Agastic anemia in the narrow sense of the word includes anemia that occurs in connection with the complete removal of the stomach (gastrectomy).

In practical terms, it is important to emphasize that the most widely used in peptic ulcer gastric surgery - partial resection and gastroenteroanastomosis, as a rule, are not accompanied by the development of anemia. Only in a part of patients (mainly women) anemia of an iron deficiency character is observed.

Contradictory data on the frequency of post-resection anemia are explained by the fact that resections were performed for various diseases, at which they removed different areas stomach. Anemia often develops during resections for gastric cancer. On the contrary, in patients with gastric ulcer who underwent resection, as a rule, severe anemia is not observed.

M. S. Dultsin's observations confirm the possibility of developing "surgical" anemia with chlorosis stigmata 5-12 years after gastric resection only in the case of additional factors - bleeding, ovarian dysfunction, infections.

According to our observations, the development and nature of anemia in patients with an operated stomach depend on the following circumstances: 1) the state of the body before surgery; 2) the underlying disease for which the operation was performed; 3) the nature of the surgical intervention; 4) the time elapsed since the operation.

From the point of view of modern ideas about the main role of the fundic glands in the development of an internal anti-anemic factor, resp. haetromucoprotein, which is necessary for the absorption of vitamin B12, the development of agastric anemia of the B12-deficient (pernicious) type can occur only if complete removal or at least subtotal resection of the stomach.

The relative rarity of pernicious anemia of agastric origin is explained by the fact that gastrectomy is performed mainly by patients with gastric cancer, whose life after surgery often does not exceed 1-2 years, which is an insufficient period for the development of pernicious anemia.

At present, in connection with the improvement of surgical techniques, the life span of gastric cancer patients subjected to gastrectomy has lengthened, as a result of which cases of pernicious anemia in gastrectomy patients have become more frequent.

According to statistics from Macdonald et al., out of 27 patients who lived for more than 3 years after total gastrectomy and who obviously did not take hepatic, resp. B12-containing drugs, 12 people developed macrocytic anemia. Tomoda followed 4 patients for 5 years after total gastrectomy. During the first 2 years, patients had hypo- or normochromic anemia, on the 3rd year hyperchromic macrocytic anemia developed, and after 5-6 years they had typical pernicious anemia, which was successfully treated with vitamin B12 or folic acid and recurred after discontinuation of treatment. According to the observations of Pitney, Beard, who systematically determined the content of vitamin B12 in the blood of the operated patient for 19 months, a decrease in the latter was first noted 16 months after the operation. According to Reimer, who observed 20 patients who underwent total gastrectomy, all patients developed severe pernicious anemia after 4-5 years. AI Goldberg and co-workers provide observations on numerous patients with agastric pernicious and macrocytic anemia that developed 2-4 years after total gastrectomy.

We observed 24 patients with agastric pernicious anemia, which developed over various periods, mostly from 2 to 6 years, after operations of subtotal resection of the stomach and gastrectomy, performed for gastric cancer (8 cases), gastric ulcer (8 cases) and gastric polyposis (8 cases).

The known period (on average 3-5 years) required for the development of pernicious anemia after complete removal of the stomach should be explained by the compensatory role of the liver, which contains significant reserves of folic acid and vitamin B12-

Based on the normal content of vitamin B12 in the liver, which is 2?/g, it should be considered that a normal liver weighing 1500 g contains 3000 of vitamin B12. The total reserves of vitamin B12 in the body of a healthy person (including the liver, kidneys, muscles) are about 4000-5000 ?, which, with a minimum daily requirement the body in 2-3 years should be enough for 4-5 years.

If the development of agastric B12-deficiency anemia due to total gastrectomy is considered a natural phenomenon, then the development of such anemia after subtotal, and even more so partial resection of the stomach requires an explanation, since these operations do not affect the fundus of the stomach, which produces gastromucoprotein. As studies by Badenoch and co-workers who biopsied the stump of 6 patients with agastric pernicious anemia after resection of the stomach for peptic ulcer showed, atrophic changes were found in the mucosa of the preserved part of the stomach. The B12-deficient nature of anemia in these individuals is confirmed by the Glass test: the radioactive vitamin B12 introduced orally is not absorbed, but the addition of an internal factor contributes to its absorption. Thus, post-resection pernicious anemia can rightfully be classified as “agastral” (according to our nomenclature) B12-deficiency anemia.

The development of typical anemia B12-deficient, resp. pernicious, the type is preceded by a period of latent B12 deficiency, manifested in the form of symptoms of the so-called agastric asthenia (A. A. Busalov), paresthesia, glossitis.

According to A. I. Goldberg and colleagues, the most early symptom B12 deficiency is the appearance of macrocytosis of erythrocytes (the average diameter of erythrocytes reaches 8 microns, while the content of vitamin B12 in the blood is still within the physiological norm. Macrocytosis of erythrocytes usually appears on the 6th month after surgery and gradually increases over 2 years ( Fig. 45).

Agastric anemia of pernicious type usually appears within 3 to 5 years after gastrectomy.

In some cases, however, anemia of the pernicious type and even funicular myelosis can develop even earlier - 1-1.5 years after the operation.

With all the similarities with the classic pernicious Addison-Birmer anemia, agastric pernicious anemia differs from the latter in a number of ways: less pronounced symptoms of hyperhemolysis and the absence of hypersideremia. Often there is a decrease in the level of plasma iron associated with a violation of the processes of ionization and absorption of dietary iron.

Rice. 45.

According to our observations, the content of vitamin B12 in the blood of patients with agastric pernicious anemia of the pernicious type is sharply reduced, amounting to traces or no more than 16-75 microns / ml, which corresponds to the data obtained in patients with pernicious Addison-Birmer anemia in the relapse stage. In persons with a resected stomach without anemia, the content of vitamin B12 in the blood is usually normal, amounting to 300-800 microns / ml. Only in individuals with erythrocyte macrocytosis can a slight decrease in the level of vitamin B12 be detected in the blood, preceding the development of anemia of the pernicious type (the so-called prepernicious state).

This operation has so far often become the method of choice for the treatment of cancer and some forms of gastric polyposis, and in PU it is widely used in complicated forms and in cases that are difficult to treat conservatively. About 60-70 thousand resections of the stomach are performed annually in our country for PU. True, in last years this figure begins to gradually decrease as organ-preserving operations become more widespread (vagotomy with pyloroplasty, selective proximal vagotomy in combination with anthroectomy, etc.). Due to the sharp changes in the anatomical and physiological relationships and relationships of the digestive organs as a result of surgery, a number of such patients experience severe post-resection disorders.

According to the currently most common classification, the latter can be divided into organic, functional and combined complications after gastric resection [Vasilenko V. X., Grebenev A. L., 1981]. Functional disorders include: early and late (hypo-hyperglycemic) dumping syndromes and conditionally afferent loop syndrome, caused by a violation of its evacuation activity (it sometimes has an organic condition), postgastro-resection asthenia (dystrophy) and anemia.

Complications of an organic nature include: peptic ulcer of the anastomosis or jejunum, cancer and ulcer of the stomach stump, cicatricial deformities and narrowing of the anastomosis, fistulas, as well as various organ damage associated with technical errors during the operation.

A somewhat less defined group of associated disorders include: anastomositis, gastritis of the stump, cholecystitis, pancreatitis, etc.

Among all post-resection disorders, the leading place is occupied by dumping syndrome, which combines a number of symptom complexes similar in clinical picture that occur in patients at different periods of time after eating. It occurs with one or another severity in 50-80% of persons who have undergone surgery.

