Gastroesophageal reflux (K21), Gastroesophageal reflux without esophagitis (K21.9), Gastroesophageal reflux with esophagitis (K21.0)

Gastroenterology

general information

Short description

Purpose of publication
To acquaint practitioners with the latest data on methods of adequate diagnosis, treatment tactics and features of rational pharmacotherapy of gastroesophageal reflux disease (GERD), based on the principles of evidence-based medicine.

Key points
In terms of prevalence, GERD ranks first among gastroenterological diseases. The leading symptom of GERD - heartburn - is detected in 20-40% of the population of developed countries. In Russia, the prevalence of GERD is 18-46%. Diagnosis of GERD in the early stages is based on primary referral and analysis of the clinical picture of the disease. Esophagogastroduodenoscopy (EGDS) makes it possible to determine the presence of reflux esophagitis, assess its severity, and identify cylindrocellular metaplasia of the esophageal epithelium. In case of a refractory course of the disease (lack of convincing clinical and endoscopic remission within 4-8 weeks of therapy with a proton pump inhibitor - PPI - in a standard dose), as well as the presence of complications of the disease (strictures, Barrett's esophagus), it is necessary to conduct an examination in a specialized hospital or gastroenterological clinics, including in the outpatient departments of these institutions. If necessary, patients should undergo endoscopy with a biopsy of the esophageal wall and histological examination of biopsy specimens to exclude Barrett's esophagus, adenocarcinoma, and eosinophilic esophagitis; intraesophageal daily pH-metry or pH-impedancemetry; high resolution esophageal manometry; x-ray examination of the esophagus and stomach.

Treatment of patients with GERD should be individualized according to the clinical manifestations of the disease and the severity of symptoms. The goal of treatment is to eliminate symptoms, in case of erosive esophagitis - healing of erosions and prevention of complications, in case of Barrett's esophagus - prevention of progression and development of esophageal dysplasia and adenocarcinoma.

To date, PPIs are considered the most effective and safe drugs for the treatment of GERD. PPIs are used for long-term basic (at least 4-8 weeks) and maintenance (6-12 months) therapy. A pathogenetically substantiated therapeutic method for reducing the "acid pocket" and neutralizing acid in the area of ​​the esophageal-gastric junction in patients with GERD is the intake of alginates, which form a mechanical barrier-raft that prevents the contents of the stomach from being thrown into the esophagus. Antacids are used both as a monotherapy for rare heartburn that is not accompanied by the development of esophagitis, and in complex therapy regimens for GERD to quickly eliminate symptoms. Adsorbents are used both as monotherapy for non-erosive reflux disease and as part of complex therapy for GERD, especially for mixed (acid + bile) reflux. Prokinetic preparations contribute to the restoration of the normal physiological state of the esophagus by acting on the pathogenetic mechanisms of GERD, reducing the number of transient relaxations of the lower esophageal sphincter and improving esophageal clearance by stimulating the motor function of the underlying parts of the digestive tract. Prokinetics can be used as part of the complex therapy of GERD together with PPIs.

Antireflux surgical treatment is indicated for complicated course of the disease (repeated bleeding, peptic strictures of the esophagus, development of Barrett's esophagus with high-grade epithelial dysplasia, often occurring aspiration pneumonia). Surgical treatment of GERD is more effective in patients with its typical manifestations and in the case of the effectiveness of PPI treatment.

Conclusion
The implementation of clinical recommendations can help improve the quality of medical care for patients with GERD and prevent complications, in particular, while observing the necessary terms of treatment, conducting active outpatient monitoring of the relevant groups of patients.

Keywords Key words: gastroesophageal reflux disease, gastroesophageal reflux, reflux esophagitis, non-erosive reflux disease, acid pocket, proton pump inhibitor, alginate, angtacid, prokinetic drug.

Introduction

Over the past 3 years since the release of clinical guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD), new data have been obtained on effective methods for diagnosing and treating patients with this disease, which made it necessary to publish this edition of the recommendations.

The problem of GERD is still very relevant. In terms of prevalence, GERD ranks first among gastroenterological diseases. Heartburn - the leading symptom of GERD - is observed in 20-40% of the population of developed countries. In Russia, the prevalence of GERD is 18-46% [Ivashkin V.T., Maev I.V., Trukhmanov A.S., 2011]. The relevance of GERD is also due to the fact that it leads to a significant decrease in the quality of life of the patient, especially with nocturnal symptoms, the appearance of extraesophageal symptoms (chest pain, persistent cough) and the risk of complications such as bleeding from ulcers and erosions, the development of peptic strictures and, that causes the greatest suspicion, adenocarcinoma of the esophagus (AKA) against the background of Barrett's esophagus. Certain difficulties arise in the treatment of patients with GERD. If the healing time of duodenal ulcers (duodenal ulcers) averages 3-4 weeks, gastric ulcers - 4-6 weeks, then the duration of healing of esophageal erosions in many patients can reach 8-12 weeks. At the same time, some patients show refractoriness to antisecretory drugs and low adherence to treatment. After discontinuation of medication, a relapse of the disease quickly occurs, which is the main risk factor for the development of Barrett's esophagus, a precancerous pathology of the esophagus.

Target of these recommendations is a presentation of the latest reliable data on the methods of adequate diagnosis, treatment tactics and features of rational pharmacotherapy for GERD based on the principles of evidence-based medicine.

Definition

GERD- a chronic relapsing disease caused by a violation of the motor-evacuation function of the organs of the gastroesophageal zone and characterized by regularly repeated reflux of the contents of the stomach and sometimes duodenum into the esophagus, which leads to the appearance of clinical symptoms that worsen the quality of life of patients, damage to the mucous membrane (SO) of the distal esophagus with the development in it of dystrophic changes in non-keratinized stratified squamous epithelium, catarrhal or erosive-ulcerative esophagitis (reflux esophagitis), and in some patients - cylindric metaplasia.

non-erosive reflux disease(NERD) and erosive esophagitis should be considered as two forms of GERD. NERD is a subcategory of GERD characterized by the presence of reflux-induced and quality-of-life debilitating symptoms without erosions of the esophageal mucosa seen on routine endoscopy, in the absence of current antisecretory therapy. Testing with proton pump inhibitors (PPIs), detection of pathological reflux by pH-metry, or specific endoscopic signs of esophagitis during studies using high-tech methods (high-resolution magnification, narrow-spectrum endoscopy) can confirm the diagnosis of NERD.

NERD should be differentiated from functional heartburn, in which there is no pathological gastroesophageal reflux. In patients with functional heartburn, constituting a small heterogeneous group, the mechanisms of development of symptoms are different. Drug tests using antisecretory drugs cannot be considered specific, but their negative result demonstrates a high probability of the absence of GERD.
Barrett's esophagus is the replacement of squamous epithelium with glandular metaplastic columnar epithelium in the mucosa of the distal esophagus, detected during endoscopic examination and confirmed by the presence of intestinal metaplasia in the histological examination of the biopsy, in some cases increasing the risk of developing AKP.

ICD‑10 coding

K21 Gastroesophageal reflux

K21.0 Gastroesophageal reflux with esophagitis (reflux esophagitis)

K21.9 Gastroesophageal reflux without esophagitis

K22.1 Ulcer of esophagus

Etiology and pathogenesis

The main factors of pathogenesis

GERD is an acid-dependent disease in which gastric hydrochloric acid is the main damaging factor in the development of clinical symptoms and morphological manifestations of GERD. Pathological reflux in this case occurs due to insufficiency of the lower esophageal sphincter (LES), i.e. GERD is a disease with an initial violation of the motor function of the upper gastrointestinal tract.

A key factor in the pathogenesis of GERD is a pathologically high frequency and / or duration of episodes of reflux of stomach contents into the esophagus. The integrity of the esophageal mucosa is determined by the balance between the factors of aggression and the ability of the mucosa to resist the damaging effect of the stomach contents thrown during gastroesophageal reflux (GER). Disruption of this balance in a large proportion of patients is accompanied by a significant slowdown in the recovery of pH in the distal esophagus after each episode of reflux. The clearance of the esophagus is impaired due to the influence of several factors: weakening of the peristalsis of the thoracic esophagus, decreased secretion of saliva and mucin.

The first barrier that gives a cytoprotective effect is the mucus layer covering the epithelium of the esophagus and containing mucin. The mucous layer is one of the key components of the chemical clearance of the esophagus and the restoration of pH in it to normal levels, the violation of which contributes to the deterioration of the purification of the esophagus from the acidic, slightly acidic or slightly alkaline contents of the stomach that have entered it. The secretion of mucins in the mucus in GERD decreases depending on the severity of esophagitis, which is an additional factor predisposing to the development of erosive esophagitis in the context of ongoing GER, therefore, an additional increase in the protective properties of the mucosal barrier along with acid suppression is an important component of the treatment of GERD. .

With a significant increase in the secretion of hydrochloric acid in the stomach, the risk of GERD increases significantly.

In the vast majority of patients with GERD, reflux episodes occur mainly during transient relaxation of the lower esophageal sphincter (PRNSP), when the antireflux barrier between the stomach and esophagus usually disappears for 10-15 seconds, regardless of the act of swallowing. PRNPS, the principal mechanism of reflux, in patients with GERD is carried out through the same pathways from the dorsal vagus nucleus (nucleus dorsalis and nucleus ambiguus) that mediate esophageal motility and PRNPS in a healthy person. Mechanoreceptors located in the upper part of the stomach respond to an increase in pressure inside the organ and send signals to the hindbrain along the afferent fibers of the vagus nerve. In the centers of the hindbrain that receive these signals, motor programs of the PRNPS are formed, reaching the NPS along descending pathways. Efferent pathways are carried through the vagus nerve, where nitric oxide is a postganglionic neurotransmitter. The contraction of the crura of the diaphragm is controlled by the respiratory center located in the brainstem and the nucleus of the phrenic nerve. With an increase in intra-abdominal pressure, if it coincides with PRNPS, the likelihood of acid reflux increases significantly.

At present, in understanding the mechanism of GER, one should be guided by the paradigm of the mutual influence of PRNPS and the consequences of destructuring the zone of the esophageal-gastric junction. The weakness of the crura of the diaphragm leads either to a delay in the onset of action, or to a significant degradation of the actual compression effect of the diaphragm contraction on the LES. Hiatus hernia (HH), depending on its size and structure, has a mechanical effect on the LES: worsens the antireflux function during PRNPS and/or reduces the actual tonic component of the sphincter. The most important consequence of destructurization of the gastroesophageal junction is the reflux of relatively large volumes of gastric fluid into the esophagus during PRNPS.

In a significant number of patients, episodes of GER develop with normal LES pressure. The mechanism of GER is associated with a high pressure gradient between the stomach and esophagus, due to various reasons: in some patients - a violation of the evacuation of the contents of the stomach, in the other - high intra-abdominal pressure. In these cases, GER develops due to the inability of the obturator mechanisms to counteract the high pressure gradient between the stomach and esophagus.

In addition, after a meal, an acid layer (average pH 1.6) forms on the surface of the stomach contents in the esophageal-gastric junction, called the "acid pocket", which is formed both in healthy people and in patients with GERD. This is an area in the stomach cavity and/or the gastroesophageal junction that forms after a meal and is characterized by relatively high acidity and is a reservoir of acidic contents thrown into the esophagus during GER.

The risk of developing acidic GER is determined by the position of the "acid pocket" relative to the diaphragm. Moving it above the level of the diaphragm leads to the development of pathological acid refluxes not only in the postprandial period. This suggests that the "acid pocket" may be a promising target for the treatment of GERD, especially if postprandial heartburn needs to be reduced. (UDD 1, UR A).

Thus, from a pathophysiological point of view, GERD is an acid-dependent disease that develops against the background of a primary violation of the motor function of the upper digestive tract. In the pathogenesis of NERD, the features of the esophageal mucosa play a special role.

Epidemiology

The prevalence of GERD among the adult population is up to 40%. The results of extensive epidemiological studies indicate that 40% of people constantly (with varying frequency) experience heartburn, which is the main symptom of GERD. In Russia, the prevalence of GERD among the adult population is 18-46%, and esophagitis is found in 45-80% of patients with GERD. In the general population of the population, the prevalence of esophagitis is estimated at 5-6%, while 65-90% of patients have mild and moderate esophagitis, and 10-35% have severe esophagitis. The incidence of severe esophagitis in the general population is 5 cases per 100,000 population per year. The prevalence of Barrett's esophagus among patients with esophagitis approaches 8%, ranging from 5 to 30%.

In recent decades, there has been an increase in the incidence of AKP, which develops against the background of the progression of dysplastic changes in the intestinal-type metaplastic epithelium of the mucosa of the distal esophagus. AKP and high-grade dysplasia develop annually in 0.4-0.6% of patients with Barrett's esophagus with intestinal metaplasia. AKP is formed annually in 0.5% of patients with a low degree of epithelial dysplasia, in 6% with a high degree, and in less than 0.1% in the absence of dysplasia.

Clinical picture

Symptoms, course

Clinical picture

Esophageal manifestations

The most widely used in the world is the Montreal classification of clinical manifestations of GERD, in which they are divided into two large groups: esophageal and extraesophageal. Esophageal manifestations include such clinical syndromes as a typical symptom complex of reflux and non-cardiac chest pain, as well as syndromes in which, in addition to patient complaints, there are endoscopic signs of the disease (esophagitis, Barrett's esophagus, strictures, etc.).

