Functional non-ulcer dyspepsia. Non-ulcer dyspepsia. Etiology and pathogenesis


Babak O.Ya., doctor medical sciences, Professor.

Institute of Therapy of the Academy of Medical Sciences of Ukraine (Kharkov)

Dyspepsia refers to digestive disorders associated with functional and organic changes not only in the stomach, but also in the intestines, pancreas, and liver.

The term “non-ulcer dyspepsia” refers to digestive disorders associated with diseases of the esophagus, stomach and intestines, of non-ulcer, often of functional origin. Synonyms for non-ulcer dyspepsia: gastric dyskinesia, irritable stomach, essential dyspepsia, neurotic gastritis, gastric neurosis, functional syndrome of the upper abdomen, functional dyspepsia.

Functional (non-ulcer) dyspepsia is considered chronic if more than 3 months pass from the onset of its occurrence.

Non-ulcer dyspepsia can have several manifestations. These are: ulcer-like, reflux-like, dyskinetic, nonspecific.

Regardless of the prevailing variant of non-ulcer dyspepsia, the presence of “vegetative syndrome” is characteristic varying degrees expressiveness. Vegetative syndrome may manifest itself fatigue, sleep disturbances, decreased performance, periodic feelings of heat, sweating, “irritation” Bladder (frequent urination in small portions).

The absence of vegetative syndrome rather indicates the presence of organic pathology.

Ulcer-like non-ulcer dyspepsia is characterized by intense pain or a feeling of pressure in the epigastric region or on the right at the level of the navel, occurring spontaneously or one to two hours after eating. Sometimes it can be "night" or "fasting" pain, which decreases or disappears during or after eating. The secretory function of the stomach is usually increased.

For the reflux-like variant of non-ulcer dyspepsia, the following symptoms are most typical: heartburn, especially when bending forward and horizontal position, after meal; chest pain with short-term relief after drinking soda; nausea, dull pain and a feeling of heaviness in the epigastric region. Gastric secretion is usually increased. There is a connection between the appearance of these symptoms or their severity and the intake of spicy and sour foods (marinades, mustard, pepper), alcoholic drinks. This option often occurs cyclically: periods of exacerbations of different durations are replaced by the spontaneous disappearance of all symptoms.

The dyskinetic variant of non-ulcer dyspepsia is associated mainly with motor disorders of the stomach and intestines and resembles the picture of chronic gastritis. This is manifested by a feeling of heaviness and fullness in the epigastric region, rapid satiety during meals, intolerance various types food, pain spread with varying intensity throughout the abdomen, nausea.

Sometimes, in a small number of patients with non-ulcer dyspepsia, the main complaint is frequent painful belching of air (aerophagia). Its distinctive features are that it is loud, occurs regardless of food intake, more often with nervous excitement. This belching does not bring relief; it intensifies when eating, especially quickly. Belching can be combined with cardialgia and disorders heart rate in the form of extrasystole, a feeling of heaviness in the epigastric region.

In half of the patients, non-ulcer dyspepsia can transform into organic pathology: reflux esophagitis, chronic gastritis, duodenitis, peptic ulcer.

Treatment of non-ulcer dyspepsia is based on the characteristics of the variant of manifestation and is essentially symptomatic.

To reduce the secretory function of the stomach or neutralize it in case of “acidism syndrome” - i.e. heartburn, sour belching, pain in the epigastric region, relieved after taking alkalis, occurring against the background of increased gastric secretion, the use of pirenzepine is also indicated. The prescription of the drug is due to the peculiarities of its pharmacodynamics, in particular, relatively low bioavailability, insignificant penetration through the blood-brain barrier, the absence of pronounced interindividual fluctuations in absorption, distribution and elimination of the drug, low level metabolism in the liver.

Pirenzepine slows down the evacuation of contents from the stomach, however, unlike other atropine-like drugs, it does not affect the tone of the lower esophageal sphincter, which thus eliminates the risk of occurrence or intensification of gastroesophageal reflux.

The most famous pirenzepine drug is Gastrozepin (Boehringer Ingelheim, Germany).

At the Institute of Therapy of the Academy of Medical Sciences of Ukraine, a study was conducted to determine the indications and evaluate the effectiveness of gastrocepin, produced by Boehringer Ingelheim, when included as a basic drug for the treatment of patients with non-ulcer dyspepsia. The study of the drug made it possible to identify, along with the antisecretory effect, also its stimulating effect on gastric mucus formation and an increase in the concentration of mucus glycoproteins in gastric juice. The side effects of gastrocepin were not as numerous as those of other atropine-like drugs. In addition, they occurred less frequently and were, as a rule, less pronounced. The most common side effects (dry mouth, accommodation disorders) were usually observed with very high doses gastrocepin (150 mg/day). At average therapeutic doses of the drug (100 mg/day), the frequency of side effects decreases to 1-6%.

The best effect of pharmacological correction of motor and secretory disorders of the stomach in non-ulcer dyspepsia is usually observed with the additional use of psychopharmacological drugs. If there is a tendency towards depressive actions, it also has anticholinergic activity.

With a high level of neuroticism, the most indicated is the prescription of sibazon (diazepam) 1-2 tablets per day.

The duration of treatment for non-ulcer dyspepsia is short - from 10 days to 3-4 weeks.

We conducted a study to determine the indications and evaluate the effectiveness of gastrocepin, produced by Boehringer Ingelheim, when included as a basic drug for the treatment of patients with non-ulcer dyspepsia.