The first description of the "resetting stomach" after the imposition of gastroenteroanastomosis belongs to C. Mix (1922), but the term "dumping syndrome" was proposed only 25 years later by J. Gilbert, D. Dunlor (1947). Distinguish between early (comes immediately after a meal or 10-15 minutes after it) and late (develops 2-3 hours after a meal) variants of the dumping syndrome, which have a different development mechanism. It should be noted that early and late dumping syndromes can occur in isolation or combined in the same patients who underwent surgery. The pathogenesis of the dumping syndrome is complex and largely unexplained. Its development is due to the loss of the reservoir function of the stomach, the lack of portioned intake of food masses into the small intestine, due to the elimination of the pylorus mechanism, as well as the shutdown of the passage of food through the duodenum, where, under its influence, the production of important digestive hormones (gastrin, secretin, cholecystokinin, etc.). According to the most accepted point of view, in patients who have undergone gastric resection, there is a rapid discharge, "failure" of unprocessed food from the stomach stump into the small intestine; at the same time, the osmotic pressure sharply increases in its upper section, which leads to a reflex change in the microcirculation in the intestine (vasodilation, slowing of blood flow) and diffusion of blood plasma and intercellular fluid into the intestinal lumen. The resulting hypovolemia is accompanied by irritation of press receptors in the vascular bed, followed by excitation of the sympathetic-adrenal system, accompanied by an increased release of catecholamines, serotonin, and bradykinin. Violated hemodynamics, there is hypotension, tachycardia. In such patients, almost immediately after a meal rich in easily digestible carbohydrates, a kind of "vegetative storm" develops, in many ways resembling a sympathetic-adrenal crisis. Sometimes a "dumping attack" can have the features of a vagotonic crisis, which is important to keep in mind when developing an adequate treatment strategy. It is believed that in such patients there is a re-irritation of the interoreceptor apparatus of the jejunum; excessively secreted biologically active substances, gastrointestinal hormones, which enter the blood in excess, which leads to a "vegetative explosion" involving various organs and systems.

The development of late dumping syndrome is explained as follows: the accelerated entry of food chyme into the jejunum is accompanied by increased and rapid absorption of carbohydrates with insufficient glycogen synthesis in the liver, hyperglycemia (usually asymptomatic), followed by hypoglycemia caused by uncoordinated excessive release of insulin by the pancreas. The latter may be due to excessive vagal stimulation. In contrast to the early dumping syndrome, this symptom complex is characterized by inconstancy, short duration, occurrence before or against the background of its onset of an excruciating feeling of hunger. IN severe cases it ends with a prolonged fainting spell. During less formidable attacks, the patient is forced to lie down, take carbohydrate food. After an attack, weakness and adynamia usually persist. We should agree with the opinion that dumping syndrome often develops against a predetermined background in patients with neurovegetative dystonia and a labile neuropsychic status. From this position, it is not surprising that somewhat smoothed clinical symptoms of dumping syndrome can also occur in healthy young people with rapid evacuation of food chyme from the stomach and an inadequate response of the pteroreceptor apparatus of the small intestine, leading to a short-term overexcitation of the autonomic nervous system.

Early dumping syndrome is often provoked by a large meal, the use of sugar, cakes, chocolate, less often - milk and fat. Patients during or immediately after eating experience severe weakness, feeling of fullness in the epigastrium, nausea, dizziness, palpitations, perspiration. The skin is hyperemic or, on the contrary, becomes pale, the pupils narrow, tachycardia occurs, less often - bradycardia and tachypnea. Arterial pressure moderately increases or, conversely, decreases. Dumping attack lasts 1-2 hours. Late dumping syndrome has similar, but less clearly defined clinical manifestations, often accompanied by bradycardia.

In the treatment of patients with dumping syndrome, the dominant importance is given to the regimen and nature of nutrition. The diet of patients who have undergone gastric resection should be mechanically and chemically sparing only during the first 3-4 months, then it gradually expands and approaches the usual. It is important to note that diet therapy is essential not only for treatment, but also for the prevention of the development of dumping syndrome. The diet should be strictly individualized, but in all cases easily digestible carbohydrates are completely excluded. Food should be varied, high-calorie, high in protein (140-170 g), fat (up to 100 g), and vitamins. All dishes are prepared boiled, stewed or steamed. Frequent, fractional (6-8 times a day) nutrition often stops the manifestations and even prevents the development of seizures, but it is not always practically feasible. Hot and cold foods should be avoided, as they are quickly evacuated; should eat slowly, chewing food thoroughly. It is recommended to take liquid and solid food separately (with an interval of 20-30 minutes) in order to reduce the possibility of the formation of hyperosmotic (hyper-osmolar) solutions. Patients with severe dumping attacks are advised to eat lying down. Often, patients with dumping syndrome are better able to tolerate coarse, mechanically unprocessed food, especially 1-2 years after the operation. It is advisable to acidify products, for this purpose use a solution of citric acid (on the tip of a table knife in /z-/z a glass of water). It must be taken into account that such patients are especially intolerant of sugar, jams, sweet compotes, egg yolks, semolina, rice porridge, lard, milk, apples. Many recommend that patients regularly keep a food diary.

Taking into account that post-resection dumping syndrome often occurs in individuals with certain manifestations of neurovegetative dystonia, which largely determines the specific clinical symptoms of each attack (dumping attack), the importance of therapy becomes clear. ssda-tive And tranquilizers. Small doses are used phenobarbital(0.02-0.03 g 3 times a day), benzo-diazepine derivatives, infusion of valerian, motherwort. In cases where the dumping attack resembles a sympathetic-adrenal crisis, it is advisable to prescribe an rh-blocker pyrroxan(0.015 g 3 times a day before meals), as well as reserpine(0.25 mg 2 times a day) and carefully oktadine (ismeline, isobarine) in an individually selected dose. The last two drugs have not only a sympatholytic, but also an antiserotonin effect, and serotonin, released in excess by the mucous membrane of the small intestine and entering the blood, is given a certain importance in the pathogenesis of dumping syndrome. The course of treatment is 1.5-2 months; taking the considered drugs is contraindicated in patients with hypotension. According to T. N. Mordvinkina and V. A. Samoilova (1985), against the background of taking reserpine, dumping attacks proceeded less severely and for a longer time. Offered with therapeutic purpose use long term prodectine(1 tablet 3 times a day), taking into account its antikinin effect. Worthy of note in this respect peritol(4 mg 3 times a day for / g hour before meals), as endowed with anti-serotonin and anti-histamine action. In order to slow down the evacuation of food chyme into the small intestine, one can resort to prescribing non-selective anticholinergics(extract belladonna, atropine, metacin. platifillin V usual doses). They can be combined with myotropic antispasmodics (papaverine, no-shpa, halidor). Patients with late dumping syndrome at the height of hypoglycemia are recommended by some authors to prescribe sympathomimetics(0.1% solution adrenaline or 5% solution ephedrine 1 ml), if necessary, again, but this is unrealistic. More acceptable is the appointment of ephedrine orally at 0.025-0.05 g or izadrin 0.005-0.01 g under the tongue 20-30 minutes before the expected manifestations of the syndrome.

In general, the effectiveness of pharmacotherapy in patients with dumping syndrome should be assessed with extreme restraint. The range of drugs used here is limited, and therefore reasonable dietary recommendations are more useful.

Chronic afferent loop syndrome is divided into functional, arising as a result of hypotension, dyskinesia of the duodenum, afferent loop, sphincter of Oddi and gallbladder, and mechanical, due to an obstacle in the afferent loop (kinks, strictures, adhesions). Patients with this pathology note a feeling of fullness in the epigastrium that occurs after eating, often accompanied by flatulence. There is regurgitation of bile or food mixed with bile, aggravated in a bent position. In more severe cases, recurrent profuse vomiting of bile occurs. Patients complain of painful, almost constant nausea, which increases after taking sweets, milk and fatty foods. The diagnosis is finally established after X-ray examination. Treatment is usually surgical, but initial manifestations may be appointed cerucal orally or parenterally at the usual dosage. With severe flatulence, which is one of the symptoms of the "syndrome of bacterial colonization of the small intestine", short repeated courses are indicated. antibiotic therapy.

Post-gastroresection dystrophy usually occurs in a longer period after surgery and is, in fact, one of the variants of the "impaired digestion syndrome". Disorders of intestinal digestion and absorption in such patients are caused by disorders of secretion and motility of the stump of the stomach and intestines, secretion of bile and pancreatic juice, changes in the microflora of the small intestine, inflammatory-dystrophic changes in its mucosa, sometimes reaching a degree of deep atrophy. At the same time, progressive weight loss, diarrhea with steatorrhea, polyhypovitaminosis, anemia, hypoproteinemia, disorders of electrolyte and vitamin metabolism develop. Treatment is symptomatic and is carried out in accordance with the principles of treatment of impaired digestion of any other etiology (see Chapter 5). In connection with the development of significant violations of some functions gastrointestinal tract associated with the surgical removal of the stomach or part of it, usually recommend enzyme therapy. However, it should be noted that one should not place unnecessary hopes on it. In conditions of throwing alkaline intestinal contents into the stomach stump and accelerated emptying, hydrochloric acid and pepsin are hardly able to show their effect. The administration of pancreatic enzymes makes more sense, but their effect seems to be modest.