A typical reflux symptom complex includes heartburn, belching, regurgitation, odynophagia, which are painful for patients, significantly impair their quality of life, and have a negative impact on performance. The quality of life of patients with GERD, in whom its clinical symptoms occur at night, is especially significantly reduced.

Heartburn, the most characteristic symptom observed in 83% of patients, occurs due to prolonged contact of the contents of the stomach with CO2. This symptom is characterized by an increase in its severity with errors in diet, alcohol and carbonated drinks, physical exertion, bending over and in a horizontal position.

Belching, one of the leading symptoms of GERD, occurs in 52% of patients with GERD. As a rule, it intensifies after eating and drinking carbonated drinks. The regurgitation observed in some patients with GERD is aggravated by physical exertion and posture that promotes regurgitation.

Dysphagia and odynophagia are observed in 19% of patients with GERD. Their occurrence is based on hypermotor dyskinesia of the esophagus, and erosive and ulcerative lesions of the CO can also be the cause of odynophagia. The appearance of more persistent dysphagia and a simultaneous decrease in the severity of heartburn may indicate the formation of esophageal stenosis, both benign and malignant.

Non-cardiac pain in the chest and along the esophagus can give the impression of coronary pain - the so-called symptom of "non-cardiac chest pain". These pains are stopped by nitrates, but unlike angina pectoris, they are not associated with physical activity. They arise as a result of hypermotor dyskinesia of the esophagus (secondary esophagospasm), which may be caused by a defect in the inhibitory transmitter system, nitric oxide. The starting point for the occurrence of esophagospasm and, accordingly, pain is pathological gastroesophageal reflux.

Extraesophageal manifestations

Extraesophageal manifestations of GERD include bronchopulmonary, otorhinolaryngological and dental syndromes.

A variety of symptoms and syndromes are divided into two groups: those whose association with GERD is based on fairly convincing clinical evidence (chronic cough associated with reflux, chronic laryngitis, bronchial asthma and tooth enamel erosion), and those whose association with GERD is only suspected ( pharyngitis, sinusitis, pulmonary fibrosis, otitis media).

Numerous studies have shown an increased risk of developing bronchial asthma, as well as an increase in the severity of its course in patients with GERD. In 30-90% of patients with bronchial asthma, GER occurs, causing a predisposition to its more severe course. The causes of bronchial obstruction in GERD are the vago-vagal reflex and microaspiration. In such cases, the inclusion of PPI in the complex therapy increases the effectiveness of the treatment of bronchial asthma.

Sore throat, hoarseness or even loss of voice, dry cough may be due to the reflux of stomach contents into the larynx (otolaryngological syndrome). This possibility should be considered if the patient has heartburn. In the absence of heartburn, the only method to verify the association of such symptoms with GER is 24-hour intraesophageal pH-metry/pH-impedancemetry (see below), which can establish a correlation between the onset of a symptom and episodes of reflux (symptom index > 50 %).

Dental syndrome is manifested by damage to the teeth due to damage to the tooth enamel by the aggressive contents of the stomach. In patients with GERD, the development of caries and the formation of dental erosions are possible. In rare cases, aphthous stomatitis develops.

Inflammatory changes in the mucous membrane of the esophagus (complications of GERD)

Reflux esophagitis detected by endoscopic examination includes simple (catarrhal) esophagitis, erosions and ulcers of the esophagus. The severity of erosive esophagitis can be different - from stage A to stage D according to the Los Angeles classification and from the 1st to the 3rd stage according to the Savary-Miller classification - depending on the area of ​​​​the lesion, while to the 4th stages according to the Savary-Miller classification include complications of GERD: strictures of the esophagus, ulcers (bleeding from ulcers), Barrett's esophagus.

To eliminate the stricture in the future, expensive surgical and endoscopic (often repeated) procedures (bougienage, surgery, etc.) are required. Each such case should be considered as a consequence of inadequate conservative therapy, which justifies the need for its improvement to prevent the development of strictures. Bleeding caused by erosive and ulcerative lesions of the esophagus can be observed both in the presence of varicose veins of the esophagus, and in their absence.

The most severe complication of GERD, Barrett's esophagus, is the development of a cylindrical (intestinal) metaplastic epithelium in the mucosa of the esophagus, which subsequently increases the risk of developing AKP. Exposure to hydrochloric and bile acids in the esophagus, on the one hand, increases the activity of protein kinases that initiate the mitogenic activity of cells and, accordingly, their proliferation, on the other hand, apoptosis in the affected areas of the esophagus is inhibited.

Approximately 95% of cases of AKP are diagnosed in patients with Barrett's esophagus, so the main role in the prevention and early diagnosis of esophageal cancer is played by the diagnosis and effective treatment of Barrett's esophagus. After the use of PPIs in patients with Barrett's esophagus, there is a decrease in the level of proliferation markers, which is absent in those patients who have persistent pathological acid reflux (pH<4,0). Длительное применение ИПП может привести к частичной регрессии цилиндрической метаплазии на ограниченном участке.

Among the risk factors for the development of complications of GERD, the most important are the frequency of occurrence and duration of symptoms, in particular heartburn, the severity of erosive esophagitis, the frequency of its relapses, obesity, the presence of hiatal hernia and nocturnal reflux.

Rapidly progressive dysphagia and weight loss may indicate the development of AKP, but these symptoms occur only in the later stages of the disease, so the clinical diagnosis of esophageal cancer is usually delayed. As a result, prevention and early diagnosis of esophageal cancer require timely detection and adequate treatment of Barrett's esophagus.

Diagnostics

STAGE DIAGNOSIS

OUTPATIENT STAGE

Diagnosis of GERD in the early stages is based on primary referral and analysis of the clinical picture of the disease. If necessary, additional studies are carried out.

Endoscopy

In patients complaining of heartburn, endoscopic examination may show signs of reflux esophagitis of varying severity. These include hyperemia and friability of the mucosa of the esophagus (catarrhal esophagitis), erosions and ulcers (erosive esophagitis of varying severity - from 1st / A to 4th / D stage - depending on the area of ​​​​the lesion), the presence of exudate, fibrin or signs of bleeding.

Many classifications have been proposed to assess changes in esophageal mucosal fluid in reflux esophagitis, but the most widely used are the classification created by M. Savary and G. Miller (1978), and the classification developed by the International Working Group of Experts, which was first proposed at the World Congress on Gastroenterology in Los Angeles in 1994.

According to the Savary-Miller classification, 4 stages of reflux esophagitis are distinguished:

Stage 1 - diffuse or focal hyperemia of the mucosa of the distal esophagus, separate non-confluent erosions with a yellowish base and red edges, linear aphthous erosions extending upward from the cardia or the esophageal opening of the diaphragm;

2nd stage - erosions merge, but do not capture the entire surface of the CO;

3rd stage - inflammatory and erosive changes merge and capture the entire circumference of the esophagus;

Stage 4 - similar to the previous stage, but there are complications: narrowing of the lumen of the esophagus, as a result of which it is difficult or impossible to pass the endoscope to the underlying sections, ulcers, Barrett's esophagus.

The Los Angeles classification provides for a four-degree gradation of reflux esophagitis, it is also based on the prevalence of the process, but the complications of GERD (strictures, ulcers, Barrett's esophagus), which can occur at any stage, are considered separately:

stage A - one (or more) area of ​​damaged CO, up to 5 mm in size, which does not capture CO between the folds (located at the top of the fold);

stage B - one (or more) area of ​​damaged CO larger than 5 mm, which does not capture CO between the folds (located at the top of the fold);

stage C - one (or more) area of ​​damaged SO that extends to SO between two (or more) folds, but captures less than 75% of the circumference of the esophagus;

stage D - one (or more) areas of damaged SO, which captures more than 75% of the circumference of the esophagus.

In addition, there may be prolapse of the gastric mucosa into the esophagus, especially with vomiting, a true shortening of the esophagus with the location of the esophageal-gastric junction significantly higher than the diaphragm, reflux of the contents of the stomach or duodenum into the esophagus. The closing function of the cardia during esophagoscopy is difficult to assess, since the cardia can be reflexively opened in response to the introduction of an endoscope and air insufflation.

STATIONARY STAGE

In case of a refractory course of the disease (lack of convincing signs of clinical and endoscopic remission within 4-8 weeks of PPI therapy at a standard dose), as well as in the presence of complications of the disease (strictures, Barrett's esophagus), it is necessary to conduct an examination in a specialized hospital or gastroenterological clinic, in including in the outpatient departments of these institutions. If necessary, patients should be carried out:

Esophagogastroduodenoscopy (EGD) with biopsy of the esophagus and histological examination of biopsy specimens to exclude Barrett's esophagus and AKP, as well as eosinophilic esophagitis;

Intraesophageal daily pH-metry or pH-impedancemetry;

High resolution esophageal manometry;

X-ray examination of the esophagus and stomach;

Comprehensive ultrasound examination (ultrasound) of internal organs;

Registration of an electrocardiogram and other special studies (see below).

Before performing probe studies (EGDS, pH-metry), it is necessary to examine the blood for hepatitis, HIV infection, syphilis. According to the indications (differential diagnosis of extraesophageal manifestations of GERD), consultations of specialists should be held: otorhinolaryngologist, pulmonologist, cardiologist.

Histological examination

Histological examination of biopsy specimens of the esophageal mucosa is carried out to exclude Barrett's esophagus, AKP, eosinophilic esophagitis, while revealing dystrophic, necrotic, acute and chronic inflammatory changes expressed to varying degrees. With simple (catarrhal) esophagitis, the layer of non-keratinized stratified epithelium may have a normal thickness. More often, its atrophy is detected, but occasionally areas of hyperplasia are also found, in particular, the basal layer, which occupies up to 10-15% of the thickness of the epithelial layer. Intercellular edema, dystrophy, and foci of necrosis of epitheliocytes (keratinocytes), expressed to varying degrees, are characteristic, especially in the surface layers. The basement membrane of the epithelium in most cases is not changed, but in some patients it can be thickened and sclerosed. As a result of necrosis of various areas of the stratified squamous epithelium, erosions (erosive esophagitis) are formed, and with deeper lesions, up to the muscular membrane and even deeper, ulcers (ulcerative esophagitis).

Along with dystrophic-necrotic changes in the epithelium, microcirculation disturbances with vascular hyperemia are noted in the mucosa. An increase in the number and change in the length of vascular-stromal papillae are characteristic. In the thickness of the epithelium and the subepithelial layer, focal (usually perivascular) and in some places diffuse lymphoplasmic cell infiltrates with an admixture of neutrophilic leukocytes and single eosinophils are detected. The appearance of intraepithelial neutrophilic leukocytes and their accumulation in the inflammatory infiltrate in the vascular stromal papillae, in the lamina propria, indicate an exacerbation and progression of the inflammatory process.

A significant increase in the number of eosinophilic leukocytes, and even more so the presence of intraepithelial eosinophilic cell microabscesses in combination with subepithelial sclerosis of the lamina propria, serve as criteria for the diagnosis of eosinophilic esophagitis. The smooth muscle cells of the lamina propria show signs of severe dystrophy or atrophy, and in rare cases, a state of coagulative necrosis.

Inflammatory, necrotic, or hyperplastic changes may also extend to the esophageal glands. In a small number of patients, signs of active current inflammation are not found on histological examination. At the same time, in the mucosa of the esophagus, there is an overgrowth of loose, and in some places dense fibrous connective tissue (sclerosis), as in the bottom of persistent erosions and ulcers.

Histological examination may reveal metaplasia of the stratified squamous non-keratinizing epithelium of the esophagus, which leads to the appearance in its place of a cylindrical (glandular) epithelium with glands of the cardiac or fundal (gastric) type. Cardiac type CO usually has a villous surface, often characterized by small pits without well-formed glands (foveolar type), although the latter may be fully formed (glandular type), but always represented only by mucous cells, do not contain parietal, chief or goblet cells. SO of the fundic (gastric) type is distinguished by the presence of acid-producing parietal and chief cells in the glands, and typical ridges covered with integumentary pit epithelium are sometimes formed from the integumentary epithelium. At the same time, the glands are often few in number, "compressed" by growths of connective tissue and diffuse lymphoplasmic cell infiltrate with an admixture of neutrophilic leukocytes.

In case of metaplasia of the esophageal mucosa of the cardiac, cardiac acid-producing or fundic type, the risk of developing AKP does not increase. However, if metaplasia leads to the appearance of the so-called specialized epithelium, as in a number of sources the glandular epithelium of the intestinal type is called, the risk of malignancy increases. The specialized epithelium is an intestinal metaplasia of the glandular epithelium, and the main criterion for its

histological diagnosis - the appearance of goblet cells (at least one such cell within the biopsy, since the changes are mosaic in nature).

The morphological substrate of NERD can be considered the expansion (edema) of intercellular spaces, especially in the basal layer of the epithelium, and degenerative changes in keratinocytes.

High resolution manometry

The study of the motor function of the esophagus is carried out using high-resolution manometry. With GERD, it is used to detect a decrease in LES pressure, the presence of HH, an increase in the number of PRNPS, quantitative indicators of the total peristaltic activity of the organ wall, esophagospasm, atypical cases of achalasia of the cardia, and diagnose syndromes of rumination and supragastric eructation. The study allows you to verify the position of the LES for pH-metry. It is a necessary attribute of the examination of the patient, which is carried out to resolve the issue of surgical treatment of GERD. When analyzing high-resolution manometry results, the Chicago Classification of Esophageal Motility Disorders (ELD 1, LEL A) should be used.

pH meter

The main method for diagnosing GER is pH-metry. The study can be carried out both on an outpatient basis and in stationary conditions. When diagnosing GER, the results of pH-metry are evaluated by the total time during which the pH is maintained.<4,0, общему количеству рефлюксов за сутки, количеству рефлюксов продолжительностью более 5 мин, наибольшей длительности рефлюкса.

