Detection of an ulcerative defect. Gastric ulcer (Gastric ulcer) Treatment regimen for Helicobacter pylori

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Stomach ulcer (K25)

Gastroenterology

general information

Short description

Stomach ulcer(GD) is a multifactorial chronic disease accompanied by the formation of ulcers in the stomach with possible progression and development of complications.

The first morphological stage of peptic ulcer is erosion Erosion is a superficial defect of the mucous membrane or epidermis
, which is a shallow defect (damage) of the mucous membrane within the boundaries of the epithelium and is formed by necrosis of an area of ​​the mucous membrane.
Erosions, as a rule, are multiple and are localized mainly along the lesser curvature of the body and the pyloric part of the stomach, less often in the duodenum. Erosion can have different shapes and sizes - from 1-2 mm to several centimeters. The bottom of the defect is covered with fibrinous plaque, the edges are soft, smooth and do not differ in appearance from the surrounding mucous membrane.
Healing of erosion occurs through epithelization (complete regeneration) in 3-4 days without scar formation; if the outcome is unfavorable, it may develop into an acute ulcer.

Acute ulcer is a deep defect of the mucous membrane, which penetrates to the muscular plate of the mucous membrane and deeper. The reasons for the formation of acute ulcers are similar to those for erosions. Acute ulcers are often solitary; have a round or oval shape; in cross-section they look like a pyramid. Size of acute ulcers An ulcer is a defect of the skin or mucous membrane and underlying tissues, the healing processes of which (development of granulations, epithelization) are disrupted or significantly slowed down.
- from several mm to several cm. Localized on the lesser curvature. The bottom of the ulcer is covered with fibrinous plaque, it has smooth edges, does not rise above the surrounding mucous membrane and does not differ from it in color. Often the bottom of the ulcer has a dirty gray or black color due to the admixture of hematin hydrochloride.
Microscopically: mild or moderate inflammatory process at the edges of the ulcer; after rejection of necrotic masses at the bottom of the ulcer - thrombosed or gaping vessels. When an acute ulcer heals within 7-14 days, a scar forms (incomplete regeneration). In rare cases, an unfavorable outcome may lead to a chronic ulcer.

For chronic ulcers characterized by severe inflammation and proliferation of scar (connective) tissue in the area of ​​the bottom, walls and edges of the ulcer. The ulcer has a round or oval (less often linear, slit-like or irregular) shape. Its size and depth may vary. The edges of the ulcer are dense (callous ulcer), smooth; undermined in its proximal part and flat in its distal part.
Morphology of a chronic ulcer during an exacerbation: the size and depth of the ulcer increases.

There are three layers at the bottom of the ulcer:
- upper layer- purulent-necrotic zone;
- middle layer- granulation tissue;
- bottom layer- scar tissue penetrating into the muscle membrane.

The purulent-necrotic zone decreases during the period of remission. Granulation tissue, growing, matures and turns into coarse fibrous connective (scar) tissue. In the area of ​​the bottom and edges of the ulcer, the processes of sclerosis intensify; the bottom of the ulcer is epithelialized.
Scarring an ulcer does not lead to a cure for peptic ulcer disease, since an exacerbation of the disease can occur at any time.

Classification

There is no generally accepted classification of peptic ulcer disease.

From the point of view of nosological independence, the following types of disease are distinguished:
- peptic ulcer associated with H. pylori;
- peptic ulcer not associated with H. pylori;

Symptomatic gastroduodenal ulcers.

Depending on the location, there are:
- gastric ulcers (cardial and subcardial sections, body of the stomach, antrum, pyloric canal);
- ulcers of the duodenum (bulb or postbulbar);
- combined ulcers of the stomach and duodenum.

Ulcers can be located on the lesser or greater curvature, the anterior and posterior walls of the stomach and duodenum (duodenum).

By the number of ulcerative lesions It is customary to distinguish between single ulcers and multiple ulcers.

Depending on the size of the ulcerative defect exist:
- small ulcers (up to 0.5 cm in diameter);
- medium (0.6-2 cm);
- large (2-3 cm);
- gigantic (more than 3 cm).

When formulating diets, it is noted stage of the disease:
- exacerbation;
- scarring (with endoscopically confirmed stages of “red” and “white” scar);
- remission.
The presence of cicatricial and ulcerative deformation of the stomach and duodenum is also reflected.

The disease may have acute course(for newly diagnosed peptic ulcer disease) and chronic course with repeated exacerbations.
Periods of exacerbation in patients may be rare(once every 2-3 years) or frequent(2 times a year or more often).

Depending on the timing of scarring, it is customary to separately identify difficult-to-scar (long-term non-healing) ulcers, the duration of scarring of which exceeds 12 weeks.

When formulating a diagnosis, indicate complications of peptic ulcer:
- bleeding;
- perforation;
- penetration;
- perigastritis;
- periduodenitis;
- cicatricial ulcerative pyloric stenosis.
Anamnestic complications and previous operations for peptic ulcer are also indicated.

Etiology and pathogenesis

The most common cause of peptic ulcer is the bacterium H. pylori (75-80%).
The second most common cause is the use of non-steroidal anti-inflammatory drugs (NSAIDs).
Rare causes include Zollinger-Ellison syndrome, liver cirrhosis, collagenosis, HIV infection; diseases of the lungs, heart, kidneys and stress ulcers, which are combined into a group of so-called symptomatic ulcers.

Hereditary predisposition is considered an important factor in the development of gastric ulcer. The family history of peptic ulcer disease in children is about 15-40%.

Pathogenesis is a consequence of an imbalance between the factors of “aggression” and “defense” of the gastric mucosa. Factors of “aggression” include hydrochloric acid, pepsin, impaired evacuation of gastric contents, duodenogastric reflux Duodenogastric reflux is the reflux of the contents of the duodenum into the stomach.
.