Treatment of peptic ulcers of the anastomosis and gastritis of the stump of the stomach is no different from that of exacerbation of peptic ulcer or the usual forms of chronic gastritis. The literature describes post-resection pancreatitis, in the genesis of which surgical trauma, hypotension and duodenostasis are important. They are treated according to the same rules as pancreatitis in general.

Iron deficiency anemia can develop both after total gastrectomy and after resection of the stomach in various modifications, and more often it occurs as a complication of the last surgical intervention. Discussing the pathogenesis of this type of anemia, one should take into account a slight decrease in the content of iron in the diet, an increase in its losses with feces and the absence of an increase in its absorption from food that is adequate to reduce reserves [Ryss E. S., 1972]. Achlorhydria does not play a significant role in the formation of anemia. Iron deficiency anemia occurs 1-3 years after surgery.

Msgaloblast 1H (.sk; 1st B^-difficile anemia refers to rare and late (after 5 years) complications of gastric resection. In its development, atrophic gastritis of the stomach stump is of primary importance, leading to disruption of the production of internal factor and a decrease in the absorption of vitamin Bia. Separation of Agastri - "ecKiix aiiCMKi"! on iron-is B,.-deficient is conditional, since in such patients there is a simultaneous deficiency of these hematopoietic substances, and in some patients there is a lack of folic acid, protein and some trace elements (cobalt, copper). In other words, anemia that develops in patients who have undergone gastric resection is always polyvalent, of mixed origin, and requires complex therapy. The latter is carried out general rules, developed for the treatment of similar forms of anemia. However, such patients often have intolerance to iron preparations when they are administered orally, which forces them to resort to parenteral administration of the appropriate drugs. Among them, the most noteworthy ferrum lsk, which is administered every other day or daily intramuscularly at 2-4 ml or intravenously at 5 ml; course of treatment - 15-20 days. Maintenance therapy with iron preparations in these patients is carried out "on demand". After a course of treatment, more often inpatient, patients with post-resection disorders are subject to dispensary observation, and 1-2 times a year they undergo the necessary examination, diet is corrected, and medication is prescribed according to indications or for preventive purposes. Patients can be deregistered not earlier than 3 years after the operation in the absence of any post-resection disorders during this period; good general condition and well-being [Vasilenko V. X., Grebenev A. L., 1981].

Assessing the results of treatment of post-gastroresection disorders in a more general form, one should not be overly optimistic. Although severe forms these disorders are not so common, but even with their moderate severity, it is far from always possible to provide satisfactory treatment results. Sometimes it is difficult to explain why, with similar postoperative anatomical changes, some patients have almost no complaints, while others have severe and resistant to conservative treatment of painful phenomena, and then one has to resort to reconstructive operations.

Atrophy of the gastric mucosa is a pathological process characterized by a change in the cellular composition and inhibition of the function of the inner layer of this organ. Due to the steady progression of the disease, it requires a serious attitude in terms of diagnosis and subsequent ongoing therapy.

Causes and mechanism of the development of the disease

Chronic atrophic gastritis autoimmune. Atrophy of the gastric mucosa in autoimmune gastritis develops due to the fact that the immune system produces antibodies to parietal cells that produce hydrochloric acid and the internal factor of Castle, which is necessary for the absorption of vitamin B12. These antibodies cause their death. As autoimmune inflammation progresses, there are fewer and fewer such cells in the stomach. Because of this, there is:

• atrophy of the mucous membrane;
• decline in production of hydrochloric acid, up to its complete absence;
• development of B12-dependent anemia.

The causes of autoimmune gastritis are not fully understood, but it is believed that important role This is where heredity comes into play.

Chronic atrophic gastritis is multifactorial. Most experts believe that almost any type of chronic inflammation of the stomach sooner or later ends with the death of mucosal cells and its atrophy. On average, it takes about 17-19 years from the moment of diagnosis of ordinary superficial gastritis, which can be accompanied even by increased acidity, until the loss of parietal cells.

It is believed that the gastric mucosa undergoes atrophy due to the fact that its regenerative ability gradually weakens. Normally, mucosal cells are renewed every 2-6 days. Any surface of an ulcer or erosion can close with new cells already in the first days due to the fact that cells migrate from the nearest mucosal folds. But in the case of frequent exacerbation of the inflammatory process, the resources for recovery are more and more depleted, so hyperacid gastritis eventually turns into gastritis with normal, and then reduced production of hydrochloric acid (HCl).

The following factors contribute to the appearance of prolonged inflammation and the subsequent development of atrophy:

• spicy and fatty foods;
• duodenogastric reflux - periodic reflux of bile and duodenal contents (duodenum) into the stomach;
• related chronic ailments that worsen the blood supply to this organ;
• availability in stomach Helicobacter pylori;
• taking NSAIDs, hormones and other drugs that irritate the gastric mucosa;
• smoking;
• alcohol;
• addiction to hot spices;
• heredity;
• chaotic daily routine;
• autoimmune reactions and much more.

Types and characteristic symptoms

Chronic hyper- or normacid gastritis. Although usually with this type of inflammation, mass cell death does not occur, however, when the process spreads deeper, focal atrophy of the mucosa in the antrum of the stomach is observed in places. Also, inflammation often affects the duodenum, causing duodenitis. In this case, you may observe:

• constipation;
• heartburn;
• belching sour, air;
• occasional nausea.

Pain in this form of gastritis, especially in combination with duodenitis, often resembles those with peptic ulcer - at night, on an empty stomach, 1.5-2 hours after eating (however, unlike ulcers, they are less intense and less often associated with seasonality, subside when the diet is followed and occur when it is inaccurate).

• Contrast x-ray - dysmotility, thickening of the folds inner shell stomach, signs of hypersecretion of gastric juice on an empty stomach.
• FGDS - redness, swelling of the mucous membrane, the presence of mucus or bile in the stomach.
• Histology - a picture of superficial gastritis and focal atrophy in the antrum of the stomach, unchanged mucous or superficial gastritis in the fundus.
• Palpation of the abdomen - moderate or slight pain in the epigastric region and slightly to the right.
• pH-metry - normal or increased secretion of HCl.

Chronic atrophic gastritis with secretory insufficiency. It occurs predominantly in the elderly and middle-aged. As a rule, the main symptoms of this form of gastritis are:

• flatulence, increased rumbling in the abdomen;
• feeling of heaviness in the epigastric region, stomach fullness;
• belching;
• loss of appetite;
• nausea;
• bad aftertaste.

Due to low acidity, a violation of digestion and assimilation of food develops, which can manifest itself:

• intestinal dysbacteriosis;
• stool disorder like diarrhea;
• weight loss;
• deficiency of various vitamins and minerals - seizures in the corners of the mouth, peeling of the skin, brittle nails, hair loss, etc.

If atrophy of the gastric mucosa is noted for a long time, then other body systems also suffer. This is accompanied by general weakness, decreased sexual function, reduced blood pressure etc. In addition, such patients may:

• general weakness, irritability, arrhythmias;
• with the addition of B12-dependent anemia - pain and burning in oral cavity, paresthesia of the upper and lower extremities, loss of interest in life, decreased vitality;
• dumping-like syndrome - hiccups, sweating, sudden weakness, drowsiness, pallor that occur after eating.

Symptoms that are detected using laboratory and instrumental methods:

• FGDS - pallor of the mucous membrane, thinning and smoothing of the folds.
• Histological examination - atrophy of the gastric mucosa, the appearance of cells characteristic of the intestine or the pyloric part of the stomach.
• Contrast radiography - a decrease in peristalsis and tone, smoothing the folds of the inner lining of the stomach.
• pH-metry - reduced secretion of hydrochloric acid or its absence (achilia).

Possible complications of the disease

The most typical complications of atrophic gastritis:

• the formation of ulcers;
• indigestion due to a decrease in the concentration of hydrochloric acid in the gastric juice;
• malignancy (degeneration into cancer);
• bleeding from formed ulcers or erosions.

In addition, there is the appearance of other diseases of the intestine, gallbladder, pancreas - pancreatitis, cholecystitis, enteritis, etc.

Diagnostics

The symptoms that accompany gastric atrophy are also found in other diseases, including cancer and peptic ulcers. Therefore, if any signs of gastritis appear, it is imperative to see a doctor. He will prescribe a comprehensive examination, including:

• FGDS, biopsy of the gastric mucosa with subsequent histological examination;
• test for Helicobacter (Hp-diagnosis);
• study of acidity (pH) of gastric juice;
• general and biochemical blood tests;
• stool tests for helminth eggs, occult blood;
• coprogram.