47 patients with a verified diagnosis of non-ulcer dyspepsia aged from 20 to 50 years were examined, including 33 men and 14 women. Depending on the character clinical manifestations all patients were divided into 3 groups: 1st group - mainly with reflux type in the amount of 12 patients; Group 2 - predominantly with the dyskinetic type - 17 patients; Group 3 - with ulcer-like type - 23 patients.

As a basic drug, all patients were prescribed gastrocepin 100 mg per day for 14 days. Additionally, according to indications, metoclopramide, drugs containing pancreatic enzymes (pancreatin, panzinorm) and others were prescribed.

The criteria for assessing the effectiveness were the dynamics of the leading clinical symptoms, the state of the acid-producing function of the stomach (according to intragastric pH-metry), and the data of X-ray (fluoroscopy of the stomach) and endoscopic (FGDS) studies.

Analysis of the data obtained showed that already on days 2-3 after taking gastrocepin there was a significant improvement in clinical symptoms in almost all patients. This was expressed in a decrease in pain, heartburn, and belching. By the end of the course of treatment complete absence clinical symptoms of the disease were observed in 40 patients (85%). The best effect of the treatment was observed in the group of patients with an ulcer-like variant of non-ulcer dyspepsia. In this group of patients, by the end of the course of treatment, not a single patient had clinical manifestations of the disease. In the group of patients with reflux type discomfort in the form of sour belching and moderate heartburn persisted in 3 patients, although they were expressed to a significantly lesser extent than before the start of treatment. Moderately severe clinical symptoms persisted until the end of treatment in 4 patients from the group with the dyskinetic type of clinical manifestations of non-ulcer dyspepsia.

Gastrocepin moderately decreased gastric secretory function in all patients. The average pH levels before treatment were 1.9 and after treatment were 3.4.

According to X-ray examination and FGDS, an improvement in the motor-evacuation function of the stomach was observed in 20% of patients from all three groups.

Among the side effects, dry mouth was noted in 4 patients (accounting for 8.8% of the total number of patients), which was easily tolerated by patients and did not require discontinuation of the drug. Other side effects We have not registered gastrocepin.

Thus, gastrocepin showed itself to be highly effective drug in the treatment of most clinical manifestations of non-ulcer dyspepsia, accompanied by increased secretory and motor function of the stomach. It quickly and easily eliminated the clinical syndromes of the disease and improved the quality of life of patients already from 2-3 days from the start of its use.

The use of such a selective anticholinergic blocker as gastrocepin can and does play a leading role in the treatment of most manifestations of non-ulcer dyspepsia and can be used as a basic drug in the treatment of this pathology.

High antisecretory activity, low severity of side effects and affordable price allow us to currently consider gastrocepin the drug of choice in the treatment of most types of non-ulcer dyspepsia.

Dyspepsia refers to a complex of symptoms related to diseases upper sections Gastrointestinal tract: pain, discomfort in the abdomen, heaviness after eating, increased gas formation, nausea, vomiting. Dyspepsia can be paroxysmal, occur sporadically, the symptoms of the disease can torment the patient constantly, intensifying after eating. In 40% of cases, the causes of dyspepsia are organic; the pathology accompanies ulcerative lesions of the stomach and duodenum, reflux esophagitis, and stomach cancer. In half of the cases, the causes of dyspepsia remain unknown; this type of disease is called “non-ulcer dyspepsia.” In medicine, unfortunately, at present there are no reliable methods that make it possible to confidently make a diagnosis, distinguishing organic dyspepsia from the second form of the disease - non-ulcer.

Causes of non-ulcer dyspepsia

There are several hypotheses that describe the causes of non-ulcer dyspepsia. According to the first assumption (acid hypothesis), the symptoms of the disease are directly related to increased secretion gastric juice or increased sensitivity of the stomach walls to hydrochloric acid. According to the dyskinetic hypothesis, the cause of the disease is impaired motility of the upper gastrointestinal tract. The psychiatric hypothesis explains the occurrence of symptoms of the disease by the patient’s anxiety-depressive disorder. Another hypothesis - enhanced visceral perception - suggests that the development of non-ulcer dyspepsia occurs due to an increased reaction of the gastrointestinal tract to the action physical factors: pressure on the walls of organs, stretching of the walls, temperature changes. According to a hypothesis called the food intolerance hypothesis, dyspepsia occurs due to certain types of foods that cause a secretory, motor or allergic reaction.

Regarding the treatment of non-ulcer dyspepsia, today there is no clear opinion; the data are extensive and contradictory. Antisecretory agents, prokinetics and drugs that affect H. Pylory have been studied in most detail. However, there are general provisions which are recommended to be followed in the treatment of non-ulcer dyspepsia.

In the treatment of the disease, it is recommended to use drugs that reduce the level of acidity of gastric juice. According to researchers, the effectiveness of drugs in this series is considered moderate. According to experts, treatment of non-ulcer dyspepsia with prokinetics turned out to be much more effective.

Much controversy in medicine is associated with the question of the advisability of using complex treatment pathological process of drugs that suppress the activity of H. Pylory. Most experts agree that eradication of H. Pylory is quite justified, even if it does not have the desired effect for dyspepsia resulting from peptic ulcer disease.

From psychotropic drugs in the treatment of non-ulcer dyspepsia, antidepressants, anxiolytics, drugs that block serotonin receptors and serotonin reuptake are used.

Small doses of antidepressants, k-opioid receptor agonists, serotonin receptor blockers, and drugs from the group of somatostatin analogues are used as medications to reduce pain sensitivity. In modern treatment regimens for the disease, much attention is paid to visceral nociception, since, according to recent studies, visceral sensitivity increases in non-ulcer dyspepsia.

IN In recent years, the problem of non-ulcer or functional dyspepsia (ND) has been discussed in domestic and foreign literature.