In the formation of chronic ulcers in the stomach, the main importance is to reduce the resistance of the mucous membrane, weakening its resistance to the damaging effects of gastric juice. This occurs with the development of atrophic (autoimmune) gastritis, with a long-term course of gastritis associated with H. pylori, with prolonged exposure to chemicals and certain medications. For example, when taking NSAIDs, the production of prostaglandins is disrupted, which leads to a decrease in mucus production and suppression of the regeneration of the epithelium of the gastric mucosa.
Resistance of the mucous membrane decreases sharply at the site of local ischemia Ischemia is a decrease in blood supply to an area of ​​the body, organ or tissue due to weakening or cessation of arterial blood flow.
, which may be the result of hemorrhage, thrombosis or vasculitis against the background of an immunopathological process.
With reduced resistance of the mucous membrane, normal and even slightly reduced aggressiveness of gastric secretions becomes sufficient for the formation of ulcers.

The bulk of gastric ulcers appear in the area located on the lesser curvature of the stomach between the body and the antrum. It is called the place of least resistance (locus minoris resistentiae).

Epidemiology

Age: mostly mature and old age

Sex ratio(m/f): 1.5

Peptic ulcer disease affects from 5 to 14% of the population in different age and social groups.
According to a number of authors, H. pylori infection (as the main potential cause of ulcerative disease) is much higher and ranges from 25 to 80% in various countries. The infection rate correlates primarily with socioeconomic level. Among urban residents, the disease is registered 2-3 times more often than among rural residents. Men under 50 years of age get sick more often than women. PUD is a rarer form compared to duodenal ulcer.

In the structure of ulcerative lesions of the gastrointestinal tract in children Ipeptic ulcer disease accounts for about 13% and occurs in approximately 2 out of 10,000 children. Peptic ulcer of the duodenum occurs 8 times more often. The disease affects children aged 7 years and older. Boys and girls get sick equally often.

Risk factors and groups

The main factors contributing to the development of gastric ulcer:
- H. pylori infection;
- heredity;
- smoking;
- gastrinoma (Zollinger-Ellison syndrome) - excessive production of gastrin and histamine (carcinoid syndrome);
- hypercalcemia;
- overpopulation;
- low socio-economic level;
- professional contact with gastric and duodenal contents (healthcare workers).

Clinical picture

Clinical diagnostic criteria

Epigastric pain associated with eating, dyspepsia

Symptoms, course

The clinical picture appears pain syndrome And dyspeptic syndrome Dyspeptic syndrome is a disorder of the digestive process, usually manifested by pain or discomfort in the lower chest or abdomen, which may occur after eating and is sometimes accompanied by nausea or vomiting
.
Usually the disease occurs with periods of exacerbation and remission.

The main symptom of exacerbation of peptic ulcer disease is pain in the epigastric region to the left of the midline (with ulcers of the body of the stomach) or to the right of it (with ulcers of the pyloric canal and duodenal bulb). Pain may radiate Irradiation is the spread of pain beyond the affected area or organ.
into the left half of the chest and left scapula (usually with subcardial ulcers), right hypochondrium (with postbulbar ulcers), thoracic or lumbar spine.

Pain during exacerbation of a peptic ulcer is usually associated with food intake. They can occur immediately after eating (with ulcers of the cardial and subcardial parts of the stomach), 0.5-1 hour after eating (with ulcers of the body of the stomach).

For ulcers of the pyloric canal and duodenal bulb, late pain (2-3 hours after eating), “hungry” pain (occurs on an empty stomach and is relieved by eating), as well as night pain are typical.
The pain decreases and disappears after taking antacids, antisecretory and antispasmodic drugs, and applying heat.

In a number of patients, at the peak of pain, vomiting of acidic gastric contents occurs, which brings relief (due to this fact, patients can induce vomiting artificially). Frequent complaints of patients with exacerbation of peptic ulcer disease are nausea, belching, constipation.

The course of the disease has a number of characteristics in women, in adolescence and adolescence, as well as in old age.

Clinic of peptic ulcer with atypical course or atypical forms:
1. Pain is often localized primarily in the right hypochondrium or in the right iliac region.
2. Atypical localization of pain in the heart area ("heart mask") or in the lumbar region ("radiculitis mask") is possible.
3. The presence of “silent” ulcers, which have only dyspeptic symptoms in the absence of pain. "Silent" ulcers may manifest as gastric bleeding or perforation. Often they lead to the development of cicatricial pyloric stenosis, and patients seek medical help only if symptoms of the stenosis itself appear.

In children
The clinical picture of peptic ulcer in children differs from that in adults in some details. The most pronounced clinical features occur in children with ulcers localized in the cardial or subcardial part of the stomach.

Among the features of manifestations of ulcers of the upper stomach, mild pain syndrome, atypical localization and irradiation of pain are noted. Children often complain of a burning sensation and pressure under the xiphoid process, behind the sternum or to the left of it. The pain may radiate to the heart area, left shoulder, under the left shoulder blade; appears 20-30 minutes after eating and decreases when taking antisecretory drugs.

Patients with mediagastric ulcers are characterized by a vague pain syndrome: nagging, bursting pain that does not go away after eating. Pain sensations can radiate to the left half of the chest, lumbar region, right and left hypochondrium. Some patients with the mediogastric form of peptic ulcer experience a decrease in appetite and weight loss, which is not typical for pyloroduodenal ulcers. The stool is often unstable. Often the disease occurs latently or atypically, with a predominance of neurovegetative changes in the clinical picture.
Examination of the patient may reveal signs of hypovitaminosis, coated tongue; When palpating the abdomen, pain occurs in the epigastrium Epigastrium is an area of ​​the abdomen bounded above by the diaphragm and below by a horizontal plane passing through a straight line connecting the lowest points of the tenth ribs.
and mesogastria Mesogastrium (womb) is the area of ​​the abdomen located between the line connecting the lowest points of the X ribs and the line connecting the anterosuperior iliac spines.
.