Also, if necessary, the doctor can prescribe an ultrasound of the abdominal organs, x-rays, MRI or CT scans, stool culture for intestinal dysbacteriosis, as well as other types of studies to exclude certain diseases.

Treatment

treatment chronic gastritis a gastroenterologist deals with atrophy of the mucous membrane. With an exacerbation of the process, the doctor may prescribe:

• antibiotics to remove Helicobacter pylori;
• drugs that relieve inflammation;
• means that normalize the acidity of gastric juice and improve digestion.

In case of insufficiency of the digestive function, the following are indicated:

• enzymes;
• vitamins;
• minerals;
• symptomatic remedies that normalize stool and eliminate the phenomena of flatulence, intestinal dysbacteriosis.

During the period of remission of the disease is shown:

• treatment with mineral waters;
• physiotherapy procedures.

Chronic atrophic gastritis autoimmune. During the progression of the disease - short courses of glucocorticosteroid hormones (Prednisolone in medium therapeutic doses or its analogues).

In the presence of insufficiency of digestion and reduced acidity of gastric juice:

• drugs that improve gastric motility - Motilium, Motilak;
• gastric juice;
• diet - table number 2;
• pancreatic enzymes - Pancreatin, Panzinorm, Creon.

If B12 deficiency anemia has developed, then vitamin B12 is also indicated by injection.

Chronic atrophic gastritis with low acidity. In the presence of H. pylori, a course of antibiotic therapy is mandatory. Depending on the duration of the course of the disease, the tolerance of drugs and the sensitivity of the bacterium itself to antibiotics, the following drugs may be included in the scheme:

• Amoxicillin;
• Bismuth;
• metronidazole etc.

The following drugs help restore acid secretion in the initial stage of the disease, which are taken 2-3 times a day before meals:

• Plantaglucid;
• plantain juice;
• bitterness - dandelion root, tincture of wormwood.

If there is no hydrochloric acid at all (achilia), then substitution therapy is indicated. These remedies are taken with meals:

• Pepsidil;
• Abomin;
• Betacid;
• acidin-pepsin;
• gastric juice.

For normalization intestinal digestion also shown:

• pancreatic enzymes;
• bile extract.

They are also taken with meals. As the condition improves and the inflammation subsides, their dose is gradually reduced until it is completely canceled.

Additionally, the doctor may prescribe:

• Methyluracil;
• Pentoxyl;
• aloe extract.

All of them help to improve the nutrition of the cells of the gastric mucosa and are taken for 3-4 weeks, usually 2 times a year.

In the absence of appetite, a significant loss of body weight against the background of gastritis with zero acidity, anabolic hormones are used:

• Retabolil;
• Nerobol and others.

Chronic gastritis with increased or normal acidity against the background of focal atrophy of the mucosa. As in the case of other forms of atrophic gastritis, drugs are prescribed:

• accelerating healing;
• relieve inflammation and spasms of the stomach;
• a course of antibiotic therapy to eliminate H. pylori.

During an exacerbation with increased acidity and hunger pains, diet No. 1 is shown, drugs that reduce the production of hydrochloric acid:

• H2-histamine receptor blockers;
• proton pump inhibitors - Ranitidine, Omez, etc.

To quickly neutralize its excess amount in the stomach, such antacids help:

• Almagel;
• Rennie and others

Nutrition principles

First of all, the diet for atrophy of the stomach depends on the stage of progression of the disease and the level of acidity of gastric juice.

With exacerbation of gastritis, food should be taken in small portions and often enough (up to 5-6 times a day).

In the case of increased acid formation, its basis should be products that are neutral in relation to the production of hydrochloric acid, and all food should be served warm. Of the methods of culinary processing, preference is given to boiling, steaming, stewing.
Allowed:

• liquid and semi-liquid cereals;
• dairy products;
• baked apples;
• mashed potatoes;
• boiled dietary meat (table No. 1 according to Pevzner).

As the aggravation subsides, the diet expands.

At low acidity food, on the contrary, should be stimulating the production of gastric juice and improve appetite, which in most cases is reduced.

At low pH values ​​are allowed:

• stewed / baked vegetables, fruits;
• ham;
• juices;
• fresh apples;
• cereals on water / milk;
• fat-free meat and fish broths;
• dill, parsley;
• black bread;
• herring;
• dairy products;
• sparkling water.

However, due to the weakness of digestion, those foods that cause irritation of the mucous membrane, require long digestion, or cause fermentation processes are also prohibited. If, along with inflammation of the stomach, symptoms of pancreatitis or cholecystitis are observed, then appropriate changes are made to the diet.

As a rule, a strict diet is indicated only during an exacerbation of the disease, which averages 1-2 months, but its basic principles should be followed for several years.

Prevention

Prevention of exacerbation of the disease in atrophic gastritis includes:

• to give up smoking;
• stress management;
• adherence to the diet recommended by the doctor;
• treatment of concomitant diseases;
• passage in the autumn-spring period of preventive courses of treatment;
• FGDS examination 1-2 times a year.

Disease prognosis

Unfortunately, chronic atrophic gastritis gradually progresses. And the production of HCl is approaching zero. However, timely detection of the disease, diet, a healthy lifestyle and proper treatment can significantly slow down this process.

Whether it is necessary to remove or not a polyp in the stomach

The polyp is benign education, which appears on any part of the mucous membrane. In medicine, it is often observed, but mostly it does not manifest itself clinically.

Basically, such growths in the stomach are detected during a routine medical examination or during the study of other diseases. Often such growths appear in people over 40 years old.

Men are more susceptible to disease. As provoking factors are gastritis, Helicobacter pylori microorganisms, genetic predisposition.

As a therapy in many situations, the complete elimination of polyps in the stomach is prescribed.

Removal of polyps in the stomach

A polyp in the gastrointestinal tract is an epithelial formation on the walls of the stomach with a smooth or segmented upper layer, which is attached by means of a thin or wide stalk.

The initially benign form of these growths, due to the formation of the disease, can cause stomach cancer.

This disease is diagnosed in different ages, however, the formation of the disease is often observed in people in adulthood.

This infection, hereditary factor, chronic form gastritis, a passive lifestyle create favorable conditions for the appearance of such a neoplasm inside the gastrointestinal tract.

Is an operation needed

Elimination of polyps in the stomach is required due to the high likelihood of adverse effects.

They are bleeding in the stomach, infection, gastrointestinal disorders, infringement of the polyp, which provokes intense sharp pain.

Most dangerous consequence- transformation into a malignant growth. This can happen in the vast majority of situations of total polyposis (a form during which the number of growths cannot be accurately calculated).

The larger the mucosal area affected by such a formation, the greater the risk and rate of their malignancy - polyposis gastric cancer.

An increased likelihood of transformation into an oncological growth, or the suspicion that the process is already taking place, is a direct indication for the surgical removal of neoplasms in the stomach.

It should not be assumed that carcinoma can form only in connection with growths large sizes and refuse to eliminate small ones.

There are situations of malignancy of the villi of polyps, outwardly benign. Such a disease is impossible to predict.

Often, polyps are detected suddenly in the process of X-ray diagnostics or with the help of gastroendoscopy.

Since patients with persistent gastric disease are at risk, frequent endoscopy is recommended to avoid possible formation growths.

The final diagnosis is carried out only after surgery to eliminate the growth inside the stomach with further histological and cytological diagnosis of tissues and cells.

Treatment tactics

Therapy of polyps in the stomach is aimed at eliminating them and preventing adverse consequences. Medications are not able to remove such growths, they are prescribed only to stop the inflammation.

With hyperplastic polyps, reaching a size of no more than 2 cm, waiting tactics are acceptable, following dietary nutrition and using anti-inflammatory drugs that regulate the pH level of the stomach and antimicrobials, effective in the process Helicobacter therapy pylori.

During this period, frequent gastroendoscopy is necessary, which allows the specialist to establish the dynamics of development, the nature of the changes and the emergence of new polyps.

In other situations, surgical removal of growths is necessary. For these purposes, abdominal or endoscopic surgery is used.

The use of newer methods (electrocoagulation and laser therapy) is likely, but they are used very infrequently.

In the process of preparations for any surgical intervention to eliminate polyps in the stomach, a comprehensive diagnosis of the general condition of the patient is required.