To define this symptom complex - various dyspeptic disorders and a state of discomfort in the upper half of the abdomen - many terms have been proposed: idiopathic, inorganic, essential dyspepsia, which brings certain difficulties to the work of practitioners. This is explained by different methodological approaches to defining both the concept itself and the diagnosis of non-ulcer dyspepsia syndrome.

According to modern ideas nonulcerative(functional) dyspepsia is a syndrome that includes: pain in the upper abdomen, dependent on food intake and/or not associated with it, periodically occurring after physical activity or emotional stress; a feeling of heaviness in the epigastric region, flatulence, nausea, vomiting, heartburn and regurgitation. In this case, various organic diseases gastrointestinal tract (GIT): peptic ulcer of the stomach and duodenum, gastroesophageal disease, cholecystitis, pancreatitis, malformations and other diseases.

A number of researchers classify Helicobacter-positive chronic gastritis and gastroduodenitis as non-ulcer dyspepsia. Our experience allows us to agree with other gastroenterologists who believe that chronic gastritis and gastroduodenitis are diseases with characteristic morphofunctional changes in the mucous membrane, and it is not legitimate to classify them as ND syndrome.

It is generally accepted that functional disorders not accompanied by rude morphological changes in organs and tissues. The need for highlighting functional disorders in a pediatric clinic is justified by the peculiarities critical periods growth and development of the child, the state of adaptation and regulatory systems. Any functional disorders are the initial manifestations chronic process, including in the digestive system.

The prevalence of dyspeptic disorders in adults and children is quite high - from 20 to 50%. However, it is difficult to establish exact figures in children without conducting clinical and epidemiological studies, since all gastroenterological diseases in children occur with symptoms of dyspepsia of varying severity. Functional disorders digestive tract manifest themselves with a wide range of symptoms and are detected in the majority of children referred for consultation to a gastroenterologist.

Classification

The clinical symptoms of ND are characterized by a wide polymorphism of symptoms. There are four forms of ND: ulcer-like, reflux-like, dyskinetic and nonspecific.

For ulcer-like form characterized by an “irritated” stomach, pain in the epigastric region before meals, sometimes at night, disappearing after eating and antacids. At reflux-like form patients are bothered by regurgitation, belching, heartburn, vomiting, and a feeling of “acid in the mouth.” For dyskinetic variant(“sluggish stomach”) typical sensations of heaviness, fullness after eating, nausea, rapid satiety, vomiting, flatulence, intolerance to fatty, dairy and other types of food. Nonspecific form ND is manifested by a combination of symptoms that are difficult to attribute to one or another form of dyspepsia.

Etiology and pathogenesis

The causes of ND can be emotional stress, mental trauma, rhythm and eating disorders, physical overload, early alcohol consumption, smoking, exposure to man-made pollution factors environment.

The decisive role in the development of ND is played by motility disorders of the upper gastrointestinal tract, which in children is manifested by incoordination of the gastroduodenal complex in the form of refluxes, insufficiency of the sphincter apparatus, various combinations of hypo- and hyperkinetic and tonic dyskinesias. This is to some extent due to the violation autonomic innervation and neurohumoral regulation. The intensity of ND symptoms in children is influenced by the level of acid formation. The significance of the degree of contamination of the mucous membrane with Helicobacter pylori (HP) in the occurrence of disturbances in the motor function of the stomach is considered controversial.

The prevalence of HP infection currently remains high; in developing countries, 80% of the population is infected by 10 years of age, which significantly increases the risk of developing certain gastrointestinal diseases. Wider detection and treatment of Helicobacter pylori infection may be considered appropriate, including in asymptomatic carriers. Primary infection with HP most often occurs at the age of 3-4 years. The detection rate of antibodies to HP is 44% in children and 88% in adults. In school-age children (7-18 years), HP infection occurs in manifest (63%) and latent (37%) forms; the frequency of latent forms increases with age. The nature of the complaints does not depend on the degree of HP infection.

In some children, ND is combined with irritable bowel syndrome, which is manifested by abdominal pain, alternating diarrhea and constipation, and a feeling incomplete emptying intestines, neurogenic bladder, vegetative-vascular dystonia.

Diagnosis

To confirm non-ulcer (functional) dyspepsia, organic gastrointestinal pathology should be excluded: gastric and duodenal ulcers, chronic gastritis and gastroduodenitis, reflux esophagitis, cholelithiasis, chronic pancreatitis, neoplasms, liver diseases and other diseases.

This requires a set of laboratory and instrumental studies, which is advisable to start with non-invasive methods. It should be emphasized that in the process of diagnosing ND, the most complete information can be obtained by studying the anamnesis and analyzing the clinical symptoms of the disease in combination with correct interpretation survey results.

The volume of research in the process of diagnosing “functional disorders” often exceeds the number of studies when making a topical diagnosis. This is due, first of all, to the doctor’s doubts about the examination results, which affects the relationship with the patients’ parents. At the same time, it is more important for the patient to get rid of unpleasant symptoms and do not subject yourself to tedious, invasive diagnostic procedures.

Diagnosis should be based on a detailed history of life and illness, clarification of hereditary factors, socio-economic and psychological nuances of the child’s life. Therefore, in our opinion, the complex of examinations must be reduced to a minimum: non-invasive research methods should be predominantly used in children, especially at the prehospital stage.

Non-invasive and minimally invasive methods:

Ultrasound examination of organs abdominal cavity with cholecystoscopy

Breath tests to detect HP

Coproscopy

Fecal occult blood test

General blood analysis

Determination of pancreatic enzyme activity in blood and urine

Biochemical tests to exclude syndromes of hepatic cell failure, cytolysis, cholestasis.

