Syndrome of insufficiency of intestinal absorption: causes, symptoms, diagnosis, treatment

Syndrome of insufficiency of intestinal absorption - a symptom complex, which is characterized by a disorder of absorption in the small intestine of one or several nutrients and a violation of metabolic processes. At the heart of the development of this syndrome lie not only morphological changes in the mucous membrane of the small intestine, but also the violation of enzyme systems, motor function of the intestine, as well as the disorder of specific transport mechanisms and intestinal dysbiosis.

Isolate the primary (hereditarily conditioned) and secondary (acquired) syndrome of impaired absorption. Primary syndrome develops with hereditary changes in the structure of the small intestine mucosa and genetically determined fermentopathy. This group includes a relatively rare congenital malabsorption in the small intestine, caused by a deficiency in the mucosa of the small intestine of specific enzymes - carriers. In this case, the absorption of monosaccharides and amino acids (for example, tryptophan) is impaired. Of primary impairments of absorption in adults, intolerance to disaccharides is more common. Secondary syndrome of insufficiency of absorption is associated with acquired lesions of the structure of the small intestine mucous membrane that arise in one or another of its diseases, as well as diseases of other organs of the abdominal cavity with involvement in the pathological process of the small intestine. Among diseases of the small intestine, characterized by a disorder of the intestinal absorption, chronic enteritis, gluten enteropathy, Crohn's disease, Whipple's disease, exudative enteropathy, diverticulitis with diverticulitis, small intestinal tumors, and extensive (more than 1 m) resection are isolated. The syndrome of insufficiency of absorption can worsen with concomitant diseases of the hepatobiliary system, the pancreas with a violation of its exocrine function. It is observed in diseases involving the small intestine, including amyloidosis, scleroderma, agammaglobulinemia, abetalipoproteinemia, lymphoma, heart failure, arteriomesenteric circulation disorders, thyrotoxicosis and hypopituitarism.

Absorption also suffers from poisoning, blood loss, beriberi, radiation damage. It has been established that the small intestine is very sensitive to the action of ionizing radiation, in which disturbances of neurohumoral regulation and cytochemical and morphological changes in the mucosa occur. Dystrophy and shortening of villi appear, a violation of the ultrastructure of the epithelium and its sloughing. Microvilli are reduced and deformed, their total number decreases, and the mitochondrial structure is damaged. As a result of these changes, the absorption process during irradiation is disrupted, especially its wall phase.

The emergence of the syndrome of insufficiency of absorption in acute and subacute states is associated primarily with the breakdown of intestinal digestion of nutrients and the accelerated passage of contents through the intestine. In chronic conditions, a disorder of the absorption process in the intestine is caused by dystrophic, atrophic and sclerotic changes in the epithelium and own layer of the small intestinal mucosa. At the same time, the naps and crypts are shortened and flattened, the number of microvilli decreases, the fibrous tissue grows in the intestinal wall, and blood and lymph circulation is disturbed. Reduction of the overall absorption surface and absorption capacity leads to a disorder of intestinal absorption. Because of this, the body in insufficient quantity receives the products of hydrolysis of proteins, fats, carbohydrates, as well as mineral salts and vitamins. Violated metabolic processes. A picture resembling an alimentary dystrophy develops.

Consequently, diseases of the small intestine, in which the processes of absorption change, are a frequent cause of malnutrition. At the same time, one should note the high sensitivity of the small intestine to protein-energy malnutrition due to daily specific nutrient losses due to the renewal of the intestinal epithelium, the period of which is 2-3 days. A vicious circle is being created. The pathological process in the small intestine, which occurs with protein deficiency, resembles that of intestinal diseases and is characterized by thinning of the mucous membrane, loss of disaccharidases of the "brush" fringe, impaired absorption of mono- and disaccharides, decreased digestion and absorption of proteins, increased transit of contents through the colon, upper parts of the small intestine by bacteria.

Due to damage to the structure of the small intestine mucosa, its passive permeability changes, due to which large macromolecules can penetrate into subepithelial tissues, the probability of functional damage of 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 fasting of the organism. Defects in the process of hydrolysis, a breakdown in the absorption and utilization of carbohydrates cause a deficit of mono- and disaccharides. Violation of the processes of splitting and absorption of lipids enhances steatorrhea. Pathology of the mucous membrane along with intestinal dysbacteriosis, decreased secretion of pancreatic lipase and violation of emulsification of fats by bile acids leads to insufficient absorption of fats. Disturbance of fat absorption arises and with excess intake of calcium and magnesium salts with food. On the deficit of water- and fat-soluble vitamins, iron, trace elements, associated with a change in the absorption of these substances in diseases of the intestine, many researchers drew attention. The causes of the disorder of their absorption, the influence of some nutrients on the absorption of others were analyzed. Thus, it was suggested that defects in absorption of vitamin B12 are associated with a primary disruption of its transport in the ileum or the effect of intestinal dysbiosis, since they are not eliminated by an internal factor. If malabsorption of nicotinic acid is impaired, protein deficiency is possible. The ratio between suction and excretion of xylose was reduced in 64% with iron deficiency and normalized with the intake of its preparations.

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

The clinical picture is quite typical: the combination of diarrhea with the breakdown of all kinds of metabolism (protein, fat, carbohydrate, vitamin, mineral, water-salt). The depletion of the patient grows up to cachexia, general weakness, decreased efficiency; sometimes there are mental disorders, acidosis. Common signs are polyhypovitaminosis, osteoporosis and even osteomalacia, B12-folia-iron deficiency anemia, trophic changes in the skin, nails, hypoproteinemic edema, muscle atrophy, polyglandular insufficiency.