If there is a need, pre-treatment is carried out for diseases of the heart and blood vessels, lungs, kidneys.

Treatment

The danger is that neoplasms of this type are capable of transforming from benign to malignant.

Directly because of this, it is very important to carry out an examination and proper therapy in time, which show whether the polyp needs to be removed.

Initially, drugs are used to treat growths.

It involves the use of funds that envelop the walls of the stomach, dietary supplements that stimulate digestive processes, drugs that relieve inflammation if present.

When prolonged drug therapy does not give the expected positive result, in this case, treatment is prescribed through surgical intervention.

Most often, removing a polyp of the stomach is required in situations where there is high probability its transformation into a malignant growth.

Indications

If there is no positive dynamics after the drug therapy indications for the prompt removal of growths inside the stomach are:

• adenomatous polyp of any size;
• an intensive increase in the size of the hyperplastic polyp, when the dimensions are over 15-20 mm;
• severe symptoms of the disease: pain, heartburn, pressure, fullness of the stomach, belching and other disorders of the digestive processes;
• general malfunctions in the functioning of the body: lethargy, weight loss, anemia, dizziness, etc.

When the need to eliminate the polyp in the stomach is identified, the specialist determines by what method this should be done.

Each type of operation has its own indications:

• endoscopy is carried out when the size of the growth is not more than 30 mm, the leg is not more than 15 mm, the polyp is single and hyperplastic;
• laparoscopic polypectomy is performed when there are several polyps, they big size and do not contain cancer cells;
• open polypectomy is done in the most difficult situations: with numerous manifestations of polyps, suspicion of malignancy, very large polyps, tissue death.

In the course of any surgical intervention, a histological diagnosis of polyp tissues is carried out. When the presence of cancer cells is detected, it is necessary to completely or partially eliminate the stomach.

Preparatory activities

Gastric polypectomy needs exercise preparatory procedures. Like any other surgical intervention, it can provoke adverse consequences.

Therefore, before removing the build-up in the stomach, the patient is sent for diagnosis:

• general and biochemical blood test;
• general analysis urine;
• blood test to establish the group, Rh factor;
• blood test for HIV, hepatitis B and C;
• coagulogram;
• fluorography;
• gastroscopy.

When there are various diseases of the internal organs, you should find out the recommendations from a specialist.

In particular, emphasis should be placed on diseases of cardio-vascular system, lungs, kidneys, liver. Probably, before surgery, it is necessary to undergo a therapeutic course.

When the operation is carried out in the morning, the last meal should be no later than 18 hours of the previous day. Taking into account the method of elimination, it is possible to carry out an enema before the procedure.

For 30 minutes, the patient is given to drink 150-200 g of sodium bicarbonate solution. It contributes to the dissolution of gastric mucus, which interferes with the implementation of surgical procedures: it complicates the capture and extraction of the build-up.

Removal Methods

At the moment, there are several ways to eliminate polyps:

• Endoscopic polypectomy. It is carried out by means of special instruments introduced into the esophagus, and then into the stomach. All actions of the surgeon are displayed on the monitor.
• Surgical polypectomy. Open or laparoscopic surgery. Needs a longer recovery period but is necessary in some situations.
• laser elimination. The operation is effective when the polyps are single and of small size. Done with the least amount of damage. Through the endoscope, a laser is injected that cauterizes polyps and blood vessels.

Municipal medical institutions rarely have the appropriate equipment and qualified specialists to carry out the task.

Endoscopy

Endoscopic removal of polyps is the most popular and safest method of therapy, despite the complexity of its implementation.

Surgical intervention is indicated when the size of the growth is not more than 3 cm and when there is no suspicion of malignancy.

Previously, the patient drinks a solution of sodium bicarbonate in order to dissolve mucus in the stomach. Manipulation is carried out laparoscopically or through a flexible endoscope.

In the first situation, the instruments are inserted using a thin puncture through the abdominal cavity without excision, in the other, the instruments are delivered to the stomach, as in the process of gastroendoscopy, having previously treated the pharynx and pharynx with dicaine (2% solution).

The patient should lie on the left side, tucking his knees under him. In rare situations, the patient is laid on his back in order to better view stomach.

To remove a polyp, you need to grab it with a metal loop and gently hook it.

It is then removed through an endoscope. When the growth is flat, an artificial leg is created for it.

The extracted material is sent for histological diagnosis. After 14 days, it is mandatory to repeat the examination of the patient.

When the neoplasms remain, another surgical intervention is likely.

Endoscopic polypectomy is prohibited during the general serious condition of the patient, the presence of a pacemaker and increased likelihood formation of gastric bleeding.

Abdominal operation

Surgical polypectomy can be prescribed during polyps of considerable size (from 3 cm), in large numbers or with an increased risk of malignancy, and also when endoscopic surgery is not possible.

The procedure is carried out under general anesthesia. At this time, a longitudinal incision is made in the anterior wall of the abdominal cavity, gastric juice is drained.

Then the polyp is scraped off with a scalpel and sent for histological diagnosis.

When the results of the study show that there are no cancer cells in the growths, the stomach is sutured. The presence of atypia in the cells is an indication for gastric resection.

The affected area of ​​the organ is removed completely, in order to prevent metastasis. Resection is indicated during pinching of the polyp pedicle and tissue death.

Treatment with coagulation

Electrocoagulation is carried out in the same way as endoscopic polypectomy. The difference is that biopsy forceps with current are used instead of a metal loop.

This has its own advantage. The likelihood of bleeding is greatly reduced, since cauterization of the leg of the growth coagulates the blood in the vessels in this area.

Approximately in the same way, electroexcision is carried out, however, instead of forceps, the polyp is removed with a dielectric loop.

Elimination of polyps with a laser is carried out endoscopically. It is used when it is impossible to carry out a standard endoscopic polypectomy or electroexcision.

During this, the laser beam is focused at a distance of 6-7 mm from the neoplasm and cauterized in layers.

But similar procedure there are a lot of downsides. It is not performed to eliminate polyps larger than 1 cm or on a thin long base.

In the process of cauterization, visibility is reduced, since the process is associated with smoke. It is extremely difficult to keep the beam at one point of the laser due to the peristalsis of the stomach.

It is not possible to take material for histological diagnosis.

After operation

The recovery period after surgery is faster, the code was carried out laser removal of polyps. After 10 days, the final restoration of the gastric mucosa occurs.

During laparoscopy and open polypectomy of the stomach, rehabilitation lasts longer.

After a classic operation with an incision in the peritoneum and stomach, the likelihood of adverse effects increases.

Bleeding develops. inflammatory processes, slow tightening of wounds comes to light. Until the final recovery, 15-60 days will pass, taking into account how many polyps and stomach tissues have been eliminated.

For a speedy recovery, you must follow the general instructions for the postoperative period: do not overheat or overcool the body, avoid excessive stress, gradually increase physical activity.

You also need to follow a diet. The first day after the operation, it is forbidden to eat and drink. On day 2, drinking and special mixtures in milk are already acceptable.

After surgery, the gastric mucosa is irritated and susceptible to temperature and chemical attack. Therefore, smoking, drinking alcohol and highly carbonated water are prohibited.

During rehabilitation, it is necessary to limit the consumption of sausages, flour, coffee, and some dairy products. The basis of the diet are soups, cereals on the water, cottage cheese and kefir, lean meats and fish.

It is necessary to adhere to the diet: eat food products 56 times a day and in small portions, avoid excessive distension of the stomach and prolonged exposure to hydrochloric acid.

In many situations, a polyp in the stomach needs to be eliminated: some of them can be transformed into oncological neoplasms, and large ones can disrupt the proper functioning of the stomach and become a provoking factor in intestinal obstruction.

Taking into account the number and size of these growths, the specialist can choose the type of surgical intervention: laser, endoscopic, laparoscopic or open polypectomy of the stomach.

During the detection of dead tissues, oncological cells, polyps and part of the stomach are eliminated (in difficult situations, the entire organ).

A polyp is a benign growth as a slight lump on the leg. Surgical removal polyps in the stomach is considered one of the best options for treating the disease.

It is used in situations where conservative treatment did not give the expected result.

Life After Pancreatic Surgery: Consequences and Recovery Tips

The pancreas is a glandular formation of mixed secretion, which simultaneously takes part in the regulation of the process of food processing and carbohydrate metabolism. Normally, the body secretes the amount of digestive enzymes and insulin that the body needs. The pancreas after surgery may begin to function differently, which leads to significant changes in the functioning of the human body.