The main indications for carrying out pH-metry:

Characteristic manifestations of GERD in the absence of endoscopic changes in the esophagus;

Extraesophageal manifestations of GERD: chest pain not associated with diseases of the cardiovascular system;

Planned surgical treatment of GERD and monitoring the effectiveness of treatment with persistent symptoms of the disease;

Selection of drugs and monitoring the effectiveness of ongoing conservative treatment.

Daily pH-metry has a very high sensitivity (88-95%) in the diagnosis of GERD and, in addition, helps in the individual selection of drugs (ELL 1, LL A).

pH impedancemetry

Esophageal impedancemetry is a method of recording liquid and gas refluxes, based on measuring the resistance (impedance) that the contents of the stomach provide to the electric current, entering the lumen of the esophagus. This is a technique for diagnosing refractory GERD, which allows you to determine episodes of reflux into the esophagus, regardless of the pH value of the refluxate, as well as the physical state (gas, liquid) and clearance of the bolus that entered the esophagus during

reflux.

The main indications for pH-impedancemetry:

Atypical forms and extraesophageal manifestations of GERD: chronic cough, bronchial asthma, chronic pharyngitis, severe belching;

Evaluation of the effectiveness of antisecretory therapy for GERD without discontinuation of the drug in the presence of persistent symptoms of the disease;

Evaluation of the effectiveness of surgical treatment of GERD (LEV 1, LE A).

X-ray examination

X-ray examination of the esophagus is not used to diagnose GERD, but it can detect HH, diffuse esophagospasm, esophageal strictures and suspect a short esophagus in those patients who are planned for surgical treatment.

Other diagnostic methods

In highly specialized institutions, in the diagnosis of GERD, methods such as measuring the impedance of the esophageal CO2, determining the content of pepsin in saliva, and impedance planimetry can be used.

The introduction of high resolution endoscopy, NBI endoscopy, ZOOM endoscopy (magnifying endoscopy) helps to detect metaplastic changes in the esophageal epithelium and perform targeted biopsy in order to obtain material for histological examination.

Endoscopic ultrasound of the esophagus is the main method for detecting endophytically growing tumors.

Treatment

Conservative treatment

Treatment of patients with GERD should be individualized and oriented in accordance with the clinical manifestations of the disease and their severity. The goal of treatment is to eliminate symptoms, and in case of erosive esophagitis, to heal erosions and prevent complications. In patients with Barrett's esophagus, the goal is to prevent the progression and development of dysplasia and AKP.

Treatment should be aimed at reducing the severity of reflux, reducing the aggressive properties of the refluxate, improving esophageal clearance and protecting the esophageal mucosa. Currently, the main principles of GERD treatment are the appointment of PPIs and long-term basic (at least 4-8 weeks) and maintenance (6-12 months) therapy. If these conditions are not met, the likelihood of a recurrence of the disease is very high. Studies conducted in many countries around the world have shown that more than 80% of patients who do not receive adequate maintenance treatment develop a relapse within the next 26 weeks, and the probability of relapse within a year is 90-98%. It follows from this that maintenance treatment is necessary.

Lifestyle modification should be considered a prerequisite for effective antireflux treatment in patients with GERD. First of all, it is necessary to reduce body weight, if it is excessive, and stop smoking. Patients should avoid overeating and stop eating 2 hours before bedtime. At the same time, the number of meals should not be increased: it is necessary to observe 3-4 meals a day and refuse the so-called snacks. Recommendations for frequent fractional meals are unfounded.

It is important to avoid situations that increase intra-abdominal pressure as much as possible (wearing tight belts, corsets and bandages, lifting weights of more than 8-10 kg on both hands, work that involves bending the torso forward, physical exercises associated with overstrain of the abdominal muscles). Patients who develop heartburn or regurgitation when lying down should raise the head of the bed.

Dietary recommendations should be strictly individual, taking into account the results of a thorough analysis of the patient's history. It is necessary to avoid the use of tomatoes in any form, sour fruit juices, foods that increase gas formation, fatty foods, chocolate, coffee. It is necessary to limit the use of alcohol, very hot and cold food, carbonated drinks as much as possible.

Patients should be warned about the side effects of drugs that reduce the tone of the NPS (nitrates, calcium ion antagonists of the nifedipine group, theophylline, progesterone, antidepressants), and those that themselves can cause inflammation (non-steroidal anti-inflammatory drugs, doxycycline, quinidine).

Medical treatment includes well-known groups of drugs.

Alginates
A pathogenetically substantiated therapeutic method for reducing the "acid pocket" and neutralizing acid in the area of ​​the esophageal-gastric junction in patients with GERD is the intake of alginates, which form a mechanical barrier-raft that prevents the stomach contents from being thrown into the esophagus. By creating a protective barrier on the surface of gastric contents, these drugs are able to significantly and for a long time (more than 4.5 hours) reduce the number of both pathological acidic GER and weakly alkaline duodenogastroesophageal reflux (DGER), thereby creating optimal physiological conditions for the esophageal mucosa. . In addition, alginates have a cytoprotective and sorption effect. The pharmacological compatibility of alginates with antisecretory drugs in the treatment of GERD has been proven. Alginates are taken 10 ml 3-4 times a day 30-40 minutes after meals and 1 time at night until persistent relief of the symptoms of the disease, and then - in the "on demand" mode (UDD 1, UR A).

Antacids
Antacids (aluminum phosphate 2.08 g, combined preparations - aluminum hydroxide 3.5 g and magnesium hydroxide 4.0 g in the form of a suspension, aluminum hydroxide 400 mg and magnesium hydroxide 400 mg, as well as calcium carbonate 680 mg and magnesium hydroxycarbonate 80 mg tablet) is used to treat moderate and infrequent symptoms, especially those associated with non-compliance with the recommended lifestyle (ELL 1, LL A).

Antacids can be used both as a monotherapy for rare heartburn that is not accompanied by the development of esophagitis, and in combination therapy regimens for GERD, as they are effective in quickly relieving symptoms. Antacids should be taken depending on the severity of symptoms, usually 1.5-2 hours after meals and at night. There is not enough evidence to support their continued use (EL 2, LL B).

Adsorbents(dioctahedral smectite) have a complex effect: firstly, they neutralize the hydrochloric acid of gastric juice, and secondly, they give a pronounced adsorbing effect, binding the components of the contents of the duodenum (bile acids, lysolecithin) and pepsin. Thus, dioctahedral smectite increases the resistance of esophageal mucosa to the damaging effect of refluxate. Adsorbents can be used both as monotherapy for clinical manifestations of NERD, and as part of complex therapy for GERD, especially for mixed (acid + bile) reflux. Dioctahedral smectite is prescribed 1 sachet (3 g) 3 times a day (UDD 1, SD A).

Prokinetics contribute to the restoration of the physiological state of the esophagus, affecting the pathogenetic mechanisms of GERD, reducing the amount of PRNPS and improving esophageal clearance by stimulating the motor function of the underlying parts of the digestive tract. Prokinetics can be used as part of complex therapy for GERD along with PPIs. The prokinetic drug itopride hydrochloride (50 mg 3 times a day) refers to the means of pathogenetic treatment of GERD, since it normalizes the motor function of the upper digestive tract (LEA 1, LE A).

In the presence of both esophageal and extraesophageal manifestations of GERD, effective PPIs - drugs, inhibiting the activity of the enzyme H +, K + -ATPase, located on the apical membrane of the parietal cell and carrying out the last step in the synthesis of hydrochloric acid. PPIs are considered the most effective and safe drugs for the treatment of GERD. In clinical trials, PPIs have consistently demonstrated the greatest efficacy in the treatment of erosive esophagitis and in the management of GERD-associated symptoms (EL 1, LRL A).

A decrease in acid production is considered the main factor contributing to the healing of erosive and ulcerative lesions. In the presence of single erosions of the esophagus (A / 1st stage of esophagitis), the likelihood of their healing within 4 weeks of treatment is high, therefore, the duration of the main course in this case can be 4 weeks using a standard dose of PPI: rabeprazole 20 mg per day (ELL 1 , REL A), or omeprazole 20 mg twice daily, or dexlansoprazole 60 mg daily (ELV 1, REL A), or pantoprazole 40 mg daily, or esomeprazole 40 mg daily, preferably with follow-up endoscopic examination.

If multiple esophageal erosions (B-C/2-4th stage of esophagitis), as well as complications of GERD, are detected, the duration of treatment with any drug from the PPI group should be at least 8 weeks, since in this case 90-95% efficiency can be achieved .

With an unreasonable reduction in the course of treatment of multiple esophageal erosions to 4 weeks, the frequency of their healing is much lower. In addition, such an unreasonable reduction in the duration of treatment for erosive forms of GERD may be the cause of rapid subsequent recurrence, as well as the development of complications. Patients with typical reflux symptoms who do not respond adequately to standard once daily PPI therapy may be advised to take twice daily PPIs. It should be borne in mind that such a dosage is not approved in the instructions for use of these drugs. The duration of maintenance therapy after healing of erosions should be at least 16-24 weeks. In the event of complications of GERD, maintenance therapy should be carried out with PPI also in a full dose (ELL 1, LL A).

PPIs effectively control pH in the lower third of the esophagus, so symptoms rapidly decrease and disappear in patients with both erosive esophagitis and NERD. In the absence of esophageal erosions, half-dose PPIs, including rabeprazole 10 mg once daily, as a course of treatment and on an on-demand regimen, can be given to treat NERD, which is pharmacoeconomically justified (ELL 1, LEL A), and also dexlansoprazole 30 mg once a day (EL 1, LL A).

When treating patients with GERD, it is recommended to use an individual approach to prescribing antisecretory therapy and choosing a drug, based on a thorough analysis of the clinical picture and the results of endoscopy. First of all, the patient's complaints are analyzed, in particular for heartburn (in addition to heartburn, other proven symptoms of GERD can be taken into account). The criteria for evaluating complaints are the frequency of their occurrence: rarely (1-2 times a week) and often (more than 2 times a week), as well as the duration of existence: small (less than 6 months) and significant (more than 6 months). When assessing the patient's status and history, male gender and age over 50 years are taken into account as risk factors for relapse, indications of the presence of erosive esophagitis during endoscopy in the past, and the stage of previously existing erosive esophagitis is essential. When assessing the patient's status, one should also pay attention to the presence of overweight (BMI> 25), obesity (BMI> 30) and HH. It is necessary to exclude the presence of "anxiety symptoms" (dysphagia, weight loss, anemia).

It is necessary to take into account the characteristics of individual antisecretory drugs. Thus, H2 receptor blockers should not be used as first-line therapy due to their significantly lower efficacy compared to PPIs.

Due to the high dissociation constant pKa, rabeprazole is able to quickly accumulate in a large number of parietal cells and lead to a rapid and pronounced inhibition of acid secretion by binding the proton pump, which ensures a high rate of action and a lasting antisecretory effect after 1 day of taking the drug. The pharmacokinetic features of rabeprazole determine the effective relief of daytime and control of nighttime heartburn from the 1st day of therapy, a high rate of healing of esophageal erosions and the maintenance of long-term remission of GERD, including when using the drug in the "on demand" mode (ELV 1, LVR A).

Dexlansoprazole is the only modified-release PPI. Its capsule contains two types of granules that release the active substance depending on pH in different parts of the small intestine: the release begins in its upper part 1-2 hours after taking the drug and continues in the distal part after 4-5 hours. The double delayed release of the active substance allows to prolong its action and helps to reduce the secretion of hydrochloric acid for a long time. Prolongation of the effect of dexlansoprazole provides effective control of nocturnal symptoms of GERD (EL 1, LRL A).

In general, PPIs show a low frequency of side effects (less than 2%), among which diarrhea, headache, nausea can be observed. Rabeprazole is characterized by a high level of safety in terms of the frequency of side effects and tolerability, and its metabolism is minimally dependent on the cytochrome P450 system (LEA 1, LE A). When prescribing PPIs in high doses for a long time, the possibility of developing side effects such as osteoporosis (although the use of PPIs should not be considered as an independent and independent risk factor for osteoporosis), bacterial overgrowth, Clostridium dificile infection and pneumonia, in patients from risk groups, primarily over 65 years of age. For long-term treatment, PPIs can be used on an on-demand basis and in intermittent courses.

The decision on the duration of maintenance therapy for GERD should be made on an individual basis, taking into account the stage of esophagitis, existing complications, the age of the patient, as well as the cost and safety of PPI treatment. With GERD, there is no need to determine the H. pylori infection and, moreover, its eradication, however, the presence of H. pylori infection should be established and its eradication should be carried out when prescribing PPI therapy for a long time.

It has not been proven that PPI treatment can lead to a decrease in the effectiveness of clopidogrel when they are used together.
It should be emphasized that symptomatic improvement with PPI therapy can also be observed in other diseases, including malignant neoplasms of the stomach, therefore, such diseases should be excluded.