If symptoms of “anxiety” are detected, such as an increase in ESR, anemia, blood in the stool, fever, weight loss, etc., an in-depth study in a hospital is indicated.

Instrumental and laboratory methods(II order):

Endoscopic examination (esophagogastroduodenoscopy) with targeted biopsy of the mucosa

Intragastric pH-metry, 24-hour monitoring as indicated

X-ray examination

Serological test for the presence of antibodies to HP (if HP is not detected in the biopsy).

Treatment

Approaches to therapy are determined by the leading clinical manifestations and the form of ND. If there are good social and living conditions, sick children should be treated on an outpatient basis.

Important importance in the treatment program is given to the organization of the regime, normalization of the rhythm of sleep and wakefulness, principles rational nutrition in compliance with dietary recommendations, elimination stressful situations, streamlining physical activity.

An individual approach to a patient with functional dyspepsia is key point therapy. It is advisable to start it with psychotherapeutic correction, and in case of persistent chronic course it is necessary to involve specialists - a neuropsychiatrist, a psychotherapist. As our clinical experience shows, often even a change in the environment already has a beneficial effect on the course of the disease.

Taking into account modern ideas about the leading role of the motor-evacuation function of the stomach and duodenum in ND, most researchers consider the use of prokinetics to be the means of choice in the treatment of patients. This group includes the dopamine receptor blocker domperidone and the serotonin receptor activator cisapride. Currently, the use of the dopamine antagonist metoclopramide is limited due to severe side effects in the form of extrapyramidal reactions and prolactinemia. Unlike metoclopramide, domperidone and cisapride do not have these side effects.

Domperidone increases the tone of the lower esophageal sphincter, enhances peristalsis, accelerates gastric emptying, improves anthro-duodenal coordination; extrapyramidal symptoms occur very rarely when prescribed. Cisapride restores motor function of the upper gastrointestinal tract by activating serotonin receptors, releasing acetylcholine, with virtually no side effects. Another no less effective drug that normalizes the motor activity of the digestive tract is trimebutine, an antagonist of opiate receptors. Trimebutine does not change normal motor skills and is prescribed to children from the first year of life. Effective in the treatment of concomitant irritable bowel syndrome.

Prokinetics are well tolerated by patients and can be used both in hospital and clinic settings. Often these drugs are used as monotherapy, which significantly reduces the drug burden on a sick child.

For the ulcer-like variant of ND, antisecretory drugs are indicated - H2-histamine blockers (famotidine, ranitidine), proton pump inhibitors (omeprazole), when there is proven hyperacidity.

In case of a nonspecific variant of ND, symptomatic therapy is prescribed taking into account clinical manifestations, their frequency and intensity, and prokinetics according to indications. Insoluble antacids and cytoprotectors can be included in the complex of therapy.

In Helicobacter-positive patients with ND, it is recommended to carry out eradication therapy using bismuth-containing drugs in combination with metronidazole and an antibiotic (clarithromycin, amoxicillin, tetracycline) or furazolidone, since the lack of eradication in such children threatens the development of peptic ulcer disease.

In the presence of exocrine pancreatic insufficiency, the use of enzyme preparations(digestal, etc.).

Taking into account the tendency of ND to recur, the therapeutic program takes quite long time and is not limited to one course of drug therapy, its positive effect must be reinforced by rehabilitation measures: physiotherapy, complexes physical therapy, Spa treatment.

Thus, when diagnosing “non-ulcer dyspepsia syndrome,” the doctor must remember that this symptom complex may hide a certain nosological form that requires clarification and appropriate dynamic monitoring.

Literature:

1. Jones R., Lydeards S Prevalence of symptoms of dyspepsia in the community // R.M.J 1989; 298: 30-2.

2. Tatley N, Silverstein M, Agreus L et al. // Evaluation of dyspepsia. Gastroenterology, 1998; 114: 582-95.

3. Vantrappen G. Gastrointestinal motility.// World Gastroenterology.-April.1999; 11-4.

4. Mazurin A.V. Syndrome of “non-ulcer dyspepsia” // Russian Pediatric. zhur., 1998; 4: 48-53.

5. Chernova A. A. Differential diagnosis syndrome of non-ulcer dyspepsia in children./Author... Ph.D. diss. M., 1998; 23.

6. Lam S.K. The role of Helicobacter pylory in functional dyspepsia. - Ibid. 42-3.

7. Champion M.S., Mac.Cannel K.L. Thomson A.B. et al. A double-blind, randomized trial of cisapride in the treatment of non-ulcer dyspepsia. //Can. J. Gastroenterol. 1977; 11: 127-34.

8. Nandurkar S., Talley N.J. Xia H et al. Dyspepsia in the community is linked to smoking and aspirin use bat not to Helicobacter pylory infection. //Arch. Intern. Hed. - 1998; 158: 1427-33.

9. Sheptulin A.A. Modern principles of treatment of dyspeptic disorders // Practitioner. 1999; 16:8.

10. Malaty H., Paycov V., Bykova O. et al. Helicobacter pylori and socioeconomic factors in Russia. Helicobacter, 1996; 1 (2): 82-7.

11. Koch K.L. Motility disorders of the stomach. // Innovation towards better GJ care 1. Janssen -Cilag congress Abstracts.- Madrid., 1999; 20-1.

12. Diseases of the digestive system in children./ Ed. A.A. Baranova, E.V. Klimanskaya, G.V. Rimarchuk. -M., 1996; 310.

13. Richter J. Stress and psychological and environmental factors in dyspepsia. // Scand. J. Gastroenterol., 1991; 26:40-6.