Diagnostics

Diagnosis of peptic ulcer disease is based on a combination of clinical examination data, results of instrumental, morphological and laboratory research methods.

Instrumental diagnostics. Diagnosis of the presence of an ulcer

Mandatory studies
The main significance is endoscopic examination, which allows you to clarify the location of the ulcer and determine the stage of the disease. The sensitivity of the method is about 95%. An ulcer is a defect in the mucous membrane that reaches the muscular and even serous layer. Chronic ulcers may be round, triangular, funnel-shaped or irregular in shape. The edges and bottom of the ulcer may be thickened by connective tissue (callous ulcer). When a chronic ulcer heals, a scar forms, often with deformation of the stomach.

If it is impossible to carry out endoscopy, it is carried out fluoroscopy of the stomach, which allows you to detect an ulcer in approximately 70% of cases. The diagnostic accuracy is increased by the double contrast method. The ulcer crater (niche) looks like a depression on the contour of the stomach wall or a persistent contrasting spot. The folds of the stomach converge to the base of the ulcer, surrounded by a wide inflammatory shaft (Hampton's line). The ulcer crater is smooth, round or oval in shape.
X-ray examination is more often used to identify complications (scar deformities, penetration).

Diagnosis of H. pylori(Helicobacteriosis), as the main cause of ulcerative disease, is of great importance.

Invasive methods:
- biopsy staining according to Giemsa, Warthin-Starry;
- CLO-test - determination of urease in mucosal biopsy;
- bacterial culture of the biopsy sample.

Non-invasive methods:
- determination of antigen in stool (chromatography with monoclonal antibodies);
- breath test with urea labeled with a carbon isotope (C13-14);
- serological methods (determination of antibodies to H. pylori).

Bismuth preparations, proton pump inhibitors and others suppress the activity of H. pylori, which leads, for example, to false negative results of a urease test, histological examination, and determination of antigen in stool. Thus, diagnostic methods should be used on average 4 weeks after the end of antibiotic therapy or 2 weeks after the end of other antiulcer therapy (PPI). It is also possible to increase the reliability of studies by multiplying them - for example, multiple biopsies from more than 2 areas of the stomach increase the specificity of this diagnostic method.

Additional Research
Daily pH measurements and a study of intragastric proteolytic activity of the stomach are performed. To assess the motor function of the stomach, ultrasound, electrogastrographic, X-ray examinations, and antroduodenal manometry are used.
Ultrasound of the abdominal organs is performed to diagnose concomitant pathologies of the hepatobiliary system and pancreas.

Laboratory diagnostics

Mandatory studies: general blood and urine analysis, coprogram Coprogram - recording the results of a stool examination.
, stool occult blood test, tests for Helicobacter pylori infection, determination of blood type and Rh factor

Additional Research(carried out to diagnose so-called “endocrine and symptomatic” ulcers): determination of the level of parathyroid hormone, alkaline phosphatase, liver tests, creatinine.
Determination of calcium and phosphorus in urine and blood is also recommended.

Although endocrine gastric ulcers in Zollinger-Ellison syndrome Zollinger-Ellison syndrome (syn. gastrinoma) - a combination of peptic ulcers of the stomach and duodenum with adenoma of the pancreatic islets, developing from acidophilic insulocytes (alpha cells)
are many times less common than duodenal ulcers or gastrojejunal ulcers, determination of gastrin levels should be considered mandatory in treatment-resistant ulcers. In doubtful cases, provocative tests with intravenous administration of calcium (5 mg/kg per hour for 3 hours) or secretin (3 units/kg per hour) are used. When the gastrin content in the blood serum increases by 2-3 times compared to the basal level, the test is considered positive.

Indications for determining gastrin levels in relation to YaBZh:
- peptic ulcers in combination with diarrhea;
- recurrent postoperative peptic ulceration;
- multiple ulceration Ulceration is the process of ulceration, that is, the formation of ulcer(s)
;
- family history of peptic ulceration;
- peptic ulcers in combination with hypercalcemia or other manifestations of multiple endocrine neoplasia Multiple endocrine neoplasia (MEN) is a group of inherited autosomal dominant syndromes caused by tumors or hyperplasia of several endocrine glands
Type I (Wermer syndrome Wermer's syndrome (multiple endocrine neoplasia type I, MEN-I) is a hereditary combination of endocrine adenomatosis and peptic ulcers of the small intestine. Includes a combination of hormonally active tumors arising from endocrine cells and hormonally inactive tumors arising from other (non-endocrine) cells of the body
);

X-ray or endoscopic signs of hypertrophy of the folds of the gastric mucosa.

In patients over 60 years of age, ulcers can form due to circulatory decompensation, against the background of hypertension and atherosclerotic lesions of the abdominal aorta and its visceral branches; in this regard, for this group of patients it is recommended to determine laboratory parameters corresponding to the listed changes.

Differential diagnosis

First of all, it is necessary to differentiate peptic ulcer disease as such from symptomatic ulcers of the stomach and duodenum, the pathogenesis of which is associated with certain underlying diseases or with specific etiological factors (for example, with the use of NSAIDs).

Symptomatic gastroduodenal ulcers(especially medicinal) often develop acutely, sometimes manifesting as sudden gastrointestinal bleeding or perforation of an ulcer, and may occur with atypical clinical manifestations (erased pattern of exacerbation, lack of seasonality and frequency).

