Intestinal absorption failure syndrome: causes, symptoms, diagnosis, treatment

Intestinal malabsorption syndrome is a symptom complex characterized by a disorder of absorption of one or more nutrients in the small intestine and a disruption of metabolic processes. The development of this syndrome is based not only on morphological changes in the mucous membrane of the small intestine, but also on disturbances in enzyme systems, intestinal motor function, as well as a disorder of specific transport mechanisms and intestinal dysbacteriosis.

There are primary (hereditary) and secondary (acquired) malabsorption syndromes. Primary syndrome develops with hereditary changes in the structure of the small intestinal mucosa and genetically determined enzymopathy. This group includes a relatively rare congenital disorder of absorption in the small intestine, caused by a deficiency in the small intestinal mucosa of specific enzymes - carriers. In this case, the absorption of monosaccharides and amino acids (for example, tryptophan) is impaired. Of the primary absorption disorders in adults, intolerance to disaccharides is most common. Secondary malabsorption syndrome is associated with acquired damage to the structure of the small intestinal mucosa, which occurs with certain diseases, as well as diseases of other abdominal organs with the involvement of the small intestine in the pathological process. Among the diseases of the small intestine characterized by a disorder of the intestinal absorption process, chronic enteritis, gluten enteropathy, Crohn's disease, Whipple's disease, exudative enteropathy, diverticulosis with diverticulitis, tumors of the small intestine, as well as extensive (more than 1 m) resection are distinguished. The syndrome of insufficient absorption can be aggravated by concomitant diseases of the hepatobiliary system, pancreas with a violation of its exocrine function. It is observed in diseases involving the small intestine in the pathological process, in particular in amyloidosis, scleroderma, agammaglobulinemia, abetalipoproteinemia, lymphoma, heart failure, disorders of arteriomesenteric circulation, thyrotoxicosis and hypopituitarism.

Absorption also suffers in cases of poisoning, blood loss, vitamin deficiency, and radiation damage. It has been established that the small intestine is very sensitive to the effects of ionizing radiation, which causes disturbances in neurohumoral regulation and cytochemical and morphological changes in the mucous membrane. Dystrophy and shortening of villi, disruption of the ultrastructure of the epithelium and its sloughing appear. Microvilli decrease and become deformed, their total number decreases, and the structure of the mitochondria is damaged. As a result of these changes, the absorption process is disrupted during irradiation, especially its parietal phase.

The occurrence of malabsorption syndrome in acute and subacute conditions is associated primarily with a disorder of intestinal digestion of nutrients and accelerated passage of contents through the intestine. In chronic conditions, the disorder of the intestinal absorption process is caused by dystrophic, atrophic and sclerotic changes in the epithelium and proper layer of the small intestinal mucosa. In this case, the villi and crypts shorten and flatten, 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 a disorder 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 resembling alimentary dystrophy develops.

Consequently, diseases of the small intestine, in which absorption processes are altered, are a frequent cause of malnutrition. At the same time, it should be noted that the small intestine is highly sensitive to protein-energy malnutrition due to daily specific losses of nutrients due to the renewal of the intestinal epithelium, the period of which is 2-3 days. A vicious circle is created. The pathological process in the small intestine that occurs with protein deficiency resembles that in intestinal diseases and is characterized by thinning of the mucous membrane, loss of disaccharidases of the "brush" border, impaired absorption of mono- and disaccharides, decreased digestion and absorption of proteins, increased time of transport of contents through the intestine, colonization of the upper parts of the small intestine with bacteria.

