the first 10 years of a child’s life. Survival depends on the type of pathology that caused the syndrome.

Causes: lactase deficiency, intestinal diseases, diabetes mellitus and others

Malabsorption syndrome is a multifaceted and complex process. The human body contains many enzymes and nutrients, and disruption of the absorption of one of them causes negative changes. The following reasons can lead to the formation of a congenital type of disorder:

lactase deficiency;
celiac disease;
Hartnup's disease;
disaccharide deficiency;
disruption of amino acid transport.

The acquired form is associated with exposure to a specific disease or intervention:

Bowel changes:
Crohn's disease;
fistulas;
diverticula;
surgical intervention;
strictures.
Disorders within the intestinal lumen as a result of:
failure of bile acid secretion;
diseases of the pancreas (chronic pancreatitis, cystic fibrosis). Common causes of malabsorption in children and adults
Pathological changes that do not relate to the intestines:
formations of a malignant nature;
pathologies of the parathyroid and thyroid glands;
collagenosis;
diabetes;
Addison's disease.

Symptoms of the syndrome

The main signs of malabsorption syndrome include:

frequent stomach rumbling;
diarrhea;
weight reduction;
discomfort in the abdominal area;
change in skin condition.

Specific signs are also characteristic of the pathology:

peeling of the skin;
changes in mucous membranes, tongue and skin;
convulsions;
intense hair loss;
pain in muscles and bones;
weakness;
swelling;
blurred vision in the dark;
changes in the sexual sphere: disruption of the menstrual cycle, decreased libido and impotence.

Depending on the severity, the disease can have a mild, moderate or severe course.

Establishing diagnosis

Such a complex disorder requires a complete diagnosis of the patient, so several examination methods are used:

Blood test:
general analysis - anemia is detected;
identifying the level of coagulation - helps to detect vitamin K deficiency;
determination of the content of substances in the blood: sodium, calcium, electrolytes, vitamin B12 and iron.
Additional research:
determination of autoantibodies - necessary for the development of celiac disease;
Diagnosis of the secretory function of the pancreas.
Test samples:
Schilling test - assess the degree of malabsorption of vitamin B12;
pancreolauryl and stimulated secretin test - study pancreatic insufficiency;

To confirm pathology and differential diagnosis, instrumental research methods are used:

biopsy of the intestinal mucosa - reveals the disease or tumor that caused the disorder;
magnetic resonance and computed tomography;
endoscopy of the duodenum and colon, as well as the stomach and esophagus - detect diseases and other causes of the syndrome;
ultrasound examination of the abdominal cavity;
X-ray diagnostics - detect anatomical changes indicating bacterial growth.

Treatment methods

The goal of therapy is to eliminate the signs of the disorder, but this is impossible without eliminating the cause of malabsorption. Treatment is carried out in several stages:

elimination of symptoms;
weight normalization;
identifying the cause and eliminating it;
neutralization of consequences;
adherence to the regimen to prevent relapse.

Note! Traditional medicine is ineffective for the treatment of malabsorption syndrome, so they are not used.

Prescription of medications is one of the methods of treating malabsorption. Depending on the type of disorder, the following may be prescribed:

vitamins and minerals (Folacin, Nicotinamide, Sufer, Ferrum Lek) - elements that are not absorbed by the body are used;
antibiotics (Gentamicin, Amoxicillin, Novosef, Doxycycline, Bactrim) - used for infectious lesions;
hormonal therapy (Prednisolone) - prescribed for Crohn's disease, celiac disease and other inflammatory processes;
pancreatic drugs (Mezim, Pangrol, Creon) - compensate for the lack of pancreatic enzymes;
choleretic agents (Allohol, Nikodin, Ursofalk) - increase the secretion of bile;
probiotics (Enterozermina, Linex) – improve the absorption of substances and intestinal microflora;
drugs to reduce the secretion of peptides and reduce the production of gastric juice - Sandostatin;
antidiarrheal drugs (Lopedium, Imodium) - inhibit intestinal motility;
antacids (Rennie, Gastal, Omeprazole, Maalox) - reduce the risk of developing ulcers and other lesions;
analgesics (Spazmalgon, Analgin) - to reduce pain.