Gastroduodenal ulcers in Zollinger-Ellison syndrome, unlike ordinary peptic ulcers, they have a very severe course; They are characterized by multiple localization (often even in the jejunum) and persistent diarrhea. When examining such patients, a sharply increased level of gastric acid secretion (especially under basal conditions) and an increased gastrin content in the blood serum (3-4 times compared to the norm) are noted.
To recognize Zollinger-Ellison syndrome, provocative tests (with secretin, glucagon) and ultrasound examination of the pancreas are used.

Gastroduodenal ulcers in patients with hyperparathyroidism differ from peptic ulcers in their severe course with frequent relapses, a tendency to bleeding and perforation, and the presence of signs of increased function of the parathyroid glands (muscle weakness, bone pain, thirst, polyuria). The diagnosis is established based on determining the concentration of calcium and phosphorus, elevated levels of parathyroid hormone in the blood serum, signs of hyperparathyroid osteodystrophy, characteristic symptoms of kidney damage and neurological disorders.

When ulcerative lesions are detected in the stomach, it is necessary to make a differential diagnosis between benign ulcers, malignant ulcers and the primary ulcerative form of gastric cancer. The malignant nature of the lesion is supported by the very large size of the ulcer (especially in young patients), the localization of the ulcer on the greater curvature of the stomach, the presence of an increase in ESR and histamine-resistant achlorhydria.

In children

Since the clinical picture of gastric ulcer does not have specific symptoms, in children it is necessary to carry out differential diagnosis with other diseases of the digestive tract, which manifest themselves with similar pain and dyspeptic syndromes.

Esophagitis, chronic gastroduodenitis (CGD), duodenal ulcer are excluded using endoscopic and morphological studies.
To exclude acute cholecystitis and exacerbation of chronic cholecystitis, the clinic, indicators of inflammation activity, ultrasound data, and analysis of the composition of bile are taken into account.
Acute pancreatitis and exacerbation of chronic pancreatitis, along with clinical manifestations, are differentiated based on the appearance of steatorrhea in the coprogram, increased amylase in the urine and pancreatic enzymes in the blood, and ultrasound data of the pancreas.

If an ulcerative defect of the gastric mucosa is detected, differential diagnosis is carried out with symptomatic ulcers, among which the most common (much more often than gastric ulcers) occur in children acute ulcers:

Stress ulcers that occur with burns, after injuries, with frostbite;
- allergic ulcerations, mainly developing with food allergies;
- drug-induced ulcers resulting from taking drugs that disrupt the barrier functions of the mucous membrane (non-steroidal and steroidal anti-inflammatory drugs, cytostatics, etc.)

Acute ulcerations of the mucous membrane of the digestive tract do not have typical clinical manifestations. They develop very dynamically and can either heal quickly or unexpectedly lead to severe complications: bleeding, perforation.
When performing endoscopy, acute ulcers range in size from several millimeters to several centimeters, round or oval in shape, the edges of the ulcers are swollen, hyperemic, the bottom is lined with fibrin. After healing of an acute ulcer, scars often do not remain.

Complications

The prognosis for the Helicobacter-associated process is largely determined by the success of H. pylori eradication H. pylori eradication is the name of standard treatment regimens aimed at the complete destruction of Helicobacter pylori in the gastric mucosa in order to provide favorable conditions for the healing of ulcers and other damage to the mucosa.
, as a result of which a relapse-free course of the disease is possible in most patients.

In adults, peptic ulcer is complicated by bleeding in 15-20% of cases, perforation/penetration in 5-15%, and pyloric stenosis in 2%.
The incidence of gastric cancer, as one of the complications of peptic ulcer, is 3-6 times higher in patients infected with H. pylori.
H. pylori infection is associated with the occurrence of certain other diseases (so-called extraintestinal lesions), for example, coronary heart disease, the risk of which increases by 1-20%.
H. pylori infection may present with idiopathic chronic urticaria, rosacea, alopecia areata Alopecia is persistent or temporary, complete or partial loss (absence) of hair.
.

Approximately 4% of patients with gastric ulcer childhood Complications such as bleeding, perforation, penetration, and occasionally malignancy develop.

Bleeding manifested by bloody vomiting, tarry stools and symptoms of acute vascular insufficiency. Often, as bleeding develops, the pain disappears (Bergmann's symptom). With heavy bleeding, vomiting “coffee grounds” is typical. The color of vomit is formed as a result of the transformation of hemoglobin into hematin, which has a black color, under the influence of hydrochloric acid. Scarlet blood may also be present in the vomit. Black, tarry stool appears on the 2nd day of heavy bleeding. In cases of moderate bleeding, the color of the stool does not change, but occult blood can be detected in the stool using the Gregersen test. With significant blood loss, weakness, pallor, dizziness, nausea, cold sticky sweat, and arterial hypotension occur. Hypotension is reduced hydrostatic pressure in blood vessels, hollow organs or body cavities.
, tachycardia, possible fainting. The hematocrit in the blood decreases and, later, the content of red blood cells and hemoglobin. The source of bleeding is determined by endoscopy of the stomach.

Perforation Gastric ulcer is characterized by a sudden sharp stabbing pain in the epigastrium, vomiting does not bring relief. A board-like tension in the muscles of the anterior abdominal wall occurs, and symptoms of peritoneal irritation increase. The patient's general condition quickly deteriorates, body temperature rises, and consciousness is impaired. The most significant diagnostic method is a survey x-ray examination of the abdominal cavity. It helps detect the presence of free gas in the abdominal cavity.