The highest percentage of effective treatment of GERD exacerbations and maintenance of remission is achieved with the combined use of PPIs, prokinetics, alginates/antacids/adsorbents. For rapid relief of heartburn in patients with GERD, as well as in patients who periodically experience reflux symptoms during PPI therapy, it may be recommended to take alginic acid preparations, while the pharmacokinetic properties of PPIs do not deteriorate and they do not affect the rate of formation and efficacy protective alginate barrier (UDD 1, UUR A).

In the treatment of GERD in pregnant women, an individual selection of therapy is necessary, taking into account the potential harm. Recommendations for lifestyle changes and the rules for taking alginate-containing drugs in case of clinical need and after consultation with a doctor can be considered universal. Due to the proven high efficacy and safety in all trimesters of pregnancy, alginates are the drugs of choice for the treatment of heartburn in pregnant women (ELV 1, EUR A). Since these drugs have almost no side effects, they can be recommended not only for pregnant women, but also for lactating women and healthy people with episodic heartburn.

In complicated forms of GERD, it is possible to conduct short courses of therapy using PPI forms for intravenous administration, the advantages of which are the rapid achievement of an antisecretory effect and a higher concentration of the drug in the blood.

As noted earlier, GERD is usually characterized by a chronic relapsing course. Patients in whom the clinical symptoms of the disease are not accompanied by the development of esophagitis need to take drugs in the "pro re nata" - "on demand" mode. However, in patients with erosive-ulcerative esophagitis with this regimen of maintenance therapy, there is a high (80-90%) risk of developing a relapse of the disease within a year. The likelihood of recurrence increases in cases of resistance of the initial stages of esophagitis to therapy with antisecretory drugs, as well as when low LES pressure is detected.

Patients with GERD should be under active dispensary observation with a control examination, which is carried out at least once a year (Appendix No. 1). If complications occur, such patients should be examined twice a year, including endoscopic and morphological studies.

The term "refractory GERD" is used in case of incomplete healing of esophageal mucosa and/or persistence of typical symptoms of GERD after a full course (4-8 weeks) of PPI treatment at a standard (once a day) dose.

The most common reason for a decrease in the effectiveness of ongoing therapy is the lack of adherence of patients to treatment, i.e., their failure to comply with recommendations for lifestyle changes and the rules for taking PPIs. For representatives of this group of drugs, an increase in activity is shown when taken in the morning 30 minutes before meals. It should be borne in mind that, according to the instructions for the use of rabeprazole, neither the time of day nor food intake affect its activity.

Compliance (or non-compliance) with the recommendations prescribed by the doctor is primarily influenced by the presence and severity of symptoms, knowledge of the basics of the pathogenesis of the disease, concomitant therapy, taste and consistency of the drug taken, side effects, age, socio-economic status, patient motivation. Of course, the implementation of the doctor's recommendations, including the diet and normalization of body weight, should be considered the basis of successful treatment. The reasons for the ineffectiveness of therapy are also often the incorrect prescription of PPIs, non-compliance with their dosage and timing of therapy.

A risk factor for the development of refractory GERD is a genetic polymorphism of CYP2C19. The risk of developing refractoriness to PPI therapy is higher in rapid metabolizers of CYP2C19 than in slow metabolizers. Genetic polymorphism of CYP2C19 affects the pharmacokinetics and pharmacodynamics of PPIs, causing differences in the severity of their antisecretory action and clinical efficacy in GERD, with pronounced interindividual and interethnic differences. In the European population, there is a high prevalence of CYP2C19 genetic polymorphism with a predominance of fast metabolizers - more than 70%. At the same time, fast metabolizers have a lower rate of healing of esophageal mucosal erosions and a higher rate of GERD recurrence during therapy due to faster clearance, low plasma concentrations, and possible insufficient antisecretory effect due to the peculiarities of PPI metabolism.

Currently, another type of CYP2C19 isoenzyme metabolizers has been identified, called "ultrafast", which can often be found in the European population. In metabolizers of this type, the metabolism of drugs that break down with the help of the CYP2C19 isoenzyme occurs especially quickly, which must be taken into account when evaluating their effectiveness.

A PPI dosing regimen based on CYP2C19 genotype characteristics may be a therapeutic strategy to overcome insufficient gastric acid inhibition in patients with refractory GERD. Rabeprazole has been proposed as the PPI least affected by the CYP2C19 genotype, as it is metabolized predominantly as a result of a non-enzymatic process. (UDD 2, LLB B). In the treatment of some of these patients, it is necessary to use antisecretory drugs in high doses, which should be verified using 24-hour pH-metry.

The timing of taking some PPIs is important, as it has a significant impact on their effectiveness. So, after taking omeprazole and lansoprazole before breakfast, it is much easier to control the level of gastric pH than after taking them without a subsequent meal. Dexlansoprazole can be taken at any time of the day, with or without food (ELV 2, LRL B).

The reasons for the ineffectiveness of hydrochloric acid secretion inhibitors may be the presence of weakly acidic reflux, as well as the predominance of duodenal contents in the refluxate with a predominantly alkaline environment, when heartburn and other symptoms of GERD occur as a result of the action of bile components and pancreatic enzymes on the esophageal mucosa. Reflux is predominantly acidic in 50% of patients with GERD, acidic in nature with a bile component in 39.7%, and bile reflux occurs in 10.3% of patients. The components of the contents of the duodenum that cause damage to the esophageal mucosa are bile acids, lysolecithin and trypsin. The action of bile acids, which seem to play a major role in the pathogenesis of damage to the esophageal mucosa in DGER, has been best studied.

In mixed reflux (acidic with a bile component), the clinical effect of PPI is due not only to the suppression of acid production itself, but also to a decrease in the total volume of gastric secretion, which leads to a decrease in the volume of refluxate. However, increasing PPI doses to relieve symptoms is not indicated in this case.

in the event of DGER, the following drugs can be prescribed in various combinations (including with PPIs): adsorbents, alginates, antacids, prokinetics, ursodeoxycholic acid. In mixed / biliary reflux, adsorbents (dioctahedral smectite) are used not only to neutralize hydrochloric acid, but also to adsorb bile acids and lysolecithin, as well as increase the resistance of CO to the action of damaging aggressive factors.

The secretion of mucins in the mucus in GERD decreases depending on the severity of esophagitis, which is an additional factor predisposing to the development of erosive esophagitis in the context of ongoing GERD. The dual mechanism of action of rabeprazole - acid suppression along with cytoprotective properties: stimulation of mucin secretion and increase in their concentration in the mucus of the esophagus - its additional advantages in the treatment of GERD (ELV 4, LL C).

If treatment of patients with GERD is ineffective within 4 weeks, the presence of GER should be confirmed using an objective research method - 24-hour pH impedancemetry. Patients with persistent symptoms who do not show pathological refluxes on pH-impedancemetry and do not correlate refluxes with the onset of symptoms most likely do not have GERD, but so-called "functional heartburn".

Surgery

Antireflux surgical treatment is considered indicated for complicated course of the disease (recurrent bleeding, peptic strictures of the esophagus, development of Barrett's esophagus with high-grade epithelial dysplasia, proven by two morphologists, frequent aspiration pneumonia). In some cases, if a patient cannot undergo conservative therapy for GERD for one or another objective or subjective reason, surgical treatment should be considered even in its uncomplicated course. Surgical treatment may be more effective in those patients with GERD who have typical manifestations of the disease and who are also treated with PPIs. If PPIs are ineffective, as well as in the presence of extraesophageal manifestations, surgical treatment will be less effective.

It is necessary to consider the issue of surgical treatment together with an experienced surgeon in this field, if all measures to normalize the lifestyle have been completed, the presence of pathological gastroesophageal reflux has been proved using pH-impedancemetry, and the absence of pronounced violations of the peristalsis of the thoracic esophagus using manometry.

Management of patients with Barrett's esophagus

The need for active dispensary monitoring of patients with Barrett's esophagus is due to the fact that in the case of early diagnosis of epithelial dysplasia, the development of AKP can be prevented. Verification of the diagnosis of Barrett's esophagus and the establishment of the degree of dysplasia is carried out using a histological examination. If at the same time low-grade dysplasia is detected, it is necessary to prescribe a PPI and repeat the histological examination after 3 months. If low-grade dysplasia persists, patients are advised to continue continuous full-dose PPIs and conduct a histological examination after 3 and 6 months, then a histological examination is performed annually. If high-grade dysplasia is detected, it is necessary to prescribe PPI in a double dose with a parallel assessment of the results of histological examination and subsequent decision on the method of treating the patient - endoscopic or surgical. More detailed algorithms for managing patients with Barrett's esophagus are presented in special clinical recommendations.

Conclusion

These clinical guidelines are intended for general practitioners, general practitioners (family doctors), gastroenterologists, surgeons, endoscopists, healthcare organizers, medical workers with a secondary medical education.

Conservative treatment of patients with GERD can be carried out on an outpatient basis with the participation of a gastroenterologist. Inpatient treatment is carried out in a day or round-the-clock hospital in specialized gastroenterological and therapeutic departments in the presence of specialized gastroenterological beds and a specialist who has undergone professional retraining in the specialty "gastroenterology".

The implementation of clinical recommendations can have a positive impact on the quality of medical care for patients with GERD and the prevention of complications, in particular, if the necessary terms of treatment are observed, and active outpatient monitoring of the relevant groups of patients is carried out. The authors hope that this methodological manual will help practitioners and healthcare organizers to achieve these goals.

Information

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Jacobson B.C., Somers S.C., Fuchs C.S. Body-mass index and symptoms of gastroesophageal reflux in women. N Engl J Med 2006; 354:2340-8. 64. Kaltenbach T., Crockett S., Gerson L.B. Are lifestyle measures effective in patients with gastroesophageal reflux disease? An evidence-based approach. Arch Intern Med 2006; 166:965-71. 65. Ness-Jensen E., Hveem K., El-Serag H. et al. Lifestyle intervention in gastroesophageal reflux disease. Clin Gastroenterol Hepatol 2016; 14(2):175-82. 66. Piesman M., Hwang I., Maydonovitch C. Nocturnal reflux episodes following the administration of a standardized meal. Does timing matter? Am J Gastroenterol 2007; 102:2128-34. 67. Stanciu C., Bennett J.R. Effects of posture on gastroesophageal reflux. Digestion 1977; 15:104-9. 68. Hamilton J.W., Boisen R.J., Yamamoto D.T. Sleeping on a wedge diminishes exposure of the esophagus to refluxed acid. Dig Dis Sci 1988; 33:518-22. 69. Kwiatek M.A., Roman S., Fareeduddin A., Pandolfino J.E., Kahrilas P.J. 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Fass R., Sontag S.J., Traxler B. Treatment of patients with persistent heartburn symptoms: A double-blind, randomized trial. Clin Gastroenterol Hepatol 2006; 4:50-6. 94. Vigneri S., Termini R., Leandro G. A comparison of five maintenance therapies for reflux esophagitis. N Engl J Med 1995; 333:1106-10. 95. Hatlebakk J.G., Katz P.O., Kuo B. Nocturnal gastric acidity and acid breakthrough on different regimens of omeprazole 40mg daily. Aliment Pharmacol Ther 1998; 122:1235-40. 96. Hammer J., Schmidt B. Effect of splitting the dose of esomeprazole on gastric acidity and nocturnal acid breakthrough. Aliment Pharmacol Ther 2004; 19:1105-10. 97. Moayyedi P., Santana J., Khan M. et al. Medical treatments in the short term management of reflux oesophagitis. Cochrane Database Syst Rev 2011; (2): CD003244. 98. Weijenborg P.W., de Schepper H.S., Smout A.J. Effects of antidepressants in patients with functional esophageal disorders or gastroesophageal reflux disease: A systematic review. 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Curr Med Res Opin 2009; 25:627-38; 3. 117. Shin J. M., Kim N. Pharmacokinetics and Pharmacodynamics of the Proton Pump Inhibitors. J Neurogastroenterol Motil 2013; 19:25-35. 118 Fass R. et al. The Effect of Dexlansoprazole MR on Nocturnal Heartburn and GERD-Related Sleep Disturbances in Patients With Symptomatic GERD. Am J Gastroenterol 2011; 106(3):421-31. 119 Freedberg D.E., Kim L.S., Yang Y.X. The Risks and Benefits of Long-term Use of Proton Pump Inhibitors: Expert Review and Best Practice Advice From the American Gastroenterological Association. Gastroenterology 2017; 152(4):706-15. 120. Moayyedi P., Delaney B., Forman D. Gastrooesophageal reflux disease. Clin Evid 2005; (14):567-81. 121. Robinson M., Fitzgerald S., Hegedus R., Murthy A., Jokubaitis L. Onset of symptom relief with rabeprazole: a community-based, open-label assessment of patients with erosive oesophagitis. Aliment Pharmacol Ther 2002; 16(3):445-54. 122. Ogawa R., Echizen H. Drug-drug interaction profiles of proton pump inhibitors. Clin Pharmacokinet 2010; 49(8):509-33. 123. Targownik L.E., Lix L.M., Leung S. Proton-pump inhibitor use is not associated with osteoporosis or accelerated bone mineral density loss. Gastroenterology 2010; 138(3):896-904. 124. Ngamruengphong S., Leontiadis G.I., Radhi S. Proton pump inhibitors and risk of fracture: a systematic review and meta-analysis of observational studies. Am J Gastroenterol 2011; 106(7):1209-18. 125. Bavishi C., Dupont H.L. Systematic review: The use of proton pump inhibitors and increased susceptibility to enteric infection. Aliment Pharmacol Ther 2011; 34:1269-81. 126. Eom C.S., Jeon C.Y., Lim J.W. Use of acid-suppressive drugs and risk of pneumonia: A systematic review and meta-analysis. CMAJ 2011; 183:310-9. 127. Johnstone J., Nerenberg K., Loeb M. Meta-analysis: Proton pump inhibitor use and the risk of communityacquired pneumonia. Aliment Pharmacol Ther 2010; 31(11):1165-77. 128. Lind T., Havelund T., Lundell L. On demand therapy with omeprazole for the long-term management of patients with heartburn without oesophagitis - a placebo-controlled randomized trial. Aliment Pharmacol Ther 1999; 13(7):907-14. 129. Pace F., Tonini M., Pallotta S. Systematic review: Maintenance treatment of gastro-oesophageal reflux disease with proton pump inhibitors taken on-demand. Aliment Pharmacol Ther 2007; 26(2):195-204. 130. Juurlink D.N., Gomes T., Ko D.T., Szmitko P.E., Austin P.C., Tu J.V., Henry D.A., Kopp A., Mamdani M.M. A population-based study of the drug interaction between proton pump inhibitors and clopidogrel. CMAJ 2009; 180(7):713-8. 131. Gerson L.B., McMahon D., Olkin I. Lack of significant interactions between clopidogrel and proton pump inhibitor therapy: Meta-analysis of existing literature. Dig Dis Sci 2012; 57(5):1304-13. 132. Chen M., Wei J.F., Xu Y.N. A meta-analysis of impact of proton pump inhibitors on antiplatelet effect of clopidogrel. Cardiovasc Ther 2012; 30(5):227-33. 133. Reimer C., Lødrup A.B., Smith G., Wilkinson J., Bytzer P. Randomised clinical trial: alginate (Gaviscon Advance) vs. placebo as add-on therapy in reflux patients with inadequate response to a once daily proton pump inhibitor. Aliment Pharmacol Ther 2016; 43(8):899-909. 134. Dettmar P.W., Little S.L. Baxter T. The effect of omeprazole pre-treatment on rafts formed by reflux suppressant tablets containing alginate. J Int Med Res 2005; 33(3):301-8. 135. Washington N., Wilson C.G., Williams D.L., Robertson C. An investigation into the effect of cimetidine pre-treatment on raft formation of an anti-reflux agent. Aliment Pharmacol Ther 1993; 7(5):553-9. 136. Bordin D.S., Yanova O.B., Berezina O.I., Treiman E.V. Advantages of the combination of alginate and PPI in the elimination of heartburn and regurgitation in the early days of GERD. Ros journal gastroenterol hepatol coloproctol 2016; 25(6):39-45. . 137 Strugala V. et al. 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Information