The skin becomes dry, often hyperpigmented in places, edema occurs as a result of disturbed protein and water-electrolyte metabolism, subcutaneous tissue is poorly developed, hair falls out, and brittle nails are increased.

Due to the deficiency of various vitamins, the following symptoms appear:

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

The clinical signs associated with the violation of the metabolism of electrolytes include tachycardia, arterial hypotension, thirst, dry skin and tongue (sodium deficiency), pain and weakness in muscles, weakening of tendon reflexes, changes in heart rate, often in the form of extrasystoles (potassium deficiency), a positive symptom of the "muscular cushion" due to increased neuromuscular excitability, a feeling of numbness in the lips and fingers, osteoporosis, sometimes osteomalacia, bone fractures, muscle spasms (calcium deficiency), decreased sexual function (manganese deficiency).

Changes in the endocrine organs are clinically manifested by a violation of the menstrual cycle, the appearance of impotence, an insipid syndrome, 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 predominantly proximal parts leads to an impairment of absorption of group B vitamins, folic acid, iron, calcium, and the damage to its middle sections and proximal gut - amino acids, fatty acids and monosaccharides. For the predominant localization of the pathological process in the distal departments, a disorder of absorption of vitamin B12, bile acids is characteristic.

A lot of research has been devoted to modern methods of diagnosing absorption disorders in various diseases of the intestine.

The diagnosis is based on an assessment of the clinical picture of the disease, the determination of the total protein content, protein fractions, immunoglobulins, total lipids, cholesterol, potassium, calcium, sodium, iron in the blood serum. In the study of blood, in addition to anemia, hypoproteinemia, hypocholesterolemia, hypocalcemia, hypoferemia, mild hypoglycemia are revealed. A coprological examination reveals steatorea, creatoria, amylorrhea (reveal extracellular starch), increased secretion with feces of undigested nutrients. With disaccharidase deficiency, the pH of the stool is reduced to 5.0 and below, the test for sugars in feces and urine is positive. With lactase deficiency and intolerance due to this milk, lactosuria can sometimes be detected.

In the diagnosis of intolerance to disaccharides, samples with mono- and disaccharide loadings (glucose, D-xylose, sucrose, lactose) help with the subsequent determination in blood, feces, urine.

In the diagnosis of gluten enteropathy, first of all, the effectiveness of a gluten-free diet (not containing products from wheat, rye, oats, barley) is taken into account, and in the diagnosis of exudative hypoproteinemic enteropathy, the daily excretion of protein with feces and urine. Help diagnosis and allow you to understand the extent of absorption of various products of intestinal hydrolysis tests for absorption: in addition to the sample with D-xylose, galactose and other saccharides, apply iodocalylic test, studies with iron loading, carotene. To this end, 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 known: respiratory, based on the determination in the exhaled air of the isotope after oral or intravenous administration of substances labeled with ¹⁴ C; etinoperfusion and others.

The syndrome of impaired absorption 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 involvement of the small intestine, with Whipple's disease, severe gluten enteropathy, intestinal amyloidosis, exudative hypoproteinemic enteropathy, and others.

Treatment of primary (hereditary) syndrome of impaired absorption consists primarily in the appointment of a diet with the exclusion or restriction of intolerable foods and dishes that cause a pathological process in the small intestine. Thus, with intolerance to mono- and disaccharides, a diet that does not contain them or contains in an insignificant amount is recommended; Gluten intolerance (gluten enteropathy) is prescribed gluten-free diet (a diet with the exception of foods and dishes from wheat, rye, oats, barley).

With the secondary (acquired) syndrome of impaired intestinal absorption, the primary disease should first be treated. Due to the inadequate activity of the enzymes of the membrane digestion, it is prescribed coronine (180 mg / day), anabolic steroids (retabolyl, nerobol), phosphodiesterase inhibitor-euphyllin, and lysosomal enzyme inducer-phenobarbital, which stimulate membrane hydrolysis in the small intestine. Sometimes, in order to improve absorption of monosaccharides, we recommend adrenomimetic drugs (ephedrine), beta-adrenoblockers (indial, obzidan, anaprilin), deoxycorticosterone acetate. Absorption of monosaccharides, increasing it at low rates and decreasing at high, normalize kinin inhibitors (prodectin), cholinolytic (atropine sulfate) and ganglion blocking (benzohexonium) agents. In order to correct metabolic disorders, protein hydrolysates, intralipid, glucose, electrolytes, iron, vitamins are administered parenterally.

As a replacement therapy, pancreatic enzymes (pancreatin, mezim-forte, trienzyme, panzinorm, etc.) are shown, abomin in high doses, if necessary - in combination with antacids.

In the syndrome of impaired absorption caused by intestinal dysbacteriosis, antibacterial drugs are prescribed (short courses of broad-spectrum antibiotics, bactrim antibiotics, naphthyridine derivatives - neviramone) followed by the use of biological agents such as bifidumbacterin, colibacterin, bifikol, lactobacterin. When intestinal absorption is disturbed associated with a disorder of the ileum (with terminal ileitis, resection of this part of the small intestine), preparations that adsorb unboiled bile acids are shown, promoting their isolation with feces (lignin), or forming with them in the intestine non-absorbable complexes (cholestyramine ), which also increases their excretion from the body.

Among the symptomatic agents used in the syndrome of impaired absorption, cardiovascular, spasmolytic, wind-related, astringent and other drugs are recommended.

The prognosis for the syndrome of impaired intestinal absorption, as in any pathology, depends on the timely diagnosis and early appointment of targeted therapy. This is associated with the prevention of secondary malabsorption in the small intestine.