14. Kasumyan S.A., Alibegov R.A. Functional and organic disorders of the patency of the duodenum. Smolensk 1997; 134.

15. Achem S.R., Robinson M.A. Prokinetic Approach to Treatment of Gastroesophageal Reflux Disease. //Dig. Dis. 1988; 16: 38-46.

16. Akimov A.A. Prevalence and clinical and endoscopic comparisons of Helicobacter pylori infection in school-age children. Author's abstract... Ph.D. diss. St. Petersburg. 1999; 21.

17. Vasiliev Yu.V. Coordinax in the treatment of gastroesophageal reflux disease.// Ros. zhur. gastroenterol., hepatol., coloproctol. 1998; VIII (3): 23-6.

Enzyme preparation -

Digestal (trade name)

(ICN Pharmaceuticals)

Omeprazole -

Gastrozol (trade name)

(ICN Pharmaceuticals)


Functional non-ulcer dyspepsia

Functional dyspepsia is a disease in which symptoms such as heaviness, bloating, and discomfort in the upper abdomen occur in the absence of obvious reasons for this.

Manifestations of functional dyspepsia are similar to those of other diseases of the gastrointestinal tract (for example, gastric ulcer). With functional dyspepsia, there is no damage to the digestive system.

The exact causes of the disease are unknown. Experts believe that psychosocial factors play a certain role in the development of inorganic dyspepsia. Patients are characterized by feelings of anxiety, restlessness,...

Diagnosis of non-ulcer dyspepsia consists of excluding disorders of the digestive organs (for example, gastric ulcer, duodenal ulcer).

Treatment is conservative. Drugs are used to eliminate the symptoms of functional dyspepsia. Important role correction of the diet plays a role.

Synonyms Russian

Functional dyspepsia, inorganic dyspepsia, irritable stomach.

English synonyms

Functional dyspepsia, nonulcer dyspepsia, nonulcer stomach pain.

Symptoms

The main manifestations of functional dyspepsia include:

  • burning and discomfort in the upper abdomen;
  • bloating;
  • early feeling of stomach fullness;
  • belching.

To be diagnosed with functional dyspepsia, these symptoms must be present for at least 12 weeks (not necessarily consecutive) in the past 12 months.

General information about the disease

Functional dyspepsia is a disease in which functional digestive disorders occur. At the same time, various organic pathologies are missing. The exact causes of this disorder have not been established. The disease occurs quite often. According to various authors, the prevalence of functional dyspepsia reaches 20%.

Researchers have identified several main factors contributing to functional dyspepsia.

  • Impaired motility of the stomach and duodenum. Motility is a wave-like contraction of the muscles of the digestive organs, which is necessary for the movement of food. To improve motility of the gastrointestinal tract, they are prescribed special drugs(prokinetics). Studies have shown that the symptoms of functional dyspepsia do not always disappear, even with a confirmed improvement in the motility of the stomach and duodenum.
  • The presence of the bacterium Helicobacter pylori. It survives in the acidic environment of the stomach and gradually causes the destruction of its mucous membrane. This can lead to the development of stomach and duodenal ulcers. Can be transmitted via shared utensils, kisses. Treatment is taking antibacterial drugs. Despite this, the role of this bacterium in the occurrence of functional dyspepsia is quite controversial. The decision on the need for eradication therapy (treatment aimed at destroying H. pylori) for non-ulcer dyspepsia is made by the attending physician.
  • Psychosocial factors. Functional dyspepsia occurs more often in people who are subject to frequent psycho-emotional stress. Nervous system controls the activity of the whole organism, so disturbances in its functioning can contribute to digestive disorders (functional dyspepsia,).
  • Eating disorders. Overeating or eating too quickly can also provoke dyspepsia. To make a diagnosis of “functional dyspepsia,” organic diseases of the stomach, which can lead to similar symptoms, are excluded. These include these and other diseases:
    • peptic ulcer of the stomach and duodenum;
    • gastroesophageal reflux – reflux of stomach contents into the esophagus; in the stomach the reaction is acidic, and in the esophagus it is alkaline, resulting in heartburn and other manifestations of the disease;
    • esophageal tumors;
    • diseases of other organs - patients with coronary heart disease in some cases complain of pain in the heart, which requires additional examination.

In most patients, the disease lasts a long time. Periods of exacerbation may alternate with improvement. For some people, symptoms of functional dyspepsia may go away on their own over time.

Who is at risk?

  • Smokers
  • People who use certain types of pain medications (eg, nonsteroidal anti-inflammatory drugs)
  • Persons exposed to frequent stressful situations

Diagnostics

Diagnosis is aimed at excluding various diseases of the digestive system that can cause similar symptoms. In the absence of organic causes (damage to any organs), a diagnosis of “functional dyspepsia” is made.

Patients who have symptoms such as difficulty swallowing, prolonged diarrhea, lack of appetite, weight loss, dark-colored stools, decreased stool levels, and those over 45 years of age, require esophagogastroduodenoscopy (examination using a flexible tube equipped with a camera and special tools).

Laboratory diagnostics is of great importance.

  • . Allows you to determine basic blood parameters: quantity, . A decrease in the level of red blood cells and hemoglobin can be observed (for example, due to bleeding from a stomach ulcer). An increase in leukocyte levels is observed when inflammatory processes in organism.
  • . It increases in various diseases (for example, inflammatory diseases). Allows you to assess the severity and dynamics of the disease.

Study of pancreatic and liver function:

Literature

Mark H. Birs, The Merk Manual, Litterra. 2011. Dyspepsia, p. 85.

Vasiliev Yu.V.