As a result of damage to the structure of the small intestinal mucosa, its passive permeability changes, due to which large macromolecules can penetrate into subepithelial tissues, the probability of functional damage to intercellular connections increases. 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, a disorder in the absorption and utilization of carbohydrates cause a deficiency of mono- and disaccharides. Disruption of the processes of splitting and absorption of lipids increases steatorrhea. Pathology of the mucous membrane along with intestinal dysbacteriosis, decreased secretion of pancreatic lipase and a disorder in the emulsification of fats by bile acids lead to insufficient absorption of fats. A disorder in fat absorption also occurs with excessive intake of calcium and magnesium salts with food. Many researchers have paid attention to the deficiency of water- and fat-soluble vitamins, iron, and microelements associated with changes in the absorption of these substances in intestinal diseases. The causes of their absorption disorders and the effect of some nutrients on the absorption of others have been analyzed. Thus, it has been suggested that vitamin B12 absorption defects are associated with a primary disorder of its transport in the ileum or the effect of intestinal dysbacteriosis, since they are not eliminated by an internal factor. Protein deficiency is possible with impaired absorption of nicotinic acid. The ratio between absorption and excretion of xylose was reduced in 64% with iron deficiency and normalized when taking iron preparations.

It should be emphasized that selective deficiency of only one nutrient is extremely rare; more often, the absorption of a number of ingredients is impaired, which causes a variety of clinical manifestations of malabsorption syndrome.

The clinical picture is quite typical: a combination of diarrhea with a disorder of all types of metabolism (protein, fat, carbohydrate, vitamin, mineral, water-salt). The patient's exhaustion increases to the point of cachexia, general weakness, decreased performance; sometimes mental disorders and acidosis occur. Frequent symptoms include polyhypovitaminosis, osteoporosis and even osteomalacia, B12-folate-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 disruption of protein and water-electrolyte metabolism, subcutaneous tissue is poorly developed, hair falls out, and nails become brittle.

As a result of a deficiency of various vitamins, the following symptoms appear:

1. with thiamine deficiency - paresthesia of the skin of the hands and feet, pain in the legs, insomnia;
2. nicotinic acid - glossitis, pellagroid changes in the skin;
3. riboflavin - cheilitis, angular stomatitis;
4. ascorbic acid - bleeding gums, hemorrhages on the skin;
5. Vitamin A - twilight vision disorder;
6. vitamin B12, folic acid, and iron - anemia.

Clinical signs associated with electrolyte imbalance include tachycardia, arterial hypotension, thirst, dry skin and tongue (sodium deficiency), muscle pain and weakness, weakened tendon reflexes, changes in heart rhythm, most often in the form of extrasystole (potassium deficiency), a positive "muscle roller" symptom due to increased neuromuscular excitability, a feeling of numbness in the lips and fingers, osteoporosis, sometimes osteomalacia, bone fractures, muscle cramps (calcium deficiency), decreased sexual function (manganese deficiency).

Changes in endocrine organs are clinically manifested by menstrual cycle disorders, impotence, insipid syndrome, and signs of hypocorticism.

There is information about the dependence of clinical symptoms on the localization of the process in the small intestine. The defeat of its predominantly proximal sections leads to a disorder of absorption of B vitamins, folic acid, iron, calcium, and the defeat of its middle sections and the proximal section of the intestine - amino acids, fatty acids and monosaccharides. For the predominant localization of the pathological process in the distal sections, a disorder of absorption of vitamin B12, bile acids is characteristic.

Quite a lot of research has been devoted to modern methods of diagnosing absorption disorders in various intestinal diseases.

The diagnosis is based on the clinical picture of the disease, determination of the total protein, protein fractions, immunoglobulins, total lipids, cholesterol, potassium, calcium, sodium, and iron in the blood serum. In addition to anemia, blood tests reveal hypoproteinemia, hypocholesterolemia, hypocalcemia, hypoferremia, and moderate hypoglycemia. Coprological examination reveals steatorrhea, creatorrhea, amylorrhea (extracellular starch is revealed), and increased excretion of undigested food substances with feces. With disaccharidase deficiency, fecal pH decreases to 5.0 and below, and the test for sugars in feces and urine is positive. With lactase deficiency and the resulting milk intolerance, lactosuria can sometimes be detected.

