Gerb treatment. Gastroesophageal reflux disease (GERD): what is it, treatment, symptoms, causes, signs. Disease in children

Gastroesophageal reflux is the reflux of gastric (gastrointestinal) contents into the lumen of the esophagus. Reflux is called physiological if it appears immediately after eating and does not cause obvious discomfort to a person. If reflux occurs often enough, at night, accompanied by unpleasant sensations - we are talking about a pathological condition. Pathological reflux is considered within the framework of gastroesophageal reflux disease.

Hydrochloric acid has an irritating effect on the mucous membrane of the esophagus and provokes its inflammation. Prevention of damage to the esophageal mucosa is carried out by the following mechanisms:

1. The presence of a gastroesophageal sphincter, the contraction of which leads to a narrowing of the lumen of the esophagus and obstruction of the passage of food in the opposite direction;
2. Resistance of the mucous wall of the esophagus to gastric acid;
3. The ability of the esophagus to cleanse itself of abandoned food.

When any of these mechanisms is disturbed, there is an increase in the frequency as well as the duration of refluxes. This leads to irritation of the mucous membrane with hydrochloric acid, followed by the development of inflammation. In this case, we should talk about pathological gastroesophageal reflux.

How to distinguish physiological gastroesophageal reflux from pathological?

Physiological gastroesophageal reflux is characterized by the following symptoms:

• Occurrence after eating;
• No associated clinical symptoms;
• Low frequency of reflux per day;
• Rare episodes of reflux at night.

Pathological gastroesophageal reflux is characterized by the following symptoms:

• The occurrence of reflux and outside the meal;
• Frequent and prolonged refluxes;
• The appearance of reflux at night;
• Accompanied by clinical symptoms;
• Inflammation develops in the mucosa of the esophagus.

Reflux classification

Normally, the acidity of the esophagus is 6.0-7.0. When gastric contents, including hydrochloric acid, are thrown into the esophagus, the acidity of the esophagus falls below 4.0. Such refluxes are called acidic.

With an acidity of the esophagus from 4.0 to 7.0, they speak of weakly acid reflux. And finally, there is such a thing as superreflux. This is acid reflux, which occurs against the background of an already reduced acidity level of less than 4.0 in the esophagus.

If gastrointestinal contents, including bile pigments and lysolecithin, are thrown into the esophagus, the acidity of the esophagus rises above 7.0. Such refluxes are called alkaline.

Causes of GERD

Gastroesophageal reflux disease (GERD) is a chronic disease caused by spontaneous and systematically repeated throwing of gastric (gastrointestinal) contents into the esophagus, leading to damage to the esophageal mucosa.

The development of the disease is influenced by eating habits and the nature of nutrition. The rapid absorption of a large amount of food with the swallowing of air leads to an increase in pressure in the stomach, relaxation of the lower esophageal sphincter and reflux of food. Excessive consumption of fatty meat, lard, flour products, spicy and fried foods leads to a delay in the food bolus in the stomach and even an increase in intra-abdominal pressure.

The symptoms that appear in GERD can be divided into two subgroups: esophageal and extra-esophageal symptoms.

Esophageal symptoms of gastroenterologists include:

• heartburn;
• belching;
• regurgitation;
• Sour;
• Swallowing disorder;
• Pain in the esophagus and epigastrium;
• hiccups;
• Sensation of a lump in the chest.

Extra-esophageal lesions occur due to the ingress of the refluctant into the respiratory tract, the irritating effect of the refluctant, activation of the esophagobronchial, esophagocardial reflexes.

Extraesophageal symptoms include:

• Pulmonary syndrome (cough, shortness of breath mainly occurring in a horizontal position of the body);
• Otorhinolaryngopharyngeal syndrome (development, rhinitis, reflex apnea);
• Dental syndrome (, rarely aphthous stomatitis);
• Anemia syndrome - as the disease progresses, erosions form on the mucous membrane of the esophagus, accompanied by chronic blood loss in a small amount.
• Cardiac syndrome (,).

Complications of GERD

Of the most common complications, it is worth highlighting the formation of esophageal stricture, ulcerative erosive lesions of the esophagus, bleeding from ulcers and erosions, and the formation of Barrett's esophagus.

The most formidable complication is the formation of Barrett's esophagus. The disease is characterized by the replacement of normal squamous epithelium with a cylindrical gastric epithelium.

The danger is that such metaplasia significantly increases the risk of esophageal cancer.

In the first few months of life, gastroesophageal reflux is normal. Infants have certain anatomical and physiological features that predispose to the formation of reflux. This is an underdevelopment of the esophagus, and low acidity of gastric juice, and a small volume of the stomach. The main manifestation of reflux is regurgitation after feeding. In most cases, this symptom resolves itself by the end of the first year of life.