Penetration- spread of the ulcer beyond the stomach wall into adjacent tissues and organs, most often into the lesser omentum and body of the pancreas. During penetration, the pain syndrome intensifies. The pain is constant (regardless of food intake) and does not decrease after taking antacids. Possible increase in body temperature. In the general blood test, leukocytosis and an increase in ESR increase. On palpation in the area of ​​the pathological focus, severe pain occurs, sometimes it is possible to palpate the inflammatory infiltrate Infiltrate is an area of ​​tissue characterized by the accumulation of cellular elements that are usually unusual for it, increased volume and increased density.
. A typical sign of penetration during an X-ray contrast examination of the stomach is the appearance of an additional shadow of barium next to the silhouette of the organ.

Malignancy- a rare complication of stomach ulcers. Malignancy most often occurs in subcardial ulcers. The clinical picture of peptic ulcer disease in the early stages does not change significantly. In case of advanced disease, patients may experience increased pain, weight loss, and the appearance of hematological changes (anemia, increased ESR). The diagnosis is established by morphological examination of a biopsy specimen.

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Treatment

Non-drug treatment

Treatment of peptic ulcer, in addition to prescribing medications, should also include measures such as dietary nutrition, stopping smoking and drinking alcohol, and stopping taking ulcerogenic drugs (primarily NSAIDs).

Diet food should be frequent, fractional, mechanically and chemically gentle. In the majority of cases, diet No. 1 according to M.I. is indicated. Pevzner. Physiologically inferior diets No. 1a and 16 should be prescribed only with pronounced symptoms of exacerbation and for a very short period of time.

Physiotherapeutic procedures(heating pads, poultices, paraffin and ozokerite applications, electrophoresis with a 5% novocaine solution, microwave therapy) are additional to pharmacotherapy and are recommended for patients only in the phase of subsiding exacerbation of peptic ulcer disease in the absence of signs of ulcer bleeding. Procedures are not carried out until the benign nature of the lesions is fully confirmed.

Eradication of H. pylori with the help of any one drug is not effective enough, so it must be carried out using a combination

Several antisecretory agents. A particular regimen is considered effective if it allows eradication to be achieved in more than 80-90% of cases. Most anti-Helicobacter therapy regimens include proton pump inhibitors (PPIs, PPIs). These drugs, by increasing the pH of the gastric contents, create unfavorable conditions for the life of H. pylori and increase the effectiveness of many anti-Helicobacter drugs.

Taking this information into account, the recommendations of the last conciliation meeting "Maastricht III"(Florence, 2005) provide as first line therapy a single triple eradication regimen, including PPI (in standard doses 2 times a day), clarithromycin (at a dose of 500 mg 2 times a day) and amoxicillin (at a dose of 1000 mg 2 times a day). In addition, these recommendations contain an important clarification that the specified regimen is prescribed if the proportion of H. pylori strains resistant to clarithromycin in a given region does not exceed 20%.

The eradication therapy protocol requires mandatory monitoring of effectiveness, which is carried out 4-6 weeks after its completion (during this period the patient does not take any antibacterial drugs or PPIs).

If H. pylori is detected in the mucous membrane, a repeat course of eradication therapy using second-line therapy is indicated, followed by monitoring its effectiveness also after 4 weeks. Only strict adherence to such a protocol makes it possible to properly sanitize the gastric mucosa and prevent the risk of recurrent ulcers.
As second line therapy a 4-drug regimen is used, including PPI (in a standard dose 2 times a day), bismuth preparations in a usual dosage (for example, colloidal bismuth subcitrate 0.24 g 2 times a day), metronidazole (0.5 g 3 times a day) day) and tetracycline (daily dose 2 g). The quadruple therapy regimen remains effective in cases of H. pylori strains resistance to metronidazole.

In case of ineffectiveness of first- and second-line eradication regimens, the Maastricht-III consensus offers several options for further therapy. Since H. pylori strains do not develop resistance to amoxicillin during its use, it is possible to prescribe its high doses (0.75 g 4 times a day for 14 days) in combination with high (4-fold) doses of PPIs.
Another option may be to replace metronidazole in the quadruple therapy regimen with furazolidone (100-200 mg 2 times a day). An alternative is the use of a combination of PPIs with amoxicillin and rifabutin (at a dose of 300 mg/day) or levofloxacin (at a dose of 500 mg/day). The optimal way to overcome resistance remains the selection of antibiotics, taking into account the determination of the individual sensitivity of a given H. pylori strain.

Taking into account antibiotic resistance and other factors, " Standards for diagnosis and treatment of acid-dependent and Helicobacter pylori-associated diseases(4th Moscow Agreement)" which include the following further treatment.

First line

Option 1

Three-component therapy, including the following drugs, which are taken for 10-14 days:

One of the PPIs in a “standard dosage” 2 times a day +

Amoxicillin (500 mg 4 times a day or 1000 mg 2 times a day) +

Clarithromycin (500 mg 2 times a day), or josamycin (1000 mg 2 times a day) or nifuratel (400 mg 2 times a day).

Option 2

Quadruple therapy, which includes, in addition to the drugs in Option 1, a bismuth drug. Duration is also 10-14 days:

Indications for surgical treatment of peptic ulcer disease currently include complicated forms of the disease (perforation and penetration of the ulcer, development of cicatricial ulcerative stenosis of the pylorus, malignancy of the ulcer). If all necessary protocols for conservative treatment are followed, cases of its ineffectiveness (as an indication for surgery) can be reduced to a minimum.

In children

Treatment of peptic ulcer in children, as well as in adults, should be comprehensive, including regimen, dietary nutrition, drug and non-drug therapy, as well as prevention of recurrence and development of complications.

Non-drug treatment
During periods of intense pain, bed rest is recommended. The diet should be mechanically, chemically and thermally gentle on the gastric mucosa. Spicy seasonings are excluded from the diet, and the consumption of table salt and foods rich in cholesterol is limited. Meals should be taken 4-5 times a day. In case of exacerbation, which is accompanied by severe abdominal pain, it is advisable to prescribe diet No. 1 followed by transition to diet No. 5.