What types of surgery are there and how does this affect the subsequent work of the pancreas?

During surgery, surgeons can completely remove the gland, remove a separate part, or do without serious damage to the organ. The least traumatic operations are the opening of an abscess of the gland, the removal of benign tumors of a small size. The doctor does not affect the pancreas itself, working with the pathological focus. Actions of this kind practically do not pose a danger to the life and health of the patient.

Resection of the pancreas

Partial removal of the organ is necessary when affected by large benign tumors that cannot be isolated. Plots of the gland are resected in acute pancreatitis and pancreatic necrosis. This leads to changes, but does not drastically affect the life of the patient after discharge from the hospital.

As a result of the consequences of removing the pancreas, the life of the patient changes more if the organ is completely removed. Indication for pancreatectomy malignant tumors glands. Also, the organ is removed in case of extensive pancreatic necrosis or traumatic injury.

It is interesting to know that changes in the patient's lifestyle in the presence of cancer are caused not only by the direct removal of the pancreas, but also by the courses of chemotherapy administered to him.

What are the consequences of the operation?

The main consequence of the removal of the body or head of the organ in question is a violation of the food processing process. In this case, the patient may suffer from diarrhea or constipation, flatulence and other manifestations of dyspepsia. He has a loss of body weight, weakness, lethargy, deterioration of the psycho-emotional state. It is possible to develop diseases associated with a lack of certain components obtained by the body from food.

Such diseases include:

• iron deficiency anemia;
• hypovitaminosis;
• hypoproteinemia;
• disruption of anabolism processes, etc.

Each of these conditions is dangerous for the life of the patient.

The consequences of pancreatic surgery, in which the tail of the organ was affected, mainly relate to carbohydrate metabolism. This is due to the presence here of a large number of islets of Langerhans - structures that directly produce insulin. Insulin deficiency is life-threatening unless artificially corrected.

What treatment does the postoperative patient need?

Despite the above, people live after pancreatic surgery for a long time. The average life expectancy of patients almost does not differ from the general indicator characteristic of healthy people. This is made possible through replacement therapy and special dietary nutrition.

Immediately after surgery, the patient experiences severe pain Therefore, the basis of pharmacological therapy is painkillers, antibiotics and regenerative agents. Shortly after subsidence pain syndrome a person is transferred to the intake of enzymatic drugs necessary for the correction of digestion (if the corresponding parts of the pancreas were operated on).

One of the most common replacement drugs is Creon, containing full complex pancreatic enzymes. The cost of the medicine at the time of writing is 292 rubles for a container containing 20 capsules. Restoration of the removed parts of the gland is impossible, therefore, enzymatic substrates are taken for life.

The prognosis for removing the tail of the gland is less favorable. Such patients are forced to inject insulin parenterally for the rest of their lives, but even this does not guarantee the absence of complications caused by high content blood sugar (nephropathy, retinopathy, trophic ulcers, polyneuropathy). In the case of complete removal of the pancreas, the patient is forced to take digestive enzymes and carry out insulin replacement therapy. An insulin pump, which delivers the drug automatically, helps to make taking medications a little easier.

On a note: frequent injections of insulin in the same place lead to lipodystrophy - the destruction of the subcutaneous fat layer. Therefore, it is recommended to change the injection sites periodically (stomach, forearm, front surface of the thigh).

Throughout life, patients with damaged pancreas follow a certain diet. They are contraindicated in spicy, salty, sour, bitter and other irritating dishes. Food should be easily digestible, sparing. Enzymatic medicines should be taken after meals.

Removal of the pancreas or part of it severe consequences. However, even in such a situation, patients can lead a full life. To do this, you must follow all the recommendations of the attending physician, take prescribed drugs, completely abandon alcohol, smoking, and the use of toxic products and substances.

Catad_tema Iron deficiency anemia - articles

Iron deficiency anemia in diseases of the gastrointestinal tract

"PHARMATEKA"; Current reviews; No. 13; 2012; pp. 9-14.

D.T. Abdurakhmanov
Department of Therapy and Occupational Diseases, I.M. Sechenov First Moscow State Medical University, Ministry of Health and Social Development of the Russian Federation, Moscow

The problem of iron-deficiency anemia (IDA), which develops, including in diseases of the gastrointestinal tract, is discussed. Information is presented on the causes of IDA, pathogenesis, symptoms, diagnosis and treatment of this pathology. Particular attention is paid to the drug Ferinject (iron carboxymaltose), which is used in the complex therapy of patients with IDA due to inflammatory diseases intestines.
Keywords: iron deficiency anemia, iron deficiency, ferrotherapy, iron carboxymaltose

The article discusses the problem of iron deficiency anemia (IDA), which develops against the background of many diseases, including gastrointestinal diseases. The data on the causes of IDA, pathogenesis, symptoms, diagnosis and treatment of this disease are presented. Particular attention is paid to the drug Ferinject (ferric carboxymaltosate) used for the treatment of IDA in patients with inflammatory bowel diseases.
key words: iron deficiency anemia, iron deficiency, ferrotherapy, ferric carboxymaltosate

The most common cause of anemia in the population is iron deficiency in the body. According to the 2002 World Health Organization (WHO) Health Report, iron deficiency anemia (IDA) is one of the top ten global risk factors for disability. Thus, it has been shown that IDA occurs among 30% of the world's population. In the US, IDA occurs in 5-12% of non-pregnant women and 1-5% of men.

Metabolism of iron in the body
The total amount of iron in the body of an adult is about 3.5-4.0 g, with an average of 50 and 40 mg/kg in men and women, respectively. The main part of iron is part of the hemoglobin of erythrocytes (about 2.5 g), a significant part of iron (about 0.5-1.0 g) is deposited in ferritin or is part of heme-containing and other enzymes (myoglobin, catalase, cytochromes) of the body (about 0.4 g) and a small part of iron (0.003-0.007 g) is in the state associated with transferrin in the blood.

The balance of iron in the body is maintained by matching the amount of incoming iron to its loss. In food, iron is present in heme or as non-heme iron. Every day with food (standard diet), 10-20 mg of iron enters the human body, from which about 10% (from 3 to 15%) is normally absorbed in the intestine, which compensates for the daily loss of iron, mainly during desquamation of epithelial cells. The body ensures the balance of iron in the body by regulating the process of its absorption in the intestines. In the case of the development of iron deficiency, the body increases the percentage of absorbed iron (it can reach 25%), with an excess, it decreases. In this process, hepcidin, a protein that is synthesized in the liver, is of key importance. Dietary intake or excretion of iron is usually out of the body's control.

About 25-30 mg of iron is recycled daily after the destruction (due to aging) of erythrocytes in the spleen and enters again into the bone marrow for the synthesis of new erythrocytes. Iron, which is absorbed in the intestine, is previously reduced on the surface of the enterocyte with the participation of ferroreductases from trivalent (Fe 3+) to divalent (Fe 2+), then with the help of a specific carrier - the transporter of divalent metals (DMT1) enters the cytoplasm. Iron in the composition of heme (found in meat, fish) is absorbed directly. Subsequently, ferrous iron, with the help of another carrier, ferroportin (also mobilizes iron from ferritin), is secreted into the blood, where it is again oxidized to ferric iron (with the participation of the hephaestin protein) and binds to the plasma protein transferrin. Transferrin transports iron to the bone marrow, where it is utilized for the synthesis of red blood cells, or mainly to the liver, where iron is deposited as part of ferritin (Fig. 1).

With a decrease in iron stores, hypoxia, anemia, enhanced erythropoiesis in the liver, hepcidin synthesis decreases, which enhances iron absorption in the intestine, with chronic inflammation, hepcidin synthesis in the liver increases and, accordingly, iron absorption in the intestine decreases.

Fig 1. Regulation of iron absorption in the intestine

Ferritin is a key protein that reflects iron stores in the body. It deposits iron in a non-toxic form, which is mobilized if necessary. On average, one molecule of ferritin contains up to 4500 iron atoms. Iron is mainly deposited in the liver, bone marrow and spleen. A decrease in serum ferritin levels is a fairly reliable indicator of iron deficiency in the body, its increase, as a rule, indicates an overload of the body with iron. At the same time, it must be remembered that ferritin is a protein. acute phase inflammation, so an increase in its content in the blood may be the result of an active inflammatory process, and not just an excess of iron. In some cases, some malignant tumors have the ability to synthesize and secrete a large amount of ferritin into the blood (as part of the paraneoplastic syndrome). Normally, the content of ferritin in the blood serum is 30-300 ng/ml.