When hydrochloric acid reflux damages the lining of the esophagus, GERD develops. In infants, this ailment manifests itself in the form of anxiety, tearfulness, excessive regurgitation, turning into profuse vomiting, hematemesis, coughing can be observed. The child refuses food, gains weight poorly.

GERD in older children is manifested by heartburn, pain in the upper chest, discomfort when swallowing, a feeling of food stuck, and a sour taste in the mouth.

Diagnostics

Different methods are used to diagnose gastroesophageal reflux disease. First of all, if GERD is suspected, an endoscopic examination of the esophagus should be performed. This method allows you to identify inflammatory changes, as well as erosive and ulcerative lesions on the mucous membrane of the esophagus, strictures, areas of metaplasia.

Also, patients undergo esophagomanometry. The results of the study will allow you to get an idea about the motor activity of the esophagus, changes in the tone of the sphincters.

In addition, patients should undergo daily monitoring of esophageal ph. Using this method, it is possible to determine the number and duration of episodes with abnormal esophageal acidity, their relationship with the onset of symptoms of the disease, food intake, changes in body position, and medication.

Treatment

In the treatment of GERD, medical, surgical methods are used, as well as lifestyle correction is carried out.

Medical treatment

Drug therapy is aimed at normalizing acidity, as well as improving motor skills. The following groups of drugs are used:

• Prokinetics (domperidone, metoclopramide)- to increase the tone and reduce the lower esophageal sphincter, improve the transport of food from the stomach to the intestines, reduce the number of refluxes.
• Antisecretory agents(proton pump inhibitors, H2-histamine receptor blockers) - reduce the damaging effect of hydrochloric acid on the esophageal mucosa.
• Antacids(phosphalugel, almagel, maalox) - inactivate hydrochloric acid, pepsin, adsorb bile acids, lysolecithin, improve esophageal cleansing.
• Reparants(sea buckthorn oil, dalargin, misoprostol) - accelerate the regeneration of erosive and ulcerative lesions.

Surgery

Surgical intervention is resorted to with the development of complications of the disease (strictures, Barrett's esophagus, reflux esophagitis III-IV degree, ulcers of the mucous membrane).

Surgery is also considered as an alternative if GERD symptoms fail to improve with lifestyle changes and medication.

There are various methods of surgical treatment of the disease, but in general their essence is to restore the natural barrier between the esophagus and stomach.

To consolidate the positive result of the treatment, as well as to prevent the occurrence of recurrence of the disease, the following recommendations should be followed:

• The fight against excess weight;
• Stop smoking, alcohol, caffeinated drinks;
• Limiting the use of products that increase intra-abdominal pressure (carbonated drinks, beer, legumes);
• Restriction of the use of products with acid-stimulating action: flour products, chocolate, citrus fruits, spices, fatty and fried foods, radish, radish;
• You should eat in small portions, chewing slowly, do not talk while eating;
• Limitation of heavy lifting (no more than 8-10 kg);
• Raising the head of the bed ten to fifteen centimeters;
• Limiting the intake of medications that relax the esophageal sphincter;
• Avoiding lying down after eating for two to three hours.

Grigorova Valeria, medical commentator

Dysfunction of the esophagus, causing acid imbalance, has a negative impact not only on the upper gastrointestinal tract. Information about atypical clinical manifestations of gastroesophageal reflux disease (GERD) will help to choose an adequate therapeutic approach and prevent the development of complications.

Reflux is the physiological act of getting the contents of the stomach or the flow of gastric juice into the lower esophagus. A portion of a liquid or food slurry that has not been used for its intended purpose is called reflux. This phenomenon provokes excess pressure created in the stomach by food masses and (or) gases.

Under normal physiological conditions, gastric contents securely hold a special muscular valve at the border with the esophagus, the so-called lower esophageal sphincter (LES). The tone of the LES is regulated by fluctuations in the acidity of gastric juice: alkalization contributes to its disclosure and vice versa.
The main causes of reflux and the development of gastroesophageal reflux disease are:

• weakening of the motor functions of the esophagus;
• low muscle tone of the LES;
• excessive intra-abdominal pressure;
• disorders of gastric peristalsis;
• increased acidity of gastric juice.

These circumstances cause prolonged "acidification" of the esophagus, especially its lower section, and mucosal lesions. A feeling of constant heartburn or recurring attacks of heartburn suggest the development of GERD.