Drug treatment

Drug treatment is prescribed depending on the leading pathogenetic factor.

In forms of the disease associated with H. pylori, therapy begins with a 10-14-day 3-component course of eradication (for example, omeprazole + clarithromycin + metronidazole) followed by a 3-4-week course of antisecretory drugs, usually H+, K+ inhibitors -ATPases (omeprazole, rabeprazole, esomeprazole).
4-6 weeks after completion of the eradication course, its effectiveness is monitored (breathing helic test). If treatment is ineffective, after 4 months a second course is carried out - second-line quadruple therapy (H+, K+-ATPase inhibitors + De-Nol + 2 antibacterial drugs).

For H. pylori-negative gastric ulcer against the background of atrophic gastritis, film-forming cytoprotectors are prescribed - sucralfate (Venter, Antepsin, Alsukral), colloidal bismuth subcitrate (de-Nol).

For duodenogastric reflux, prokinetics are used - domperidone (Motilium).

In the treatment of gastric ulcer associated with long-term use of NSAIDs, synthetic prostaglandins are recommended - misoprostol (arboprostil, enprostil, cytotec, cytotect). Prescribe tablets of 0.2 mg 3 times a day orally with meals and before bedtime.

In the case of a bleeding gastric ulcer, endoscopy and endoscopic bleeding control (diathermo- or laser coagulation) are performed. Parenteral administration of hemostatic drugs (Vicasol, calcium, adroxon), as well as H2-histamine receptor blockers, is necessary. Aminocaproic acid with thrombin and adroxon is prescribed orally. In case of significant blood loss, transfusion of high-molecular blood substitutes, plasma, and in critical conditions - blood transfusion is used.

With adequate treatment in children, healing of stomach ulcers occurs within 20-23 days. At 2-3 weeks of therapy, a control endoscopic examination is performed. In the absence of positive dynamics or slow healing, Daralgin is additionally prescribed. This drug stimulates regeneration processes, improves microcirculation in the gastric mucosa and has an anti-stress effect.
During endoscopy, local laser therapy, ulcer irrigation with solcoseryl, and fibrin glue applications are also used.

Physiotherapy is of auxiliary importance in the treatment of gastric ulcer. Electrosleep, electrophoresis with bromine on the collar area and with novocaine on the epigastric region, and EHF therapy are prescribed. At the beginning of convalescence after an exacerbation, DMV-, SMV-therapy, laser therapy are used on the most painful point of the epigastrium, a little later - ozokerite, paraffin on the epigastric region.

Surgery

Surgical treatment of gastric ulcer in children is necessary in case of development of such complications of gastric ulcer as continuous massive bleeding, perforation, penetration of ulcer, malignancy.

Forecast

In adultsthe prognosis is largely determined by the success of eradication of H. pylori infection, which leads to a relapse-free course of the disease in most patients.

In children: P The prognosis is favorable subject to timely diagnosis, adequate treatment and subsequent rational management.

Hospitalization

It is advisable to carry out primary diagnosis of peptic ulcer disease in a hospital only in children. In adults, such diagnostics can be done on an outpatient basis.
All patients are hospitalized if complications are suspected.

Prevention

Prevention of gastric ulcer involves limiting exposure to triggers Trigger - trigger, provoking substance or factor
factors, carrying out epidemiological measures aimed at preventing H. pylori infection.

The basics of anti-relapse prevention are adherence to a rational diet, limiting stressors, preventive therapy “on demand”: when the first clinical symptoms of an exacerbation appear, take one of the antisecretory drugs for 1-2 weeks at the full daily dose, and then another 1-2 weeks at half the dose.

For forms of gastric ulcer associated with H. pylori, control of H. pylori infection and, if reinfection is detected, eradication are mandatory.
Dispensary observation is carried out for life. In the first year after an exacerbation, examination and endoscopy with a urease test are carried out 4 times a year, from the second year - 2 times a year.

Information

Sources and literature

1. Ivashkin V.T., Lapina T.L. Gastroenterology. National leadership. Scientific and practical publication, 2008
2. McNally Peter R. Secrets of gastroenterology / translation from English. edited by prof. Aprosina Z.G., Binom, 2005
3. General and emergency surgery. Manual / ed. Paterson-Brown S., trans. from English edited by Gostishcheva V.K., M: GEOTAR-Media, 2010
4. Roytberg G.E., Strutynsky A.V. Internal illnesses. Digestive system. Textbook, 2nd edition, 2011
5. "International clinical guidelines for the management of patients with non-variceal bleeding from the upper gastrointestinal tract", journal "Emergency Medicine", No. 5(18), 2008
6. "Endoscopic control of bleeding in Dieulafoy's disease" Shavaleev R.R., Kornilaev P.G., Ganiev R.F., journal "Surgery", No. 2, 2009

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is a chronic polyetiological pathology that occurs with the formation of ulcerative lesions in the stomach, a tendency to progression and the formation of complications. The main clinical signs of peptic ulcer disease include pain in the stomach and dyspeptic symptoms. The diagnostic standard is an endoscopic examination with a biopsy of pathological areas, radiography of the stomach, and detection of H. pylori. Treatment is complex: diet and physiotherapy, eradication of Helicobacter pylori infection, surgical correction of complications of the disease.

ICD-10

K25 Stomach ulcer

General information

Gastric ulcer (GUD) is a cyclically relapsing chronic disease, the characteristic feature of which is ulceration of the stomach wall. PUD is the most common pathology of the gastrointestinal tract: according to various sources, from 5 to 15% of the world's population suffer from this disease, and among urban residents the pathology is five times more common. Many specialists in the field of gastroenterology combine the concepts of gastric ulcer and duodenal ulcer, which is not entirely correct - ulcerations in the duodenum are diagnosed 10-15 times more often than ulcers in the stomach. However, PU requires careful study and development of modern diagnostic and treatment methods, since this disease can lead to the development of fatal complications.