List of authors:
V.T. Ivashkin 1 , I.V. Maev 2 , A.S. Trukhmanov 1 , E.K. Baranskaya 1, O.B. Dronova 3 , O.V. Zayratyants 2 , R.G. Sayfutdinov 4 , A.A. Sheptulin 1 , T.L. Lapina 1 , S.S. Pirogov 5 , Yu.A. Curly 2 , O.A. Storonova 1 , D.N. Andreev 2

1 FGAOU VO "First Moscow State Medical University named after I.I. THEM. Sechenov” (Sechenov University) of the Ministry of Health of Russia, Moscow, Russian Federation

2 Moscow State University of Medicine and Dentistry named after V.I. A.I. Evdokimov” of the Ministry of Health of Russia, Moscow, Russian Federation

3 Orenburg State Medical University, Ministry of Health of Russia, Orenburg, Russian Federation

4 Kazan State Medical Academy — branch of the Russian Medical Academy of Continuing Professional Education of the Ministry of Health of Russia, Kazan, Russian Federation

Table 1

Levels of Certainty of Evidence (Oxford Center for Evidence-Based Medicine)

Level	Diagnostic study	Therapeutic research
1a	Systematic Review of Level 1 Homogeneous Diagnostic Tests	Systematic review of homogeneous RCTs
1b	Qualitative gold standard validating cohort study	Single RCT (Narrow CI)
1s	Specificity or sensitivity is so high that a positive or negative result rules out/diagnoses	All or Nothing Study
2a	Systematic review of homogeneous diagnostic studies >2 levels	Systematic review of (homogeneous) cohort studies
2b	Exploratory cohort study with a qualitative gold standard	Single cohort study (including low quality RCTs; i.e. with<80% пациентов, прошедших контрольное наблюдение)
2s	No	Study of "outcomes"; environmental studies
3a	Systematic review of level 3b and higher homogenous studies	Systematic Review of Homogeneous Case-Control Studies
3b	Study with inconsistent recruitment or no gold standard study in all subjects	Separate case-control study
4	Case-control or low-quality or non-independent gold standard study	Case series (and low quality cohort or case-control studies)
5	Expert opinion without rigorous critical appraisal or based on physiology, laboratory animal studies, or development of "first principles"	Expert opinion without rigorous critical appraisal, laboratory animal studies, or development of "first principles"

Conventional designations. RCTs, randomized clinical trials; CI - confidence interval.

table 2

These draft recommendations have been peer-reviewed by independent experts who were asked to comment primarily on the extent to which the interpretation of the evidence underlying the recommendations is understandable. Comments from outpatient doctors were received, which were carefully systematized and discussed at meetings of the expert group.

The latest changes in these guidelines were presented for discussion within the framework of the Twenty-Second Russian Gastroenterological Week (03.10.2016-05.10.2016). The draft guidelines were re-reviewed by independent experts and outpatient clinicians. For the final revision and quality control, the recommendations were re-analyzed by the members of the expert group, who concluded that all comments and comments were taken into account, the risk of systematic errors in the development of recommendations was minimized.

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Among the diseases requiring clinical recommendations, GERD occupies one of the first places, since only in Russia the prevalence of this pathology is 18-46%.

Gastroesophageal reflux disease (GERD) is a chronic relapsing disease, the main manifestation of which is the injection of stomach contents into the esophagus, resulting in clinical symptoms that significantly reduce the patient's quality of life. According to the degree of distribution, complex clinic and the possibility of life-threatening complications, this disease is considered one of the acute problems of gastroenterology.

The reasons

Sphincter dysfunction is considered to be the main cause of GERD. This formation is designed to keep the passage between the stomach and esophagus closed and stop the backflow (reflux) of stomach contents. In case of weakening of the sphincter, the hole opens, and the stomach, contracting, throws the food clot into the esophagus. If the refluxant has damaging properties, then the walls of the organ are irritated up to pathological disorders of the mucosa.

In addition, the causes of gastroesophageal disease are:

1. Disturbances in the motor functions of the esophagus.
2. High intra-abdominal pressure.
3. Excessive acidity of the gastric juice.

The possibility of reflux disease is increased by:

• Stress.
• Smoking.
• Excess weight.
• Medications: nitrates, calcium channel blockers, beta-blockers.

Symptoms

Insufficiency of the lower alimentary sphincter (LES) causes painful symptoms of GERD, including:

1. Typical related to the digestive system:
   • heartburn;
   • belching;
   • ulceration of the walls of the esophagus.
2. Atypical, called pulmonary signs of GERD, manifested in impaired respiratory function.

A burning sensation behind the sternum, heartburn, refers to the hallmarks of pathology and is the result of persistent damage to the walls of the esophagus by acid.

Gastric juice injures the mucosa of the organ, causing a burn. Constant heartburn caused by prolonged irritation of the walls is an alarming sign of GERD.

The presence of other symptoms is characteristic of more complex cases of the disease. So, sour belching, combined with heartburn, causes a strong cough that makes it difficult to sleep at night. In addition, heartburn can manifest itself as an imitation of angina pectoris. Observed:

• drop in blood pressure;
• cardiopalmus;
• cold sweat;
• fear of death.

Additional Information! One of the most common and serious exacerbations is the formation of Barrett's esophagus, when the usual squamous epithelium is replaced by a cylindrical gastric one.

Treatment

Therapy is carried out by medical, surgical methods, as well as by conducting a healthy lifestyle. The medicinal effect is carried out in order to normalize acidity and improve motor skills.

Apply:

1. prokinetics (Domperidone, Metoclopramide) - fixes the state of the sphincter, regulates the passage of food mass in the gastrointestinal tract;
2. antisecretory drugs (blockers of H2-histamine receptors) - reduce the harmful effect of gastric juice on the mucous membrane;
3. antacids (Almagel, Maalox) - level the acidity of the stomach;
4. reparants (misoprostol and sea buckthorn oil) - contribute to the healing of erosive lesions.

Surgical intervention is used in the presence of complications:

1. Barrett's esophagus;
2. strictures;
3. reflux esophagitis III - IY degree;
4. mucosal ulcers.

The main result of the treatment is the regeneration of the physiological septum separating the stomach and esophagus.

Despite the fact that food does not linger in the esophagus, and therefore does not cause harm, rather severe pathologies of this organ are known. Many of them require surgical intervention, which is difficult due to the deep location and delicate structure of the muscular tube, which is 25 centimeters long. Consider the signs indicating violations in its work and methods of their treatment.

Symptoms of diseases of the esophagus

Diseases of the esophagus are accompanied by the following symptoms:

• Difficulty swallowing, sensation of the presence of a foreign body.
• Severe, sudden, unexplained pain, similar to an angina attack.
• Metallic taste in the mouth, profuse salivation, belching, heartburn.
• Vomiting after eating from spasm of the lower sphincter.

Thermal and chemical burns are accompanied by purulent mucous secretions. When concentrated caustic substances enter the walls of the esophagus, scars form. With malignant pathogenesis, a person’s weight decreases and he weakens before our eyes.

Such symptoms should alert and become a reason to visit a doctor. Only he can make a final diagnosis and choose an adequate treatment.

Reasons for development

Pathologies of the esophagus are sometimes congenital in nature and are formed at the stage of embryogenesis. They also occur in the presence of benign neoplasms (polyps), after swallowing foreign bodies, poisons, eating extremely hot or cold dishes. They can appear during chronic inflammatory processes, as well as due to infection of the tissues of the digestive tube, including pathogenic fungi that cause, for example, candidiasis.

Video: Diseases of the esophagus

Accurate diagnosis

If a lesion of the esophagus is suspected, in order to exclude oncology, laboratory tests are prescribed by the doctor, as well as:

• radiography;
• fibrogastroduodenoscopy;
• determination of the pH level of the gastric environment.

In parallel with endoscopy, a biopsy is performed with the collection of the affected parts of the mucosa for their histological examination. If necessary, methods are used to measure the pressure inside the tube and register the contraction of the walls of the organ.

Video: Endoscopy of the esophagus and stomach

Diseases of the esophagus

Understanding the importance of a small part of the gastrointestinal tract often comes only after its pathological degeneration, when unpleasant sensations appear that can radically change a person's life.

Prolonged stagnation of food provokes inflammation of the mucosa, that is, it contributes to the development of esophagitis. Its chronic variety is considered as a form preceding a cancerous tumor, which captures even the upper parts of the stomach.

Throwing chyme into the respiratory organs leads to pneumosclerosis, abscesses of the lung tissue, to aspiration types of bronchopneumonia. Such complications often affect the youngest children.

Achalasia cardia is diagnosed using multichannel probes that record motility and pressure inside the digestive tube.

Medical treatment of achalasia is effective only at an early stage. Thermal and mechanical sparing of food is recommended. Dealing with pain:

• calcium antagonists;
• ganglioblockers;
• nitropreparations, for example, Corinfar.

The main therapeutic technique is cardiodilatation, which expands the narrowing places.

Barrett's esophagus

It is a complication of reflux disease (GERD), when aggressive gastric or duodenal juice, including enzymes, hydrochloric and bile acids, irritates the mucosa of the digestive tube. It leads to metaplasia, that is, the replacement of squamous epithelium by its other types. Barrett's syndrome increases the risk of developing cancerous tumors.

Endoscopy with a biopsy study allows you to confirm or refute the initial diagnosis. A control biopsy is performed after a course of anti-inflammatory therapy in order to exclude a morphological error. Further treatment tactics depend on the clinical picture. If epithelial dysplasia is absent, modern techniques are used, such as:

• laser destruction.
• Photodynamic therapy.
• Argon plasma coagulation.

In cases of dysplasia, endoscopic resection is used, as well as dissection in the submucosa. Proton pump inhibitors help in the repair of squamous epithelium.

Video: Harbingers of cancer. Barrett's esophagus

Esophagospasm

A condition in which the lower sphincter is working normally and the walls of the tube are contracting spasmodically. It occurs more often in men. Patients complain of pain when swallowing. Spasm causes deformation of the esophagus, which is visualized during an X-ray examination.

Treatment of the esophagus consists in observing a sparing diet, taking nitro group drugs, antispasmodics. If medical therapy and balloon dilatation are ineffective, an operation to cut the muscle tissue is indicated.

Reflux esophagitis

Pathology occurs due to frequent reflux of chyme from the stomach upwards, which occurs due to the weakness of the lower sphincter. Hydrochloric acid irritates the delicate mucous membrane, which becomes inflamed and ulcerated. In places of scarring, the tube narrows.

Symptoms of the disease are more common in infants. Manifested in the form of belching, heartburn, burning in the sternum, spasm. Vomiting at night can trigger aspiration pneumonia. After some time, the tube narrows, and problems are created during the passage of the food bolus. The disease can cause hidden bleeding, recurrent pneumonia, scarring of the mucosa.

Video: Reflux esophagitis

Diagnosis is carried out using esophagogastroscopy, radiography with contrast, pH-metry.