Dyspepsia (general information)

It is known that a significant proportion of people are more or less constantly bothered by pain in the epigastric region, heaviness, a feeling of pressure, fullness or rapid saturation that occurs in the epigastric region during or after eating, belching, nausea, vomiting, regurgitation, decreased or lack of appetite ( sometimes flatulence, pain in the lower abdomen, abnormal stool). Another thing is known - abdominal pain or dyspeptic disorders are possible in patients with both focal and diffuse lesions of the gastrointestinal tract. As observations show, it is possible various options combinations of these symptoms, their different duration, intensity and frequency of occurrence. This or that complex of these symptoms is often combined into a single term “dyspepsia”.

It is obvious that the presence in patients of various dyspeptic disorders, which can occur with various lesions of the gastrointestinal tract, is a stereotypical response of the body to all kinds of influences. Known and various classifications dyspepsia, but most often they distinguish organic and non-ulcer (functional) dyspepsia (NFD).

Among organic lesions In humans, in which dyspepsia may occur, most often benign ulcers and erosions of the stomach and duodenum of various origins, gastroesophageal reflux disease (GERD), Barrett's esophagus, malignant lesions of the esophagus, stomach, pancreas, liver, extra- and intrahepatic bile ducts, gallbladder, intestines, as well as pancreatitis, cholelithiasis and cholecystitis, ovarian cysts and others. The progression of some of these diseases (when stenosis occurs due to for various reasons) can lead to the cessation of the passage of the food “bolus”, i.e. to the appearance of obstruction. Deterioration of gastric emptying was also observed in patients with cascading stomach.

With NFD, patients often experience pain in the epigastric region, a feeling of early (premature) satiety, fullness and bloating of the stomach that occurs during or after eating, as well as nausea and vomiting. Unlike organic dyspepsia, NFD is characterized by the absence of any organic gastrointestinal lesions.

Most of the clinical symptoms noted with NFD are also possible with organic dyspepsia. However, the complex of these symptoms, their frequency, time of occurrence, intensity and duration, according to our observations, can also be different, and not all of these disorders are always present in a particular patient (often only 1-2 symptoms are noted).

Etiopathogenesis of dyspepsia

Repeated attempts have been made to identify the causes and mechanisms of occurrence of both NFD as a whole and its individual symptoms. However, to this day this issue is not completely clear. The “relationships” between many symptoms and functional impairment are not precisely known.

The occurrence of dyspeptic disorders is often associated with disturbances in the regime and rhythm of food intake, consumption of poor-quality products, drinking alcohol, food allergies, physical and mental disorders, abnormal acid secretion and other factors; a possible connection with smoking and the use of non-steroidal anti-inflammatory drugs is assumed, however, the age of patients and the presence of Helicobacter pylori (HP) are not considered factors in the occurrence of dyspepsia.

Considering possible reasons appearance of NFD, taking into account our own observations and literature data, the following should be noted. Some researchers believe that there is a consistent relationship between some symptoms of dyspepsia, in particular between the appearance of discomfort after eating and gastric atony. Indeed, many reports indicate an increase in the incidence of symptoms characteristic of NFD after patients ingest a particular food, but there are almost no reports indicating that the intake of any food leads to a decrease or disappearance of these symptoms. No clear parallels have been established between the consumption of foods that “irritate” the stomach and duodenum, the state of the acid-forming function of the stomach and dyspeptic symptoms in patients with chronic gastritis compared with gastritis in patients who do not have dyspeptic disorders.

Psycho-emotional disorders can also lead to the appearance (increase) of intensity and greater frequency of dyspeptic disorders in patients with chronic gastritis. Perhaps this is explained by a certain connection between changes in psycho-emotional status and the reaction of the secretory and motor apparatus of the stomach to stress.

Chronic gastritis (gastroduodenitis) is often discussed as one of the causes of dyspeptic disorders. However, NFD is also possible in the absence of morphological signs of gastritis, which is most often observed in children and adolescents. The majority of patients with chronic gastritis do not present any complaints at all; dyspeptic disorders in such patients are quite rare. And although a significant proportion of patients are diagnosed with chronic gastritis (according to our observations, in all adult patients admitted to hospitals for examination and treatment), in recent years studies are increasingly questioning or even rejecting any connection between the occurrence of certain symptoms and chronic gastritis (including Helicobacter gastritis).

No definite connection has been noticed between the severity of pathological diffuse changes in the gastric mucosa (with chronic gastritis) and the intensity of certain dyspeptic symptoms or a complex of these symptoms in patients with or without any complaints. Between clinical symptoms, considered characteristic of NFD, and the presence of HP contamination of the gastric mucosa there is no connection - there are no specific symptoms, characteristic of chronic gastritis with NFD.

Obviously, though main factor The pathogenesis of NFD in most patients is a violation of the motor function of the stomach and duodenum (weakening compared to the norm), which leads to slower gastric emptying. Dyspeptic disorders with NFD occur most often in those patients with chronic gastritis who have weakened gastric motility, leading to a slower evacuation of stomach contents into the duodenum. This helps explain the presence of “chronic” constant or recurrent pain in the epigastric region or some dyspeptic symptoms.

In some patients with chronic gastritis, the appearance of dyspeptic disorders is possible with normal gastric motility. In such cases, stretching of the stomach wall is associated with hypersensitivity mechanoreceptors located in the submucosal layer of the stomach, and (or) with a change in the tone of the proximal part of the stomach. Visceral hypersensitivity occurs due to pathological contraction of the stomach and disruption of the receptor perception of normal stimuli, including muscular peristaltic contractions of the stomach and distension by air and food. There is a consistent relationship between some of the symptoms of dyspepsia, in particular the onset of discomfort after eating and weakening of the stomach tone. Obviously, a combination of various factors with a slowdown in the motility of the stomach and duodenum is also possible.