About 80% of cases of primary detection of gastric ulcers occur in working age (up to 40 years). In children and adolescents, gastric ulcers are diagnosed extremely rarely. Among the adult population, there is a predominance of men (women suffer from peptic ulcers 3-10 times less often); But in old age, sex differences in incidence are smoothed out. In women, the disease is milder, in most cases asymptomatic, and is rarely complicated by bleeding and perforation.

Gastric ulcer ranks second among the causes of disability in the population (after cardiovascular pathology). Despite the long period of study of this nosology (more than a century), therapeutic methods of influence that can stop the progression of the disease and completely cure the patient have not yet been found. The incidence of gastrointestinal ulcers throughout the world is continuously growing, requiring the attention of therapists, gastroenterologists, and surgeons.

Causes

The disease is polyetiological. There are several groups of reasons based on the degree of significance.

1. The main etiological factor in the formation of gastric ulcer is infection with H. pylori - more than 80% of patients have positive tests for Helicobacter pylori infection. In 40% of patients with gastric ulcer infected with the Helicobacter bacterium, anamnestic data indicate a family predisposition to this disease.
2. The second most important cause of gastric ulcer formation is considered to be the use of non-steroidal anti-inflammatory drugs.
3. Rarer etiological factors of this pathology include Zollinger-Ellison syndrome, HIV infection, connective tissue diseases, liver cirrhosis, heart and lung diseases, kidney damage, exposure to stress factors that lead to the formation of symptomatic ulcers.

Pathogenesis

The main significance for the formation of gastric ulcer is an imbalance between the protective mechanisms of the mucous membrane and the influence of aggressive endogenous factors (concentrated hydrochloric acid, pepsin, bile acids) against the background of a disorder of the evacuation function of the gastrointestinal tract (gastric hypokinesia, duodenogastric reflux, etc.) . Inhibition of protection and slower recovery of the mucous membrane is possible against the background of atrophic gastritis, with chronic Helicobacter pylori infection, ischemia of stomach tissue against the background of collagenosis, long-term use of NSAIDs (the synthesis of prostaglandins slows down, which leads to a decrease in mucus production).

The morphological picture of gastric ulcer undergoes a number of changes. The primary substrate for the occurrence of ulcers is erosion - superficial damage to the gastric epithelium, which forms against the background of necrosis of the mucous membrane. Erosions are usually detected on the lesser curvature and in the pylorus of the stomach; these defects are rarely isolated. The size of erosions can range from 2 millimeters to several centimeters. Visually, erosion is a mucosal defect that does not differ in appearance from the surrounding tissues, the bottom of which is covered with fibrin. Complete epithelization of erosion with a favorable course of erosive gastritis occurs within 3 days without the formation of scar tissue. If the outcome is unfavorable, erosions transform into acute gastric ulcers.

An acute ulcer is formed when the pathological process spreads deep into the mucous membrane (beyond its muscular plate). The ulcers are usually single, take on a rounded shape, and look like a pyramid when cut. In appearance, the edges of the ulcer also do not differ from the surrounding tissues; the bottom is covered with fibrin deposits. Black coloration of the bottom of the ulcer is possible when the vessel is damaged and hematin is formed (a chemical substance formed during the oxidation of hemoglobin from destroyed red blood cells). A favorable outcome of an acute ulcer consists of scarring within two weeks; an unfavorable outcome is marked by the transition of the process to a chronic form.

The progression and intensification of inflammatory processes in the area of ​​the ulcer leads to increased formation of scar tissue. Because of this, the bottom and edges of a chronic ulcer become dense and differ in color from the surrounding healthy tissue. A chronic ulcer tends to enlarge and deepen during an exacerbation; during remission it decreases in size.

Classification

Until today, scientists and clinicians around the world have not been able to reach agreement on the classification of gastric ulcers. Domestic experts systematize this pathology according to the following criteria:

• causative factor– ulcers associated or not associated with H. pylori, symptomatic ulcers;
• localization– ulcer of the cardia, antrum or body of the stomach, pylorus; greater or lesser curvature, anterior, posterior wall of the stomach;
• number of defects– single ulcer or multiple ulcerations;
• defect size– small ulcer (up to 5 mm), medium (up to 20 mm), large (up to 30 mm), giant (more than 30 mm);
• stage of the disease– exacerbation, remission, scarring (red or white scar), cicatricial deformation of the stomach;
• course of the disease– acute (the diagnosis of gastric ulcer is established for the first time), chronic (periodic exacerbations and remissions are noted);
• complications– gastric bleeding, perforated gastric ulcer, penetration, cicatricial ulcerative gastric stenosis.

Symptoms of stomach ulcer

The clinical course of gastric ulcer is characterized by periods of remission and exacerbation. Exacerbation of peptic ulcer is characterized by the appearance and increase of pain in the epigastric region and under the xiphoid process of the sternum. With an ulcer of the body of the stomach, the pain is localized to the left of the center line of the body; in the presence of ulceration of the pyloric region - on the right. Pain may radiate to the left half of the chest, shoulder blade, lower back, and spine.

Gastric ulcer is characterized by the onset of pain immediately after eating with increasing intensity within 30-60 minutes after eating; pylorus ulcer can lead to the development of night, hunger and late pain (3-4 hours after eating). The pain syndrome is relieved by applying a heating pad to the stomach area, taking antacids, antispasmodics, proton pump inhibitors, and H2-histamine receptor blockers.