Causes of iron deficiency anemia
There are three global reasons for the development of iron deficiency in the body (Fig. 2):

1. Insufficient intake from food or increased need.
2. Violation of iron absorption in the intestine.
3. Chronic blood loss.

Fig 2. The main causes of iron deficiency anemia

In a population, the most common cause of IDA is inadequate dietary intake: according to WHO, a quarter to a third of the world's population is chronically hungry due to a lack of food, especially meat. However, in clinical practice, chronic blood loss, primarily from the gastrointestinal tract, is distinguished among the main causes of IDA.

Clinical picture
With IDA, manifestations of the circulatory-hypoxic syndrome common to all anemias are observed:

pallor of the skin and sclera;

increased weakness and fatigue;

headache;

noise in ears;

flashing "flies" before the eyes;

increased heart rate (tachycardia);

systolic murmur at the apex of the heart on auscultation (anemic murmur);

In addition, there may be specific signs tissue iron deficiency:

glossitis;

angular stomatitis;

esophagitis;

change in the shape of the nails (“koilonychia” - spoon-shaped nails);

perversion of appetite;

taste perversion (desire to eat starch, chalk, clay, etc.).

Diagnostics
Laboratory diagnosis of IDA is based on the study of iron metabolism and the detection of its deficiency. There are a number of signs indicating the iron deficiency nature of anemia (Table 1).

Table 1

Laboratory signs of iron deficiency and IDA

IDA is a classical hyporegenerative, microcytic and hypochromic anemia, but on early stages diseases microcytosis and hypochromia of erythrocytes are not expressed. IDA can sometimes be accompanied by reactive thrombocytosis. The most routine laboratory findings of IDA are decreased iron saturation of transferrin (< 20 %) и уменьшение содержания железа (< 50 мкг/дл), а также ферритина (< 15 нг/мл) сыворотки. Поскольку ЖДА не развивается, пока запасы железа в костном мозге не исчерпаны, его наличие в костном мозге исключает дефицит железа как причину анемии. Исследование проводят с помощью железоспецифической окраски (берлинской лазурью) аспирата или биоптата bone marrow. However, in clinical practice, this method of IDA verification is rarely used, since bone marrow examination is a painful and expensive procedure. In addition, false positive and false negative results are common.

As a rule, clinical and laboratory manifestations of anemia (mainly a decrease in hemoglobin) develop when the body loses at least 20-30% of iron stores.

Differential Diagnosis
IDA most often needs to be differentiated from anemia chronic diseases and thalassemia. In addition, mixed forms of anemia can be observed (a combination of iron deficiency with a deficiency of folic acid and / or vitamin B12, a combination of iron deficiency anemia and anemia of chronic diseases, etc.).

The detection of anemia, as well as the establishment of its iron deficiency nature, as a rule, in most cases is not difficult. The most difficult may be to establish the cause of iron deficiency, which often requires a long differential diagnostic search, but is a necessary condition for successful treatment and improving the prognosis of the disease. By itself, iron deficiency and the anemia caused by it, as a rule, do not threaten the life of the patient (with the exception of anemic coma, which, however, is currently quite rare). The body adapts quite well to the development of iron deficiency, and the clinical manifestations of anemia usually develop only with increased functional needs of the body (stress, increased physical activity, pregnancy, in girls during the formation of the menstrual cycle, etc.). Therefore, very often anemia is asymptomatic and in most cases is detected during an accidental or preventive examination. However, diseases that cause the development of IDA, in particular malignant tumors, can be dangerous, threatening the health and life of the patient. Therefore, regardless of the severity of clinical manifestations and the severity of IDA, identifying the cause of iron deficiency is a prerequisite for a full examination of the patient.

IDA in diseases of the gastrointestinal tract
Diseases of the gastrointestinal tract (GIT) are one of the main causes of the development of IDA, which is caused by a violation of iron absorption in the intestine or its loss due to erosive-ulcerative, neoplastic or autoimmune inflammatory lesions of the intestinal mucosa (Table 2).

table 2

Diseases of the gastrointestinal tract, accompanied by the development of IDA

Note. NSAIDs are non-steroidal anti-inflammatory drugs.

Among the causes of IDA (almost 30-50% of all cases), acute or chronic blood loss from the gastrointestinal tract is primarily considered. The main cause of IDA in women before menopause is pregnancy and menstruation, in women after menopause and in men - chronic (latent) blood loss from the gastrointestinal tract. Fecal occult blood test is the main screening method for detecting occult gastrointestinal bleeding (the test is positive when at least 10 ml of blood is excreted per day). With a loss of at least 30 ml of blood per day, the test for occult blood is positive in 93% of cases. Most often, in chronic IDA, and especially in cases of a positive fecal occult blood result, esophagogastroduodeno- (EFGDS) and colonoscopy are performed. In 5-10% of cases of anemia associated with diseases of the gastrointestinal tract, EFGDS and colonoscopy fail to identify the lesion. In 25% of cases, this is due to the small size of the affected area, which is found on re-examination, in other cases, examination of the small intestine is necessary. In recent years, wireless capsule endoscopy has been most commonly used to identify the source of bleeding from the small intestine.

In 10-17% of cases, the cause of IDA in men and women over 40 years old is gastrointestinal cancer; especially colorectal cancer. IDA may be the only manifestation of right-sided colon cancer for a long time, with the tumor usually larger than 3 cm. common cause IDA - peptic ulcer of the stomach and duodenum.

With hidden blood loss caused by damage to the small intestine, tumors (lymphoma, carcinoid, adenocarcinoma, polyposis), angioectasia of the arteries (Dieulafoy's lesion), celiac disease and Crohn's disease are most often detected at the age of up to 40 years. and taking NSAIDs.

In a third of patients with inflammatory bowel diseases (Crohn's disease, ulcerative colitis), anemia is detected, which has a complex genesis (combination of IDA and anemia of chronic diseases).

In this case, iron deficiency becomes a consequence of several reasons:

a decrease in iron intake due to refusal to eat or a decrease in its quantity due to fears of an exacerbation of the disease;

chronic intestinal bleeding;

violation of iron absorption in the duodenum and jejunum (with Crohn's disease).

Treatment
Treatment of IDA primarily involves addressing the cause of the iron deficiency (if possible) and taking iron supplements (ferrotherapy). There are more than 100 different iron preparations, in the Russian Federation, about 10-15 dosage forms are most often used.

Daily therapeutic dose elemental iron in the treatment of IDA for adults is on average 100-200 mg in 2-3 doses. Multivitamin complexes containing iron are not recommended as a treatment for IDA, because they contain insufficient amounts of iron or it is poorly absorbed in the intestine.

With adequate treatment, already during the first 3 days, an increase in the number of reticulocytes in the blood is observed, on the 7-10th day there is a reticulocyte crisis (peak of reticulocytosis). By the 3-4th week of treatment, there is an increase in hemoglobin levels by 20 g/l. Iron preparations should be continued for another 3-6 months after the normalization of hemoglobin levels - until the saturation of transferrin with iron exceeds 30% and the ferritin concentration reaches 50 ng / ml (an indicator of the restoration of tissue iron stores).

Among 20-30% of patients, various dyspeptic disorders (nausea, epigastric discomfort, diarrhea or constipation) are noted as a result of taking iron preparations. The risk of developing gastrointestinal disorders can be reduced by taking the drug with meals or at night, as well as by gradually increasing the dose.

Among the reasons for the ineffectiveness of oral forms of iron, a number of factors are considered:

insufficient intake of iron;
irregular intake of iron preparations;
insufficient iron content in the drug taken.

Iron malabsorption:

simultaneous intake of substances that suppress the absorption of iron (tea, calcium preparations, antacids, tetracyclines, the content of tannins and phosphates in food);

concomitant inflammation with functional iron deficiency;

bowel disease (celiac disease, inflammatory bowel disease);

reduced secretion of hydrochloric acid (including as a result of taking proton pump inhibitors);

resection of the stomach or small intestine;

colonization of Helicobacter pylori.

Ongoing blood loss or increased need for iron:

Associated diseases or conditions:

deficiency of folic acid and / or vitamin B12;

tumor, chronic inflammation, chronic kidney failure or infection;

primary damage to the bone marrow or suppression of bone marrow hematopoiesis.