A decrease in gastric tone is normally associated with the interaction of the “work” of such reflexes as relaxation (the flow of food through the esophagus into the stomach) and accommodation (stretching of the stomach). Gastric volume is largely dependent on muscle tone, which typically decreases when the stomach is distended by food. The rate of gastric emptying depends on the composition and consistency of food, its temperature, time of consumption, and for liquid food - and on its volume (as opposed to solid food). In addition, the rate of gastric emptying is also influenced by factors such as the state of the nervous and hormonal systems, and the use of certain medications (anticholinergics, analgesics, cardiac glycosides, etc.). In particular, it has been noted that eating fatty foods leads to a delay in gastric emptying, while eating liquid foods speeds it up. Weight gain is currently considered a risk factor for constipation.

There is a hypothesis that explains one of the symptoms of dyspepsia - the weakening of accommodation (adaptation) to cause rapid satiety after eating is associated with its reserve function. Analysis of such symptoms as pain in the epigastric region, “after-dinner fullness” of the stomach, rapid (premature) satiety, nausea, vomiting, regurgitation, burning in the epigastric region and flatulence, showed that weakening of accommodation is significantly associated with rapid satiety, but not with others the above dyspeptic symptoms.

Considering the role of disorders of gastric motor function in the pathogenesis of NFD in the appearance of some symptoms of the disease associated with this disorder and the treatment of patients, we considered it possible to reflect the role of prokinetics (domperidone and metoclopramide), which affect gastric motility and are most often used in the practice of treating patients . These drugs, along with increasing the amplitude of contractions of the esophagus, as well as increasing pressure in the region of the lower sphincter, improve the clearance of acid from the lower esophagus and reduce the volume of gastroesophageal reflux, accelerating gastric emptying by increasing the frequency and amplitude of contractions of the antrum of the stomach, reducing the time transit and in the duodenum by increasing the amplitude of its contractions. The acceleration of gastric emptying caused by prokinetics is associated not only with an increase in the frequency and amplitude of contractions of the antrum of the stomach, but also with the ability of these drugs to synchronize antral and duodenal contractions.

Currently, domperidone is one of the safest prokinetic drugs used in the practice of treating patients. The effectiveness of domperidone is determined by its pharmacological profile. Domperidone is an effective selective dopamine antagonist associated with butiprofen. The main effect of domperidone is the blockade of dopamine receptors that affect the motility of the upper gastrointestinal tract. By enhancing the peristalsis of the esophagus, increasing the tone of its lower sphincter and regulating the motor function of the stomach (including increasing the duration of contractions of its antrum), as well as enhancing the peristalsis of the duodenum, domperidone accelerates the emptying of the stomach from liquids, which is almost completely regulated by the fundus of the stomach; The antrum of the stomach is mainly associated with the processing of solid nutrients.

Domperidone counteracts the gastric relaxation caused by dopamine and the inhibition caused by secretin; increases the amplitude of contractions of the antrum of the stomach, causing relaxation of the pyloric sphincter. This drug improves antroduodenal coordination, which usually refers to the propagation of peristaltic waves from the antrum of the stomach through the pylorus (pylorus) to the duodenum.

A significant difference between domperidone and metoclopramide and some antipsychotic drugs is that domperidone “not without difficulty” penetrates the blood-brain barrier, which largely indicates its peripheral action. At the same time, domperidone does not counteract the effects of dopamine on gastric emptying and contractile function. Domperidone reduces the time required to mix food swallowed by the patient and prevents the delay in gastric emptying caused by dopamine.

It is interesting to note that in chronic gastritis, pancreatitis, duodenal ulcer in remission, domperidone at a dose of 30 mg taken per os enhances the elimination of liquid food in patients with delayed gastric emptying and, according to some observations, inhibits it in patients with accelerated emptying stomach. The use of domperidone in the treatment of patients is not associated with the risk of developing extrapyramidal adverse reactions.

Therapy of dyspeptic disorders

In order to increase the effectiveness of treatment of patients with NPD, various clinical options for NPD and drug treatment regimens for patients with NPD have been proposed. Unfortunately, it is most often impossible to accurately identify one or another NFD variant according to the proposed classifications. Only in a small number of cases, when patients with NFD have a large number of symptoms, can one or another variant of NFD be more or less reliably determined.

One of the attempts to treat patients with NFD, which, according to our observations, has justified itself: influence on the main symptoms of this disease, the pathogenesis of which is already more or less known. In principle, this approach to treating patients is essentially not new. It has long been noted that the so-called “symptomatic” treatment of patients, affecting one of the factors of the appearance (exacerbation) of a particular disease, is fully justified in many diseases. For example, therapy of gastroesophageal reflux disease (GERD) only with proton pump inhibitors (omeprazole, rabeprazole or esomeprazole), the main purpose of which is to eliminate pain and heartburn, allows one to obtain good or quite satisfactory results in the treatment of patients with GERD.

Recently, the importance of HP eradication in the treatment of Helicobacter gastritis with NFD has been increasingly questioned in order to eliminate clinical manifestations. Many clinicians “experience stress when it is necessary to present the results of HP eradication in patients with chronic Helicobacter gastritis with NFD.” It was not possible to identify any significant differences in the reduction in the frequency of dyspepsia symptoms, regardless of whether patients received anti-Helicobacter therapy or not. A year after treatment, symptoms of dyspepsia in patients with successful eradication of HP are observed more often than in patients who were not previously treated with anti-Helicobacter therapy.