In addition to the pain syndrome, gastrointestinal tract is characterized by a coated tongue, bad breath, and dyspeptic symptoms - nausea, vomiting, heartburn, increased flatulence, and stool instability. Vomiting mainly occurs at the height of stomach pain and brings relief. Some patients tend to induce vomiting to improve their condition, which leads to progression of the disease and complications.

Atypical forms of gastric ulcer can manifest as pain in the right iliac region (appendicular type), in the heart (cardiac type), and in the lower back (radiculitis pain). In exceptional cases, pain syndrome with gastric ulcer may be completely absent, then the first sign of the disease is bleeding, perforation or cicatricial stenosis of the stomach, for which reason the patient seeks medical help.

Diagnostics

If a gastric ulcer is suspected, a standard set of diagnostic measures (instrumental, laboratory) is carried out. It is aimed at visualizing the ulcerative defect, determining the cause of the disease and excluding complications.

• Esophagogastroduodenoscopy. It is the gold standard for diagnosing gastric ulcers. Endoscopy allows you to visualize the ulcerative defect in 95% of patients and determine the stage of the disease (acute or chronic ulcer). Endoscopic examination makes it possible to timely identify complications of gastric ulcer (bleeding, cicatricial stenosis), conduct endoscopic biopsy, and surgical hemostasis.
• Gastrography. X-ray of the stomach is of paramount importance in the diagnosis of cicatricial complications and penetration of ulcers into nearby organs and tissues. If endoscopic visualization is not possible, radiography can verify a gastric ulcer in 70% of cases. For a more accurate result, it is recommended to use double contrasting - in this case, the defect is visible in the form of a niche or a persistent contrasting spot on the wall of the stomach, to which the folds of the mucous membrane converge.
• Diagnosis of Helicobacter pylori infection. Considering the huge role of Helicobacter pylori infection in the development of peptic ulcer, all patients with this pathology undergo mandatory tests to detect H. pylori (ELISA, PCR diagnostics, breath test, examination of biopsy specimens, etc.).

Of auxiliary value for gastric ulcers are:

• Ultrasound of the liver (detects concomitant pathology of the liver, pancreas),
• electrogastrography and antroduodenal manometry (makes it possible to assess the motor activity of the stomach and its evacuation ability),
• intragastric pH-metry (detects aggressive damage factors),
• stool occult blood test (performed if gastric bleeding is suspected).

If a patient is admitted to the hospital with a clinical picture of an “acute abdomen,” diagnostic laparoscopy may be required to exclude gastric perforation. Gastric ulcers must be differentiated from symptomatic ulcers (especially medicinal ones), Zollinger-Ellison syndrome, hyperparathyroidism, and gastric cancer.

Treatment of gastric ulcer

Conservative treatment

The main goals of therapy for peptic ulcer include repair of the ulcer, prevention of disease complications, and achievement of long-term remission. Treatment of gastric ulcer includes non-drug and medicinal treatments, and surgical methods.

1. Non-drug treatment JAB implies following a diet, prescribing physiotherapeutic procedures (heat, paraffin therapy, ozokerite, electrophoresis and microwave exposure), it is also recommended to avoid stress and lead a healthy lifestyle.
2. Drug treatment must be complex, affecting all parts of the pathogenesis of ulcerative disease. Anti-Helicobacter therapy requires the use of several drugs to eradicate H. pylori, since the use of monoschemes has shown to be ineffective. The attending physician individually selects a combination of the following drugs: proton pump inhibitors, antibiotics (clarithromycin, metronidazole, amoxicillin, furazolidone, levofloxacin, etc.), bismuth preparations.

Surgery

If you seek medical help in a timely manner and carry out a complete anti-Helicobacter treatment regimen, the risk of complications of gastric ulcer is minimized. Emergency surgical treatment of gastric ulcer (hemostasis by clipping or suturing a bleeding vessel, suturing the ulcer) is usually required only for patients with a complicated pathology: perforation or penetration of the ulcer, bleeding from the ulcer, malignancy, and the formation of scar changes in the stomach. In elderly patients, if there is a history of complications of ulcerative gastritis in the past, experts recommend reducing the duration of conservative treatment to one to one and a half months.

Absolute indications for surgery:

• perforation and malignancy of the ulcer,
• massive bleeding
• cicatricial changes in the stomach with disruption of its function,
• gastrojejunostomy ulcer.

Conditionally absolute indications include:

• ulcer penetration,
• giant callous ulcers,
• recurrent gastric bleeding during conservative therapy,
• lack of ulcer repair after suturing.

A relative indication is the absence of a clear effect from drug therapy for 2-3 years. For decades, surgeons have been discussing the effectiveness and safety of various types of surgical interventions for gastric ulcers. Today, gastrectomy, gastroenterostomy, and various types of vagotomies are recognized as the most effective. Excision and suturing of a gastric ulcer is used only in extreme cases.

Prognosis and prevention

The prognosis for gastric ulcer largely depends on the timeliness of seeking medical help and the effectiveness of anti-Helicobacter therapy. Peptic ulcer is complicated by gastric bleeding in every fifth patient, from 5 to 15% of patients suffer perforation or penetration of the ulcer, and 2% develop cicatricial stenosis of the stomach. In children, the incidence of complications of gastric ulcer is lower - no more than 4%. The likelihood of developing stomach cancer in patients with peptic ulcer is 3-6 times higher than among people who do not suffer from this pathology.

Primary prevention of gastric ulcer includes preventing infection with Helicobacter pylori infection, eliminating risk factors for the development of this pathology (smoking, cramped living conditions, low standard of living). Secondary prevention is aimed at preventing relapses and includes following a diet, avoiding stress, and prescribing an anti-Helicobacter drug regimen when the first symptoms of peptic ulcer appear. Patients with gastric ulcer require lifelong monitoring, endoscopic examination with mandatory testing for H. pylori once every six months.