From medical means the patient accepts:

• Vitamins, antihistamines.
• Calming compounds.
• Prokinetics to increase the contractile activity of the lower sphincter.
• Means with enveloping properties.
• Antispasmodics.
• Antacids.

Hernia of the esophagus

Hereditary or acquired defect of the esophageal opening in the diaphragm, when the abdominal organs are in the chest. Common symptoms include occult bleeding and anemia. If the tube is narrowed, surgical intervention is indicated. Conservative therapy aims to reduce the possibility of reflux.

Damage

The esophagus can be injured when foreign bodies enter its lumen: parts of children's toys, buttons, nails. The cause of organ damage can even be the mechanical impact of instrumental methods of diagnosis and treatment. Spontaneous rupture of the tube is possible with vomiting. Attempts to push through fish bones with a crust of bread lead to serious consequences. Those wedged into the mucosa and cause a progressive complication.

With perforation of the esophagus, the patient's condition deteriorates sharply. Subcutaneous emphysema develops.

Treatment of the disease is usually surgical. Medically eliminated only the consequences of shallow damage to the wall. For its implementation requires systematic medical supervision, monitoring the dynamics of the process.

Video: Hernia of the esophagus and heartburn: radical treatment

burns

Mucosal damage can be chemical and thermal. Occur accidentally or intentionally (hot food, aggressive compounds, a list of which is presented below). It includes:

• acids;
• potassium permanganate;
• hydrogen peroxide;
• ammonia;
• ethanol;
• phenol.

In 7 out of 10 cases, children under the age of 10 suffer from burns.

Acids are less destructive than alkalis. The formation of a kind of film prevents further tissue damage.

In case of poisoning with caustic soda, saponification of fats, denaturation of proteins occurs, cells turn into a gelatinous substance, which ultimately ends in more deplorable consequences. A through hole is formed when even 20 ml of alkali enters the initial section of the gastrointestinal tract.

First aid for chemical burns is to wash the alimentary canal. To neutralize the poison, its identification is necessary.

The acid is neutralized with a 2% soda solution (0.5 tsp per 1 liter), after which the gag reflex is stimulated.

In case of alkali burns, the affected organ is washed with vegetable oil diluted with citric or acetic acid.

The patient receives complex treatment in a hospital setting. After severe damage to the tube, a hole in the anterior wall or a gastrostomy is used to feed it.

Esophageal carcinoma

About 70% of all pathologies of the initial gastrointestinal tract are malignant in nature. Within 1-2 years, a dangerous disease does not manifest itself in any way. When the tumor reaches a large size, it prevents the promotion of a dense food bolus, the work of the larynx. Over time, difficulties also arise with the use of liquid food. A person suffers from pain behind the sternum, increased salivation, loses weight.

Gastroesophageal reflux disease (GERD) is a disease caused by the development of inflammatory changes in the distal esophagus and / or characteristic symptoms due to regularly repeated reflux of gastric and / or duodenal contents into the esophagus.

EPIDEMIOLOGY

The true prevalence is not known, which is associated with a large variability in clinical symptoms: from episodically occurring heartburn to clear signs of complicated reflux esophagitis. The true prevalence of GERD is much higher than official statistics due to the existing difficulties in the use of diagnostic methods. In addition, less than 1/3 of GERD patients see a doctor.

Symptoms of GERD are found in 20-50% of the adult population, and endoscopic signs in more than 7-10% of individuals in the population.

In the US, heartburn (the main symptom of GERD) is experienced by 10-20% of adults on a weekly basis.

There is no complete epidemiological picture in Russia. There are separate epidemiological studies conducted in different regions. So, in Moscow, 34% of women and 15% of men complain of frequent heartburn.

CLASSIFICATION

According to ICD-10, GERD is subdivided into GERD with esophagitis and GERD without esophagitis. In clinical practice, a different terminology has been adopted:

Endoscopy-negative reflux disease, or non-erosive reflux disease;

Endoscopically positive reflux disease, or reflux esophagitis.

Rice. 39-1. The severity of reflux esophagitis.

Table 39-1. Classification of reflux esophagitis

Degree gravity	Characteristic
	One (or more) mucosal lesions less than 5 mm in size and limited to the mucosal fold
	One (or more) mucosal lesion larger than 5 mm, limited to the mucosal fold (the lesion does not extend to the area between the two folds)
	One (or more) mucosal lesions extending into two or more mucosal folds but involving less than 75% of the circumference of the esophagus
	One (or more) mucosal injury involving 75% or more of the circumference of the esophagus

Complications of GERD include:

Peptic strictures;

Esophageal bleeding;

Barrett's esophagus.

Approximately 60% of patients are diagnosed with non-erosive reflux disease, 30% have reflux esophagitis, and 5% develop complications.

ETIOLOGY AND PATHOGENESIS

The reasons for the development of GERD include the following.

Weakening of the function of the antireflux barrier (the locking mechanism of the cardiac part of the stomach).

Decreased clearance of the esophagus.

Reducing the resistance of the mucosa of the esophagus to the effects of damaging factors.

An increase in the production of hydrochloric acid, pepsin in the stomach, the flow of bile into the stomach.

Since the pressure in the stomach is always higher than in the chest cavity, there is a special mechanism that prevents the reflux of gastric contents - the so-called locking mechanism of the cardia. Normally, reflux occurs rarely, for a short time (less than 5 minutes). This physiological process, observed after eating and characterized by the absence of clinical symptoms, short duration of episodes, may occur during sleep. Normal pH values ​​in the esophagus are 5.5-7.0.

Esophageal reflux is considered pathological if the time during which the pH in the esophagus reaches 4.0 and below is 1 hour / day or the total number of gastroesophageal refluxes during the day exceeds 50, they develop day and night.

The mechanisms that support the viability of the function of the esophageal-gastric junction (the locking mechanism of the cardia) include:

lower esophageal sphincter;

Diaphragmatic-esophageal ligament;

Mucous "socket";

Acute angle of His, forming Gubarev's fold;

Intra-abdominal location of the lower esophageal sphincter;

Circular muscle fibers of the cardia of the stomach.

LOWER ESophageal Sphincter

The main role in the locking mechanism belongs to the state of the lower esophageal sphincter. At rest, in a healthy person, it is closed. Normally, transient relaxation lasts for 5-30 seconds and helps to free the stomach from excess air swallowed during meals. In patients with GERD, these spontaneous episodes of relaxation of the lower esophageal sphincter are frequent and prolonged. The reason for this is a violation of the peristalsis of the esophagus, fast and plentiful food, when a large amount of air is swallowed.

The tone of the lower esophageal sphincter is reduced by:

Foods containing caffeine (chocolate, coffee, tea, coca-cola), citrus fruits, tomatoes, alcohol, nicotine and fats;

Some drugs: anticholinergics, sedatives and hypnotics, -blockers, calcium channel blockers, nitrates, theophylline and other drugs;

Vagus nerve lesions (vagal neuropathy in diabetes mellitus, vagotomy).

Pressure in the lower esophageal sphincter decreases under the influence of a number of gastrointestinal hormones: glucagon, somatostatin, cholecystokinin, secretin, vasoactive intestinal peptide, enkephalins.

Decreased antireflux barrier function can occur in three ways:

Primary decrease in pressure in the lower esophageal sphincter;

An increase in the number of episodes of his transient relaxation;

Complete or partial destruction of the sphincter, for example, with a hernia of the esophageal opening of the diaphragm, scleroderma, after surgical interventions, pneumocardiodilation.

GIS ANGLE

This is the angle of transition of one side wall of the esophagus into the greater curvature of the stomach, while the other side wall smoothly into the lesser curvature. The air bubble of the stomach and intragastric pressure contribute to the fact that the folds of the gastric mucosa, forming the angle of His, fit snugly against the right wall (Gubarev's fold), preventing the contents of the stomach from refluxing into the esophagus.

CLEARANCE REDUCTION

The esophagus is equipped with an effective mechanism that eliminates pH shifts to the acid side - esophageal clearance. In 50% of patients with GERD, esophageal clearance is reduced. In this case, the following variants of esophageal clearance suffer:

Chemical - due to a decrease in the neutralizing effect of bicarbonates of saliva and esophageal mucus;

Volumetric - due to inhibition of secondary peristalsis and a decrease in the tone of the wall of the thoracic esophagus.

The immediate cause of reflux esophagitis is prolonged contact of gastric or duodenal contents with the mucosa of the esophagus.

RESISTANCE OF THE ESOPHAGUS MUCOSA

Provided by preepithelial, epithelial and postepithelial factors.

Epithelial damage begins when hydrogen ions and pepsin or bile acids overcome the preepithelial mucus protective layer and active bicarbonate secretion.

Epithelial factor: features of the structure and functions of cell membranes, intercellular connections, intra- and intercellular transport, creating an optimal pH (7.3-7.4).

Postepithelial factor: blood supply to the mucous membrane of the esophagus, providing adequate trophic processes, optimal acid-base balance.

CLINICAL PICTURE

The peculiarity of GERD is the absence of dependence of the severity of clinical symptoms (heartburn, pain, regurgitation) on the severity of changes in the mucosa of the esophagus. Symptoms of the disease do not allow differentiating non-erosive reflux disease from reflux esophagitis.

All symptoms can be combined into two groups: esophageal (heartburn; belching with sour, bitter or food; regurgitation; dysphagia; odynophagia; pain behind the sternum) and extraesophageal (cough, asthma attacks, shortness of breath, hoarseness or hoarseness of voice, dry throat, salivation, caries, signs of anemia).

In the clinical picture, the leading place is occupied by heartburn, eructation of acidic contents that occurs when bending forward and at night. The second most common manifestation of this disease is retrosternal pain. Less commonly, dysphagia, regurgitation, and odynophagia (pain when swallowing) are observed.

HEARTBURN

A peculiar burning sensation or heat of varying intensity that occurs behind the sternum (in the lower 1/3 of the esophagus) or in the subscapular region. It is noted in 83% of patients with GERD. It occurs as a result of prolonged contact of the acidic contents of the stomach (pH ‹4) with the mucous membrane of the esophagus. The severity of heartburn does not correlate with the severity of esophagitis. It is characterized by its strengthening with errors in diet, intake of carbonated drinks, alcohol, physical exertion, forward bending and in a horizontal position.

BUCKING AND RETURNING FOOD

52% of patients complain of belching. As a rule, it intensifies after eating, taking carbonated drinks. Regurgitation of food, observed in some patients, occurs during exercise and a position that promotes regurgitation. Belching and regurgitation are characteristic of a disease with severe impairment of the motor function of the esophagus.

CHEST PAIN

It spreads to the interscapular region, neck, lower jaw, left side of the chest and can mimic angina pectoris. In the differential diagnosis of the origin of pain, it is important to establish what provokes and relieves pain. Esophageal pain is characterized by a connection with food intake, body position and their relief by taking alkaline mineral waters and antacids.

DYSPHAGIA

Dysphagia has an intermittent character, noted in 19% of patients. The appearance of persistent dysphagia and a simultaneous decrease in heartburn indicates the development of esophageal stricture. Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma.

DIAGNOSTICS

The main methods used to detect gastroesophageal reflux are:

X-ray examination;

Endoscopy;

Daily monitoring of the pH of the esophagus;

Examination of the motor function of the esophagus;

Histological examination.

X-ray study. When fluoroscopy of the esophagus, the ingress of a contrast agent from the stomach into the esophagus is determined, a hernia of the esophageal opening of the diaphragm, strictures, signs of esophagitis (thickening of the folds, changes in motility, uneven contours of the esophagus), erosion and ulcers of the esophagus are detected.

Endoscopic study. Used to diagnose reflux esophagitis and assess its severity (see above for the classification of reflux esophagitis).

Chromoendoscopy detects metaplastic and dysplastic changes in the epithelium of the esophagus by applying to the mucous membrane of substances that stain healthy and affected tissues in different ways. In addition, you can see the prolapse of the gastric mucosa into the lumen of the esophagus, which is especially noticeable during vomiting; true shortening of the esophagus with the location of the esophageal-gastric junction above the diaphragm. Evaluation of the closing function of the cardia is difficult, since it can be opened in response to the introduction of an endoscope or air insufflation.

Daily pH-metry esophagus. The most informative method for diagnosing GERD, especially non-erosive reflux disease, which makes it possible to judge the frequency, duration and severity of reflux. Compared with other methods [fluoroscopy, fibroesophagogastroduodenoscopy (FEGDS), lower esophageal sphincter pressure study], 24-hour pH-metry has a high sensitivity in detecting gastroesophageal refluxes (88-95%). The information obtained makes it possible to accurately determine how long the esophageal mucosa was exposed to hydrochloric acid, evaluate the effectiveness of esophageal clearance, compare the occurrence of refluxes with clinical symptoms, and investigate the acid-producing function of the stomach during the day.

For the diagnosis of GERD, the results of pH-metry are evaluated by the total time during which the pH value is ‹4.0, by the total number of refluxes per day, by the number of refluxes lasting more than 5 minutes and the duration of the greatest reflux.

Scintigraphy esophagus. A radioactive isotope of technetium is used to assess esophageal clearance. A delay of the received isotope in the esophagus for more than 10 minutes indicates a slowdown in esophageal clearance. The study of daily pH and esophageal clearance allows you to identify reflux before the development of esophagitis.

Manometry. A decrease in the pressure of the lower esophageal sphincter, an increase in the number of its transient relaxations, a decrease in the amplitude of peristaltic contractions of the esophageal wall are revealed.