Imodium is an antidiarrheal agent Pangrol replenishes the deficiency of pancreatic enzymes Prednisolone is necessary for inflammatory processes Sandostatin reduces the secretion of peptides and reduces the production of gastric juice Ferrum Lek replenishes the deficiency of iron

Diet for adults and children: use of mixtures Peptamen, Nutrien Elemental, Nutrilon

The principles of nutrition for malabsorption syndrome are as follows:

determine the degree of absorption of nutrients;
avoid taking foods whose elements are difficult to digest;
replace lost components with alternative foods containing essential nutrients;
plan a diet taking into account the cause of the pathology;
drink large amounts of liquid to remove toxic elements.

Doctors recommend that patients include foods in their diet that are high in protein and low in fat. In some cases, enteral (via tube) nutrition products are used, as they contain a suitable composition of proteins, carbohydrates and fats. The most commonly used semi-element mixtures are Peptamen and Nutrien Elemental.

A child is very vulnerable in the first year of his life, so choosing the right diet is an important point. If it is necessary to use infant formula, you need to choose a diet depending on the type of disorder, for example, in case of celiac disease, preference is given to gluten-free formulas. Young patients may be prescribed a special Nutrilon mixture, which improves the absorption of substances.

If there is no possibility of self-feeding, then a special probe is used through which the mixture is supplied. In severe cases, nutrients are administered intravenously.

Prognosis and Prevention

Forecast for primary M. s. depends on the timeliness of the diagnosis and the correctness of the treatment; in case of secondary MS, it depends on the underlying disease and the effectiveness of the treatment.

Prevention of secondary M. s. consists of treating the underlying disease.

Bibliography:

Badalyan L. O., Tabolin V. A. and Veltishchev Yu. E. Hereditary diseases in children, p. 231, M., 1971; Vasilenko V. X. and Vinogradova M. A. About the problem of insufficient absorption of nutrients and the classification of its form, Klin, med., t. 45, No. 2, p. 9, 1967; Veltishchev Yu. E. et al. About intolerance to disaccharides in childhood, Vopr. ocher mat. and children, vol. 14, no. 12, p. 3, 1969, bibliogr.; G at b e r g r and c A. Ya. and L and Nevsky Yu. V. Diseases of the small intestine, M., 1975, bibliogr.; Complex therapy for diseases of the digestive system, ed. H. T. Larchenko and A. R. Zlatkina, M., 1977; Loginov A. S. et al. Treatment of patients with chronic diseases of the small intestine, Sov. med., No. 2, p. 63, 1979; Tabolin V. A. et al. Issues of diagnosis and treatment of malabsorption syndromes in children, Pediatrics, No. 3, p. 3, 1974; Physiology of absorption, ed. A. M. Ugoleva et al., L., 1977; F r about l-kiye A. V. Chronic enterocolitis, L., 1975, bibliogr.; Ament M. E. Malabsorption syndromes in infancy and childhood, J. Pediat., v. 81, p. 685, 1972; Bond JH a. L evitt MD Quantitative measurement of lactose absorption, Gastroenterology, v. 70, p. 1058, 1976; Gastrointestinal disease, ed. by M. H. Slei-senger a. J. S. Fordtran, p. 259, Philadelphia, 1973, bibliogr.; L osowsky MS, Walker BE a. K e 1 1 eher J. Malabsorption in clinical practice, Edinburgh, 1974, bibliogr.; Regan PT Konservative Therapie der Malabsorption, Leber Magen Darm, Bd 7, S. 201, 1977, Bibliogr.; Schreier K. Maldigestions-und Ma-labsorptionsyndrome, in the book: Klin. Gastroenterol., hrsg. v. L. Demling, Bd 1, S. 302, Stuttgart, 1973.

A. V. Frolkis; V. A. Tabolin (ped.).