In diagnosing disaccharide intolerance, tests with a load of mono- and disaccharides (glucose, D-xylose, sucrose, lactose) with subsequent determination of them in the blood, feces, and urine are helpful.

In the diagnosis of gluten enteropathy, the effectiveness of a gluten-free diet (not containing products from wheat, rye, oats, barley) is taken into account first of all, and in the diagnosis of exudative hypoproteinemic enteropathy - daily excretion of protein with feces and urine. Absorption tests help in diagnosis and allow us to form an idea of the degree of absorption disorder of various intestinal hydrolysis products: in addition to the test with D-xylose, galactose and other saccharides, a potassium iodine test, studies with iron and carotene loading are used. For this purpose, methods based on the use of substances labeled with radionuclides are also used: albumin, casein, methionine, glycine, oleic acid, vitamin B12, folic acid, etc.

Other tests are also known: respiratory tests based on determining the isotope content in exhaled air after oral or intravenous administration of substances labeled with ¹⁴ C; jejunoperfusion, etc.

The malabsorption syndrome is pathognomonic for many diseases of the small intestine, in particular, chronic enteritis of moderate severity and especially severe course. It was observed in the widespread form of Crohn's disease with predominant damage to the small intestine, in Whipple's disease, severe gluten enteropathy, intestinal amyloidosis, exudative hypoproteinemic enteropathy, etc.

Treatment of primary (hereditary) malabsorption syndrome consists primarily of prescribing a diet with the exclusion or limitation of intolerable products and dishes that cause a pathological process in the small intestine. Thus, in case of intolerance to mono- and disaccharides, a diet is recommended that does not contain them or contains them in small quantities; in case of gluten intolerance (gluten enteropathy), a gluten-free diet is prescribed (a diet with the exclusion of products and dishes from wheat, rye, oats, barley).

In secondary (acquired) syndrome of impaired intestinal absorption, the underlying disease should be treated first. Due to insufficient activity of membrane digestion enzymes, corontin (180 mg/day), anabolic steroids (retabolil, nerobol), phosphodiesterase inhibitor - euphyllin, lysosomal enzyme inducer - phenobarbital are prescribed, which stimulate membrane hydrolysis processes in the small intestine. Sometimes, in order to improve the absorption of monosaccharides, adrenomimetic agents (ephedrine), beta-blockers (inderal, obzidan, anaprilin), deoxycorticosterone acetate are recommended. The absorption of monosaccharides, increasing it at low rates and decreasing it at high rates, is normalized by kinin inhibitors (prodectin), cholinolytic (atropine sulfate) and ganglionic blocking (benzohexonium) agents. In order to correct metabolic disorders, protein hydrolysates, intralipid, glucose, electrolytes, iron, and vitamins are administered parenterally.

Pancreatic enzymes (pancreatin, mezim-forte, triferment, panzinorm, etc.), abomin in large doses, if necessary - in combination with antacids, are indicated as replacement therapy.

In case of malabsorption syndrome caused by intestinal dysbacteriosis, antibacterial drugs are prescribed (short courses of broad-spectrum antibiotics, eubiotics - bactrim, naphthyridine derivatives - nevigramon) followed by the use of biological drugs such as bifidumbacterin, colibacterin, bificol, lactobacterin. In case of intestinal absorption disorder associated with dysfunction of the ileum (in terminal ileitis, resection of this section of the small intestine), drugs are indicated that adsorb unabsorbed bile acids, facilitating their excretion with feces (lignin), or form unabsorbable complexes with them in the intestine (cholestyramine), which also enhances their excretion from the body.

Among the symptomatic agents used for malabsorption syndrome, cardiovascular, antispasmodic, carminative, astringent and other drugs are recommended.

The prognosis for malabsorption syndrome, as for any pathology, depends on timely diagnosis and early prescription of targeted therapy. Prevention of secondary malabsorption in the small intestine is also associated with this.