As previous observations have shown, the elimination of the main symptoms of NFD leads (thanks to the ability of the human body to “self-heal”) to the disappearance of less pronounced symptoms, to which patients previously paid almost no attention (many of them did not even consider such symptoms to be a manifestation of any disease) .

The choice of treatment tactics largely depends on the disease, the presence or absence of complications, clinical manifestations of the disease, including the presence or absence of certain symptoms of dyspepsia. For organic dyspepsia, patients are advised drug treatment, the main goal of which is to improve the subjective and objective condition of patients. The leading direction of therapy is primarily the treatment of the underlying disease, including the elimination of pain and dyspeptic disorders. As symptomatic agents, in order to improve gastric motility and eliminate the symptoms of dyspepsia (in the absence of stenosis), it is advisable to prescribe prokinetics to patients. Even in cases where the patient is indicated for planned surgical treatment for any disease of the upper gastrointestinal tract, if the patient has symptoms of dyspepsia associated primarily with slowed motility (in the absence of stenosis), it is advisable in the preoperative period as one of Symptomatic agents can also be used with prokinetics, in particular domperidone.

The effectiveness of domperidone has been established in eliminating vomiting caused by cytotoxins in diseases (syndromes) such as gastroenteritis, gastritis and acetonemia, as well as vomiting that sometimes occurs in patients after eating. It should, however, be noted that domperidone in eliminating vomiting associated with food intake is effective in cases where the patient took domperidone immediately after the first vomiting.

One of the advantages of domperidone is the elimination of symptoms of dyspepsia caused by certain medications. In particular, its effectiveness in the treatment of Parkinson's disease (nausea and vomiting), which can occur when treating patients suffering from this disease with bromocriptine, is known. This allows you to increase necessary cases dosage of bromocriptine in the treatment of patients with Parkinson's disease. Domperidone also eliminates the so-called “gastrointestinal” symptoms associated with the drug levodopa, and can also be useful in improving lactation after childbirth.

When treating patients suffering from GERD, domperidone eliminates (reduces the intensity and frequency of heartburn and belching), reduces the need for the use of antacids and drugs that inhibit gastric acid formation, and also reduces the intensity and frequency of symptoms usually associated mainly with impaired motility.

Motilak

In recent years, interest has increased significantly various specialists, working in domestic healthcare, to those produced in Russia medications High Quality, one of which is Motilac (domperidone). This drug is an antagonist of peripheral and central dopamine receptors, increases the duration of peristaltic contractions of the antrum of the stomach and duodenum, accelerates emptying of the esophagus and stomach (in cases of weakened motility) and increases the tone of the lower esophageal sphincter. Motilak stimulates peristalsis of the esophagus, stomach and duodenum in the distal direction and at the same time relaxes the muscles of the outlet of the stomach, which facilitates its emptying. The drug also reduces antiperistalsis, which allows stomach contents to enter the esophagus, which is one of the causes of heartburn.

After oral administration, Motilac is well absorbed from the gastrointestinal tract (meal intake and a decrease in the acidity of gastric juice slow down and reduce its absorption). The maximum concentration in the blood is reached after 1 hour. Plasma protein binding is 91-93%. The drug undergoes intensive metabolism in the intestinal wall and liver (by hydroxylation and N-dealkylation). The half-life is 7-9 hours. It is excreted by the intestines (66%) and kidneys (10%), including unchanged - 10% and 1%, respectively. Penetrates poorly through the blood-brain barrier.

Motilak can be used as a rational, safe and effective therapy for functional non-ulcer dyspepsia or as an addition to antacid or anticholinergic drugs, as well as weak tranquilizers used in the treatment of patients who have symptoms of dyspepsia (in the absence of stenosis).

The usual therapeutic dosage of Motilac for adults is 10 mg 3 times a day 15-30 minutes before meals, if necessary, 4 times a day - 10 mg at night; for children - with a body weight of 20-30 kg - 5 mg 2 times a day, over 30 kg - 10 mg 2 times a day. At renal failure the frequency of use of the drug should be reduced.

Literature
1. Loginov A.S., Vasiliev Yu.V. Non-ulcer dyspepsia. // Russian. gastroenter. magazine.-1999.- No. 4.- P.56-64.
2. Vasiliev Yu.V., Yashina N.V., Ivanova N.G. Dyspepsia syndrome (diagnosis, treatment).// Current issues of clinical medicine. M., 2001 - pp. 77-82.
3. Brogden R.N., Carmine A.A., Heel R.C. et al. Domperidone. A Review of its Pharmacological Activity, Pharmacokinetics and Therapeutic Efficacy in the Symptomatic Treatment of Chronic Dyspepsia and as an Antiemetic. // Drugs. - 1982. - Vol. 24. - P.360-400.
4. O’Morain C., Gilvarry J. Eradication of Helicobacter pylori in patients with non-ulcer dyspepsia. // Scand. J. Gastroenterol.-1993.-Vol. 28.(Suppl.196).-P.30-33.
5. Tack J. et al (Quoted by Vantrappen G., 1999).
6. Talley N.J. A critique of therapeutic trials in Helicobacter pylori-positive functional dyspepsia.// Gastroenterology.-1994.-Vol.106.-P.1174-1183.
7. Vantrappen G. Gastrointestinal Motility.// World Gastroenterology.-April 1999. - P.11-14.
8. Jian R., Ducrot F., Ruskone A. et al. Symptomatic, radionuclide and therapeutic assessment of chronic idiopathic dyspepsia: A double blind placebo-controlled evaluation of cisapride.// Dig. Dis. Sci.- 1989.- Vol.14.-P.657-664.