Histological study. Histological examination of a biopsy of the esophageal mucosa is used to exclude Barrett's esophagus and esophageal adenocarcinoma. Histological examination reveals thinning and atrophy of the epithelium, proliferation of connective tissue (sclerosis). Metaplasia of the squamous non-keratinizing epithelium of the esophagus is found, leading to the growth of the cylindrical epithelium of the cardiac or fundal type of the gastric mucosa. If metaplasia leads to the appearance of a specialized small intestine columnar epithelium, then there is a risk of malignancy. Specialized columnar epithelium is diagnosed as incomplete small intestinal metaplasia with the presence of goblet cells.

COMPLICATIONS

Risk factors for the development of complications are the frequent occurrence and prolonged existence of symptoms, a pronounced stage of erosive esophagitis, the presence of a hiatal hernia. Complications of GERD include esophageal ulcers, bleeding, strictures, and Barrett's esophagus.

Peptic ulcers The esophagus is observed in 2-7% of patients with GERD, in 15% of them peptic ulcers are complicated by perforation, most often in the mediastinum.

Acute and chronic bleeding varying degrees are observed in almost all patients with peptic ulcers of the esophagus, and severe bleeding is noted in half of them.

Strictures occur in approximately 10% of patients with GERD: stenosis of the esophagus makes the disease more persistent (dysphagia progresses, health worsens, body weight decreases). Clinical symptoms of stenosis (dysphagia) occur when the lumen of the esophagus narrows to 2 cm.

Esophagus Barrett(See Section 39.2 Barrett's Esophagus).

TREATMENT

The choice of treatment method is associated with the characteristics of the course and the cause that caused GERD. Treatment for GERD can be medical or surgical.

THERAPEUTIC TREATMENT

Exclude loads that increase intra-abdominal pressure: do not wear tight clothes and tight belts, corsets; do not lift weights of more than 8-10 kg on both hands; avoid physical exertion associated with overexertion of the abdominal press.

Avoid large meals and do not eat at night (no later than 3 hours before bedtime); after eating, avoid bending forward and do not lie down. Limit the intake of foods that reduce the pressure of the lower esophageal sphincter and irritate the esophageal mucosa: foods rich in fats (whole milk, cream, cakes, pastries, goose, duck, pork, lamb, fatty beef), alcohol, drinks containing caffeine (coffee, cola, strong tea, chocolate), citrus fruits, tomatoes, onions, garlic, fried foods. Do not take drugs that cause reflux (sedatives and tranquilizers, calcium channel inhibitors, β-blockers, theophylline, prostaglandins, nitrates).

Sleep with the head of the bed raised.

Give up smoking.

Normalize body weight.

Medical treatment

Terms of treatment: 4-8 weeks for non-erosive reflux disease and at least 8-12 weeks for reflux esophagitis, followed by maintenance therapy for 6-12 months. Drug therapy includes the appointment of prokinetics, antacids and antisecretory agents.

Prokinetics. Increase the tone of the lower esophageal sphincter, increase esophageal peristalsis, improve esophageal clearance. Assign domperidone, metoclopramide 10 mg 3-4 times a day 30 minutes before meals. Domperidone has the advantage of not penetrating the blood-brain barrier and has fewer side effects compared to metoclopramide. In the form of monotherapy, prokinetics are used only in the treatment of mild forms of GERD.

Antacids and antisecretory drugs. The goal of antisecretory therapy is to reduce the damaging effect of acidic gastric contents on the esophageal mucosa in gastroesophageal reflux. Antacids are effective for moderate and infrequent symptoms. Antacids have a cytoprotective effect and neutralize the hydrochloric acid of gastric juice. The most convenient pharmaceutical form is gels. Usually drugs are prescribed 3 times a day 40-60 minutes after meals and at night. Each episode of pain and heartburn should be stopped, as these symptoms indicate progressive damage to the esophageal mucosa.

In the treatment of reflux esophagitis, preparations containing sodium alginate have proven themselves well. It forms a foamy antacid suspension floating on the surface of the gastric contents, and, getting into the esophagus in case of gastroesophageal reflux, gives a therapeutic effect.

Blockers H 2 -receptors histamine. With reflux esophagitis, ranitidine and famotidine are widely used, which significantly reduce the acidity of the gastric contents thrown, which contributes to the relief of the inflammatory and erosive-ulcerative process in the mucosa of the esophagus.

Inhibitors proton pump. Currently, H + , K + -ATPase blockers (omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole) are considered the drugs of choice, which, by inhibiting the proton pump, provide a pronounced and prolonged suppression of gastric secretion of hydrochloric acid. These drugs are the most powerful antisecretory agents, they are particularly effective in peptic erosive-ulcerative esophagitis, providing scarring of the affected areas in 90-96% of cases after 4-5 weeks of treatment.

SURGERY

The issue of surgical correction is decided in the case of prolonged and/or ineffective drug therapy, the occurrence of complications (esophageal stricture, repeated bleeding, Barrett's esophagus). Especially often, indications for surgery occur when GERD is combined with a hernia of the esophageal opening of the diaphragm.

FORECAST

With non-erosive reflux disease and a mild degree of reflux esophagitis, the prognosis is favorable in most cases. The prognosis worsens with a long duration of the disease, combined with frequent, prolonged relapses, with complicated forms of GERD, especially with the development of Barrett's esophagus due to an increased risk of developing adenocarcinoma of the esophagus.

39.2. Barrett's Esophagus

Barrett's esophagus is an acquired chronic metaplastic condition of the esophageal mucosa, in which the stratified squamous epithelium in some areas is replaced by a single-layer cylindrical epithelium.

Barrett's esophagus with intestinal metaplasia develops in approximately 10-20% of individuals with GERD. The chance of developing adenocarcinoma in Barrett's esophagus is 1 in 200-400 patients per year. Barrett's esophagus is 10 times more likely to develop in men (especially the elderly) than in women.

Etiology and pathogenesis. The etiology is not clear. Factors predisposing to the development of the disease are the high secretion of hydrochloric acid in the stomach and the presence of bile in the gastric contents thrown into the esophagus.

Clinical painting Barrett's esophagus does not differ from that of GERD. In this regard, it is necessary to exclude the presence of Barrett's esophagus in any patient with a long history of GERD (more than 5 years).

Diagnostics. On endoscopic examination, the columnar epithelium has a characteristic red color and velvety appearance, which distinguishes it from the adjacent thin, pale, glossy epithelium of the esophagus. To confirm the diagnosis and establish the degree of epithelial dysplasia, a biopsy is performed from four sections of the esophageal mucosa.

Treatment

If low-grade dysplasia is detected, high (doubled) doses of proton pump inhibitors are prescribed. After 3 months, a repeated histological examination is carried out. If low-grade dysplasia persists, continue treatment with proton pump inhibitors at the same doses, performing control histological studies after 3 and 6 months, and then annually.

If high-grade dysplasia is detected, proton pump inhibitors are prescribed and the issue of endoscopic treatment (laser destruction, multipolar electrocoagulation, photodynamic coagulation of metaplastic epithelial areas) or surgical intervention is decided.

39.3. esophagitis

Esophagitis is a group of diseases characterized by the development of inflammatory and destructive changes in the mucous membrane of the esophagus, and sometimes deeper layers of its wall. Depending on the morphological picture, catarrhal, erosive, hemorrhagic and necrotic esophagitis are distinguished. The clinical picture of all esophagitis is characterized by dysphagia.

INFECTIOUS ESOPHAGITS

Infectious esophagitis usually occurs in immunocompromised individuals. Esophagitis is divided into viral (most often caused by the herpes simplex virus and cytomegalovirus), bacterial (due to Mycobacterium tuberculosis and bacteria of the genus Lactobacillus) and fungal (often caused by fungi of the genus Candida).

Viral esophagitis. Esophagitis caused by the herpes simplex virus often accompanies rashes in the nasolabial triangle. Cytomegalovirus infection, in addition to damage to the esophagus, is characterized by the involvement of other internal organs. Endoscopically, in lesions of the herpes simplex virus, typical vesicles are found on the mucous membrane of the esophagus, in place of which limited ulcers are then formed with edges raised above the surface (crater-shaped ulcers). When affected by cytomegalovirus, erosions are detected in the early stages, then linear sickle-shaped ulcers are formed. The diagnosis is confirmed by virological and immunohistochemical methods, as well as by the method of hybridization. in situ. Acyclovir is considered the drug of choice for infection caused by the herpes simplex virus, and ganciclovir for cytomegalovirus infection.

Bacterial esophagitis. With bacterial esophagitis, hyperemia, mucosal edema, plaque, pseudomembranes, erosions and ulcers are detected endoscopically. To confirm the diagnosis, it is necessary, firstly, to detect signs of bacterial invasion in Gram-stained histological preparations and, secondly, to exclude the presence of a viral, fungal, or neoplastic lesion of the esophagus. In bacterial esophagitis, antibacterial agents are used, as well as a complex of astringent, enveloping and antisecretory drugs in combination with local anesthetics.

Fungal esophagitis. With fungal esophagitis, white or yellowish overlays are found endoscopically on the hyperemic mucosa of the esophagus. During bacteriological and histological examination of biopsy specimens, mycelial forms of the fungus are determined. Patients suffering from fungal esophagitis and immunodeficiencies are recommended to take drugs containing imidazole derivatives (bifonazole, oxiconazole) orally. Patients with granulocytopenia due to a high risk of dissemination of a fungal infection are prescribed amphotericin B intravenously.

MEDICINAL ESOPHAGITS

Most often, drug-induced esophagitis is caused by antibiotics (doxycycline, tetracycline, etc.), NSAIDs, quinidine, potassium chloride, etc. These drugs account for approximately 90% of all cases of drug-induced injury to the esophagus.

A characteristic clinical symptom is dysphagia, which occurs several hours or days after ingestion of the drug. Endoscopically, medicinal lesions of the esophagus are characterized by the presence of one or more separately located ulcers on the unchanged mucosa. Particles of the drug are often found at the edges of ulcers.

In uncomplicated cases, drug-induced injuries of the esophagus do not require active intervention and heal within 3 days to several weeks after discontinuation of the drug. In the presence of symptoms of GERD, antisecretory, astringent, enveloping drugs, local anesthetics are prescribed.

39.4. achalasia cardia

Achalasia (gr. a- - absence, chalasis- relaxation) of the cardia - a disease of the esophagus, in which there is no reflex relaxation of the lower esophageal sphincter during swallowing, and the tone and peristalsis of the thoracic esophagus are impaired.

Epidemiology. Achalasia of the cardia is a rather rare disease, the prevalence of which is 0.001-0.002%. Most patients are people aged 30-50 years. Most often (95% of cases) observe idiopathic achalasia of the cardia. In 2-5% of patients, achalasia of the cardia is familial (inherited in an autosomal recessive manner).

Etiology and pathogenesis. The etiology of the disease is not clear. The pathogenesis is a violation of the activity of the intramural nervous apparatus of the esophagus, possibly due to a deficiency of relaxing mediators, primarily nitric oxide.

Clinical painting. A characteristic symptom of achalasia cardia is dysphagia. At the beginning of the disease, dysphagia occurs only when taking solid food, then dysphagia gradually joins when drinking liquids. In some cases, dysphagia is relapsing in nature. As a result, patients need much more time to eat. To speed up the emptying of the esophagus, patients often resort to certain methods, for example, drink a glass of water in one gulp.

Progressive dysphagia causes weight loss in most patients. As dysphagia progresses, regurgitation develops, so patients often wake up at night coughing or choking. Hypermotor dyskinesia of the esophagus, as well as its overflow, lead to the development of pain behind the sternum of a pressing or compressive nature with irradiation to the neck, lower jaw or back.

Diagnostics. An x-ray examination performed on an empty stomach reveals the following signs:

Large amount of esophageal contents;

Violation of the evacuation of the contrast agent into the stomach;

Moderate or significant (fusiform or S-shaped) expansion of the esophagus with narrowing in the distal section (symptom of "mouse tail", "carrot tip" or "bird's beak");

No gas bubble in the stomach.

Esophagoscopy reveals an expansion of the esophagus, congestive esophagitis, sometimes with areas of epithelial metaplasia (leukoplakia). To exclude malignancy, a biopsy is performed from suspicious areas of the mucous membrane.

Manometrically, with achalasia of the cardia, hypertonicity of the lower esophageal sphincter, the absence of its reflex opening, and a violation of the peristalsis of the thoracic esophagus are revealed.

Differential diagnosis of achalasia cardia is carried out with diseases accompanied by dysphagia, primarily cancer of the esophagus and cardia of the stomach. X-ray and endoscopic examination with biopsy are of great help in this.

Treatment. The main treatment for achalasia cardia is pneumocardiodilatation (expansion of the cardiac opening of the stomach with the help of an inflated rubber balloon, resulting in a partial rupture of the muscles of the lower esophageal sphincter). The frequency of good results of this treatment method is 86-100%. The effect persists for 2-8 years or more; with the resumption of dysphagia, repeated courses of cardiodilatation are carried out.

Long-acting nitrates and calcium channel blockers reduce lower esophageal sphincter pressure and improve esophageal emptying, but are not a complete substitute for cardiodilation.

Patients with achalasia cardia should be registered with a gastroenterologist. They are shown to conduct x-ray and endoscopic examination of the esophagus at least 1 time per year.