Misdiagnosis or other causes of anemia:

anemia of chronic disease or kidney failure;

hemoglobinopathies;

other causes of anemia (hemolysis, myelodysplastic syndrome, congenital anemia, endocrinopathies.

Allocate the following indications to parenteral administration, mainly intravenous, of iron preparations:

intolerance or ineffectiveness of oral forms of iron;

iron malabsorption (eg, celiac disease, inflammatory bowel disease);

ongoing blood loss that is not replenished by oral iron supplementation;

the need to quickly restore iron stores (severe anemia or anemia that provokes an exacerbation of coronary heart disease and other chronic diseases);

patients on renal replacement therapy receiving erythropoietin.

The main danger of parenteral administration of iron is the development of severe allergic reactions, including anaphylactic shock With lethal outcome, which are observed in 0.6-1.0% of cases. These reactions are mainly characteristic of iron preparations containing dextran.

Among parenteral iron preparations, iron saccharate and iron carboxymaltose (Ferinject) are widely used, especially in the complex therapy of inflammatory bowel diseases, which, unlike iron dextran, are associated with minimal risk development of anaphylactic and other allergic reactions. So, in 2011, the results of a randomized controlled trial on Ferric Carboxymaltose for Iron Deficiency Anemia in Inflammatory Bowel Disease were published. The study compared the efficacy and safety of a new fixed-dose regimen of iron carboxymaltose (Ferinject) and individually calculated doses of iron saccharate (FS) in patients with inflammatory bowel disease and IDA. The study included 485 patients with IDA (ferritin levels< 100 мкг/л; гемоглобина 7-12 г/дл [женщины] или 7-13 г/дл [мужчины]; легкая/умеренная или скрытая ЖДА) из 88 больниц и клиник 14 стран. Пациенты получали либо Феринжект максимально 3 инфузии по 1000 или 500 мг железа, либо СЖ в дозах, рассчитанных по формуле Ганзони (Ganzoni), до 11 инфузий по 200 мг железа. Первичной конечной точкой считали изменение уровня Hb на 2 г/дл и более; вторичными конечными точками были анемия и уровень железа к 12-й неделе исследования. Проанализированы результаты 240 пациентов, получавших Феринжект, и 235 пациентов, получавших СЖ. Среди больных группы Феринжект по сравнению с лицами, получавшими СЖ, был более выражен ответ на терапию по уровню гемоглобина: 150 (65,8 %) по сравнению со 118 (53,6 %); процентное различие - 12,2 (р = 0,004), или нормализации уровня гемоглобина: 166 (72,8 %) по сравнению со 136 (61,8 %); процентное различие - 11,0 (р = 0,015). Оба препарата к 12-й неделе исследования улучшали качество жизни пациентов. Исследуемые препараты хорошо переносились. Нежелательные явления, связанные с приемом препарата, согласовывались с уже имеющимися сведениями. Таким образом, более простой режим дозирования Феринжекта был наиболее эффективным и безопасным, он способствовал большей приверженности пациентов лечению.

The efficacy and safety of Ferinject when administered intravenously have been demonstrated in the treatment of IDA and in a number of other clinical situations (in patients on hemodialysis, in the postpartum period, with severe uterine bleeding).

Transfusion of blood components (erythrocyte mass) for the treatment of IDA is used only when life threatening(anemic coma) or severe anemia (Hb< 60 г/л), сопровождающейся признаками декомпенсации.

LITERATURE

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Iron is an important element of human metabolism, which takes part in hematopoiesis. Despite the fact that its absorption occurs in the intestines, the intestines and hemoglobin are rarely associated, which often makes it difficult to diagnose the cause of anemia.

Violation of iron absorption is a fairly common pathology.

Iron malabsorption

Low hemoglobin, as a result of impaired absorption of iron in the intestine, is a fairly common problem. To understand its etiology, you need to know exactly how this element is absorbed, and what is the relationship between the intestine and the level of hemoglobin.

The amount of ferum absorbed into the blood significantly exceeds the requirements of the body. Iron is delivered to the blood by enterocytes, so the rate of the process depends on the production of apoferritin by these cells. This substance captures the ferum molecule, binding it, preventing it from being released into the blood.

If the hemoglobin level is normal or above normal, apofferitin is produced by enterocytes in large quantities. Over time, these cells “fall off” from the intestinal walls, removing iron from the body. naturally. If the hemoglobin level drops, the enterocytes practically do not produce a “trap” for iron and the blood is saturated with the necessary element.

If for some reason these processes fail, a person develops iron deficiency anemia. Malabsorption can be the result of many diseases of the gastrointestinal tract.

Causes of insufficiency of intestinal absorption

The problem may occur due to the following diseases:

• dysbacteriosis;
• violations of peristalsis;
• Crohn's disease;
• oncology;
• intestinal obstruction, etc.

The cause of poor absorption of iron in the intestine may be a recent surgical intervention.

Dysbacteriosis

Dysbacteriosis is a state of the intestine, when its non-pathological microflora lends itself to qualitative or quantitative changes, and is accompanied by various disorders of the gastrointestinal tract.

The intestinal flora constantly maintains the normal course of metabolic processes in the body, bacteria are involved in biochemical and metabolic processes. They are important part defense mechanisms of the immune system. The microflora is formed by natural physiological needs organism, therefore, a change in the number and types of microorganisms signals a malfunction.

Systemic pathologies, HIV infection and other diseases can provoke dysbacteriosis, which cause a persistent deterioration in human immunity when the body is not able to maintain the stability of the flora. Dysbacteriosis can occur after a course of antibiotic treatment. Usually the intestines recover on their own after therapy, but sometimes you need to drink pharmaceuticals to help speed up this process.

Trouble digesting certain foods due to enzyme deficiency also a common cause of pathology, for example, with lactose deficiency, intolerance to cereals, etc.

Enteritis

Inflammation of the small intestine (enteritis) is characterized by impaired functionality of the organ, which is caused by changes in the structure of the mucous membranes. An extraintestinal symptom of enteritis is malabsorption syndrome - a condition in which many elements that enter the intestine are unable to be absorbed in it.

If the pathology exists for a long time, hypovitaminosis or a lack of some trace elements develops, for example, iron deficiency anemia occurs.

Crohn's disease

- these are inflammatory processes in the deep tissues of the entire gastrointestinal tract, which begins with the ileum, spreading to the entire intestine. The differential diagnosis often does not distinguish between the initial stage of Crohn's disease and appendicitis, which is why the disease is diagnosed when surgical intervention on the appendix.

Crohn's disease implies malabsorption of vitamins, minerals, which, with prolonged development of the disease, causes anemia, which is manifested by low hemoglobin.

Violation of peristalsis

Food is transported through the intestines through muscle and hormonal interactions. Food is divided into absorbed substances and waste products, which improves the flow of nutrients into the blood. When the motility of an organ is disturbed, discomfort and various complications. Enhanced peristalsis causes excessive fecal excretion, which is why useful material, including iron, do not have time to be absorbed, which causes water-electrolyte imbalance, hypovitaminosis and anemia.

bowel cancer

Every 10-15 patients who suffer from iron deficiency anemia after 40 years of age are prone to oncology of the digestive system. Very often, low hemoglobin is the only manifestation with. In addition, lymph nodes may be enlarged. Therefore, if oncological formations are suspected, first of all, doctors do a general blood test to identify anemia, in case of diagnosing which an urgent consultation with a gastroenterologist is necessary. In men closer to 50 years, a low hemoglobin level may indicate a malignant neoplasm in the rectum.

Other reasons

Often the hemoglobin level drops with obvious or hidden bleeding, for example, with hemorrhoids, injuries, operations. Autoimmune diseases can be the cause of the problem, infectious lesions. Hemoglobin levels may be below normal with peptic ulcer or gastritis.

In addition to the pathological causes of low hemoglobin levels, there are others that are associated with poor unbalanced nutrition.

Elevated hemoglobin due to bowel obstruction

Intestinal obstruction is characterized by a narrowing of the intestinal passage, as a result of which the transport of food is disturbed. Most often, complete blockage of the lumen does not occur, which can be cured by pharmaceutical means. Sometimes it's necessary surgery, for example, if tumors or lymph nodes in the intestines are enlarged and treatment does not help.

With intestinal obstruction, there is a violation of blood circulation, which can provoke an acute vascular insufficiency. Blood test shows erythrocytosis, high level hemoglobin, change in the level of leukocytes, etc.