Forecast. The prognosis if left untreated is serious: the disease progresses and can lead to death from exhaustion. The prognosis worsens the high probability of cancer of the esophagus (2-7% of cases) and aspiration pneumonia.

39.5. TUMORS OF THE ESOPHAGUS

MALIGNANT TUMORS OF THE ESOPHAGUS

The incidence of esophageal cancer has recently increased significantly, its share is 2% of all malignant tumors and 7% of all malignant tumors of the gastrointestinal tract.

Men get sick 3-5 times more often than women. The peak incidence occurs at the age of 50-70 years.

Classification. The International Classification of Esophageal Cancer meets the accepted criteria for the TNM classification of cancer ( tumor- primary tumor nodulus- defeat of regional lymph nodes, metastasis distant metastases).

Malignant tumors of the esophagus in more than 95% of cases are squamous cell carcinoma or adenocarcinoma. In rare cases, small cell cancer, melanomas, sarcomas, malignant lymphomas, etc. are found.

Etiology and pathogenesis. The causes of esophageal cancer are unknown. Risk factors for developing squamous cell carcinoma are:

Achalasia of the cardia;

alcohol abuse;

Smoking;

Familial tilosis (hereditary hyperkeratosis of the palms and soles with a high (95%) risk of developing esophageal cancer over the age of 65);

The risk of developing adenocarcinoma is increased in the presence of Barrett's esophagus.

Clinical painting. For a long time the disease is asymptomatic. In the later stages, characteristic signs develop.

progressive dysphagia.

Regurgitation of gastric contents.

Pain behind the sternum.

Horner's syndrome (ptosis, miosis, enophthalmos), which occurs when the tumor grows into the sympathetic trunk.

Hiccups and impaired excursion of the diaphragm as a result of tumor invasion of the phrenic nerve.

Painful cough, stridor breathing when the tumor grows into the trachea and large bronchi.

Esophageal-tracheal or esophageal-bronchial fistulas, causing coughing when eating, as well as aspiration pneumonia.

Bleeding from the esophagus (streaks of blood in the vomit, anemia, a positive reaction to occult blood in the feces); when the tumor destroys the wall of a large vessel - massive bleeding.

Common symptoms include weakness, increased fatigue, decreased performance, and progressive weight loss.

Diagnostics. X-rays play an important role in the diagnosis of esophageal cancer. With exophytic tumor growth with decay and ulceration, a filling defect with uneven, corroded contours is revealed. The most informative method for diagnosing esophageal cancer is FEGDS.

The diagnosis must be confirmed histologically. The highest accuracy (90-100%) is provided with multiple biopsies of tumor tissue.

Endosonography can detect tumors up to 3 mm in size and assess the condition of the tissues surrounding the esophagus. To determine the spread of the tumor process, CT and MRI are used.

differential diagnostics. It is carried out with the following diseases characterized by symptoms of dysphagia:

Peptic and burn cicatricial strictures of the esophagus;

Esophagospasm;

Achalasia of the cardia;

Benign tumors and diverticula of the esophagus;

Lymphogranulomatosis, lymphosarcoma (characterized by an increase in the cervical and mediastinal lymph nodes);

Mediastinal pathology: mediastinal tumors, aortic aneurysm, retrosternal goiter, exudate in the pericardial cavity.

Treatment esophageal cancer in the early stages includes endoscopic resection of the mucosa with a tumor, laser and photodynamic destruction of a superficial tumor.

At later stages, in the absence of signs of metastasis, a radical surgical intervention is indicated - extirpation of the esophagus with lymphadenectomy and the creation of an artificial esophagus from the greater curvature of the stomach. If a radical operation is not possible, palliative surgical interventions are carried out aimed at providing nutrition to the patient: the imposition of bypass anastomoses, gastrostomy.

The most common type of palliative surgery for cancer of the middle and lower third of the esophagus is currently endoscopic dilatation of stenosis or recanalization of the tumor. Recanalization can be laser, thermal, chemical, or using stents.

Chemotherapy for esophageal cancer is ineffective. A combination of fluorouracil and cisplatin is usually used.

Forecast. Postoperative mortality averages 6-10%. The average five-year survival rate of patients after radical surgery at stage I is about 60%, at stage II - 30-40%, at stage III - 10-15%, at stage IV - 1-4%.

BENIGN TUMORS OF THE ESOPHAGUS

Benign tumors of the esophagus are detected approximately 80 times less often than malignant ones. Of these, most (60-70%) are leiomyomas, which are more often formed in the middle and especially the lower thirds of the esophagus and, as a rule, are asymptomatic.

Benign tumors are subject to surgical treatment in order to avoid malignant degeneration and the occurrence of complications (bleeding, inflammation, etc.).

The following signs indicate violations in the work of the esophagus:

1. Pain after or during swallowing.
2. Heartburn, belching.
3. Bad breath.
4. Hypersalivation (increased salivation).
5. Burning behind the sternum.
6. Regurgitation (reverse movement) of gastric contents into the oral cavity, bitter taste in the mouth.
7. Sensation of a lump, fullness in the throat.

Food- the basis for the prevention of diseases of the esophagus. To prevent irritation of the walls of the organ, limit fatty, sour, spicy, smoked and very salty foods. Alcohol and carbonated drinks are also recommended to be avoided. The basis of the diet should be vegetables, fruits, greens, lean meat and fish, cereals. Steam, stew, bake, boil. Dishes should not be solid, a viscous or liquid consistency is recommended.

It is also important to follow a few rules for eating:

• eat small meals;
• chew slowly and thoroughly;
• eat at the same hours;
• to improve the passage of food after eating, drink 1 glass of warm boiled water;
• to prevent stagnation and decomposition of food in the esophagus, do not take it at bedtime (preferably 3 hours before bedtime) or while lying down.

Preventive diagnostic measures help to identify violations of the body at an early stage of development. The basis of examinations is instrumental and laboratory diagnostics of the patient:

1. Laboratory: analysis of blood, urine, feces. Their study helps to detect deviations from the norm, to identify concomitant pathologies, hidden bleeding.
2. Instrumental: EGDS (examination of the esophageal mucosa with an endoscope), radiography with contrast (helps to assess the motility of the organ), manometry (helps to assess the pressure of the sphincters), MRI (the most informative for diagnosing neoplasms).

Prevention of diseases of the esophagus depending on the etiology

Prevention of esophageal cancer

To reveal the oncological process (cancer, carcinoma, lymphoma, leiomyosarcoma), annual preventive examinations.

The earlier cancer is diagnosed, the better the prognosis. Timely treatment will help prevent complications: metastasis, tumor perforation, bleeding, stenosis, aspiration pneumonia, cachexia, etc. Prevention also consists in timely treatment/elimination of predisposing factors:

• diverculae;
• achalasia;
• leukoplakia;
• hernia;
• bad habits;
• irrational and unbalanced nutrition;
• Barrett's esophagus, etc.

Prevention of Barrett's esophagus

Diseases of the esophagus are sometimes associated with the ingress of gastric acid into the organ, which leads to ulcers, erosions and changes in the structure of the mucosa. Barrett's esophagus is characterized by abnormal metaplasia. The condition has been recognized as potentially precancerous and has been associated with gastroesophageal reflux. Therefore, prevention is based on early detection and treatment of the disease:

• Visit a gastroenterologist once every six months, and if you have alarming symptoms, see your doctor regularly.
• Watch your excess weight. Obesity often causes the progression of diseases of the esophagus.

This is due to the fact that the transport of stomach contents into the duodenum slows down significantly. As a result, increased pressure is formed in the organ and the contents are ejected into the esophagus along with hydrochloric acid. In addition, an increase in intragastric pressure contributes to a change in the functional state of the lower esophageal sphincter, weakening the legs of the diaphragm. What causes reflux esophagitis.

If the patient has previously been diagnosed with reflux esophagitis or there is an increased acidity of the stomach, then drugs of the proton pump inhibitor group are prescribed for treatment or prophylactic purposes to prevent relapse. These antisecretory drugs effectively suppress the production of hydrochloric acid and have high pharmacological safety. These funds include:

Zulbeks

The drug inhibits the secretion of stomach acid. Not addictive, side effects are rare. It is recommended to take 1 tablet per day for 1 month. Contraindicated in children under 12 years of age, during pregnancy, lactation, with severe kidney and liver diseases.

Losek

The drug inhibits the release of hydrochloric acid into the lumen of the stomach. With exacerbations of acid-dependent diseases, it is recommended to take 20 mg 1-2 times a day for a month. Contraindicated in pregnancy, children, during breastfeeding and allergies to the active substance.

Ursodeoxycholic acid

If reflux of bile into the esophagus is diagnosed, then ursodeoxycholic acid is prescribed. It reduces the saturation of bile, contributes to the gradual dissolution of gallstones. Has no age restrictions. But it is not recommended for hypersensitivity to the active substance.

If there are complaints of stomach fullness, a feeling of fullness, then enzymatic drugs are prescribed that do not contain bile acids. They improve the digestion process, contain enzymes.

Creazim

The drug is designed to optimize the digestive process. Contains enzymes that help to fully absorb food components entering the digestive tract. The capsules are coated with a kilo-resistant shell, which prevents the influence of gastric acid on the active substances. It is recommended to take 1 capsule with the main meal. The duration of therapy varies from several days to several months, depending on the intensity of the disturbing symptoms. At the same time, fluid intake should be increased. Contraindicated in acute pancreatitis, hypersensitivity.

Festal

Popular enzyme preparation. It compensates for the insufficiency of the secretory function of the pancreas, and also normalizes the biliary activity of the liver. Contains enzymes that improve the absorption of carbohydrates and proteins, the breakdown of plant fiber, and other digestive processes. It is recommended to take 1-2 tablets 3 r. in a day. The duration of therapy depends on the complexity of disorders in the gastrointestinal tract. Contraindicated in hepatitis, hypersensitivity, acute pancreatitis, children under 3 years of age, with intestinal obstruction.

Prevention of cicatricial stenosis of the esophagus

Cicatricial narrowings are characterized by complete or partial overlap of the lumen of the esophagus, which interferes with the normal swallowing of food and saliva. They are more often diagnosed in patients who have suffered a chemical burn with acids, alkalis, and other aggressive liquids. Less commonly in patients with reflux esophagitis, tumors, hernias of the esophagus, gastritis. Pathology has 5 stages of development: from the free passage of any food, but uncomfortable swallowing, to the complete impossibility of taking any food and even swallowing saliva.

To prevent the progression of the pathology and eliminate the mechanical obstruction in the esophagus, an integrated approach is needed:

1. Power correction.
2. Conservative therapy: prokinetics, enzymatic agents.
3. Surgical intervention (endoscopic bougienage).

All patients are recommended diet No. 1. It has sufficient energy value (daily calorie content up to 3000 kcal) and a balanced ratio of essential nutrients. Vegetable soups, cereals, vegetables, herbs, lean meats, fish, dairy products, eggs, baked pies, etc. are allowed. Dishes should not irritate the esophageal mucosa, be hot or too cold. Pureed products with a mushy consistency are recommended. Number of meals: 5-6.

To improve the motility of the esophagus, stomach, prokinetics are prescribed. These funds prevent stagnation of food, increase the amplitude of contraction of the esophagus, and contribute to the rapid healing of erosions. Means do not affect the secretory function of the stomach. They have an antiemetic effect. Not recommended for long-term use, tk. can cause various side effects: drowsiness, anxiety, headache, weakness, etc.

Motilium

A well-known drug of the prokinetic group. Reduces the severity of dyspeptic symptoms (heartburn, bloating, belching, nausea, etc.) by accelerating the evacuation of the food bolus into the duodenum. It is also used to stop vomiting. It is recommended to take 1 tablet 15 minutes before meals. Contraindicated in gastrointestinal bleeding, pregnancy, lactation, mechanical intestinal obstruction.

Prevention of vascular pathologies of the esophagus

The main symptom of vascular disease of the esophagus is esophageal bleeding. It occurs as a result of injury to an organ or a nearby large vessel, compression of the portal vein by tumors, cirrhosis, etc. Violation of the outflow and stagnation of blood in the vascular system of the esophagus leads to various pathologies, such as varicose veins.

The basis of prevention is the timely treatment of pathologies that provoke vascular disease of the esophagus. To stop bleeding, hemostatic drugs are prescribed, for example, Pituitrin.

Pituitrin

The tool narrows the capillaries, regulates the constancy of osmotic pressure. It is administered intravenously drip 10 U in 200 ml of glucose solution (5%) or sodium chloride. Contraindicated in severe atherosclerosis, high blood pressure, thrombophlebitis.

It is also recommended to abandon heavy physical exertion, weight lifting, because. they create high pressure on the internal organs, which can cause bleeding. You can not take drugs that can cause bleeding for a long time, for example, antiplatelet agents - they are taken to prevent thrombosis (Aspirin, Upsarin Upsa, etc.).

Treatment

Prevention of the esophagus - symptoms, methods and recommendations

With the appearance of any pathology of the esophagus, diet is required. Detailed recommendations regarding treatment should be provided by a gastroenterologist after a comprehensive examination. According to the results, the doctor chooses the tactics of further therapy - hospitalization with surgery or taking medications:

• antibiotics - prevent the attachment and spread of pathogenic bacterial microflora;
• anticholinergics - suppress the secretion of hydrochloric acid, increase the protective properties of the mucous membrane of the digestive tract, reduce peristalsis and tone of the digestive tract;
• antispasmodics - eliminate attacks of spastic pain, relax smooth muscles, etc.) or.