Symptoms of pathology

LPS deficiency is the root cause of the painful symptoms of GERD: both typical (heartburn, belching, and damage to the esophageal walls), clearly associated with the digestive tract, and atypical, associated with impaired respiratory functions - the so-called pulmonary symptoms of GERD.

Heartburn

The mucous membranes of the esophagus and stomach, although they are called the same, have a completely different structure and purpose. The ingress of acidic gastric juice on the esophageal walls is not a physiological norm. On the contrary, it becomes a sharp traumatic factor, leading to a burn.

A burning sensation in the sternum - heartburn - is a classic symptom of GERD, evidence of a persistent lesion of the esophageal walls, and the more extensive it is, the stronger and longer the attacks of heartburn. IN individual cases the course of GERD does not cause inflammatory changes in the esophageal mucosa. The acidity of the reflux is crucial.

Prolonged irritation of the walls of the esophagus, causing constant heartburn, is an alarming symptom of GERD. In the future, it can lead to the formation of ulcerative lesions, the gradual thinning of the esophageal walls and their perforation (rupture). In such cases, urgent surgery is the only chance to save a person's life.

Belching

Often, dysfunction of the LES is accompanied by the release of gastric gases from the esophagus. This phenomenon occurs when the larynx is closed and is called belching. The volume of gas reflux is much greater than liquid reflux, as is the pressure it creates in the stomach. Gas reflux can cause the upper esophageal sphincter to open, reaching the larynx and even the oral cavity. This causes symptoms of GERD that at first glance have nothing to do with the digestive system.

In the case of reflux of gastric contents, the eructation has a pronounced sour taste. When reflux is cast from the duodenum, the bitter taste of eructation is due to the presence of bile acids and trypsin (pancreatic secretion).

Bile reflux is evidence of insufficiency of the lower valve of the stomach (pylorus), which separates the duodenum from the stomach, as well as diseases of the biliary tract.

Heartburn and chronic belching are typical but not the only symptoms of GERD. The adaptive reaction of the body to prolonged irritation of the mucosa becomes the degeneration of the tissues of the esophageal walls: their thickening, scarring, leading to a narrowing of the lumen of the esophagus, cell metaplasia.

Esophageal obstruction

The consequence of inflammatory processes is tissue scarring and narrowing (stricture) of the esophagus, which makes it difficult to move food masses, causing swallowing disorders (dysphagia). Over time, the movement of the food bolus begins to cause discomfort and pain when swallowing (odynophagia).

The causes of odynophagia, in addition to GERD, can also be:

• esophagitis of an infectious nature (fungal or viral lesions);
• tumors of the esophagus;
• chemical injuries of the esophageal walls.

In some cases, obstruction of the esophagus develops, leading to death from starvation.

Formation of a diverticulum

In some cases, a local expansion is formed over the site of narrowing of the esophagus, where food begins to accumulate. The greater the volume of accumulated food mass, the more the esophagus expands and its walls stretch. Part of the wall, consisting of submucosal and mucous tissue, protrudes in the form of a hernia - a diverticulum.

Which has a thin muscle layer, sometimes completely absent. Most often, diverticula form on the posterior wall of the esophagus. In the protruding part of the wall, food accumulates and an inflammatory process develops, which is accompanied by pain, bad breath and periodic regurgitation. In the event of a rupture of the diverticulum, the contents enter the surrounding tissues, the chest cavity, leading to tragic consequences.

Barrett's esophagus

Degeneration (metaplasia) of cells is a protective reaction of the body to regular damage to the upper layer of the esophageal mucosa. The lower third of the esophageal tube is most often affected.

The mucosal cells formed as a result of regeneration (recovery) are not identical to the former cells typical of this type of tissue. They are called atypical cells. The presence of such cells is a symptom of Barrett's esophagus, the first step towards the occurrence of malignant tumors, such as adenocarcinoma of the esophagus or stomach.

Congestion in the stomach: cause and effect of GERD

Digestive disorders in the stomach are caused by disorders of its motor activity. Depending on the nature of these disorders, the release of the stomach from the food mass can slow down or accelerate.

Reasons for slowing down the evacuation of food and stagnation in the stomach:

1. spasm of the pylorus caused by disorders of the nervous regulation of its muscles;
2. pyloric spasm caused by reflex irritations from other organs;
3. organic changes in the pylorus (presence of ulcers, scars, tumors, compression);
4. increased acidity of gastric juice;
5. relaxation of the stomach (atony).

Stagnation of food masses causes their bacterial decomposition. The accumulation of gases and decay products irritates the gastric mucosa, causing heartburn, a feeling of heaviness and fullness, and reflux phenomena. Abnormally rapid satiety, bloating, foul-smelling belching, and nausea are gastric symptoms of GERD.

The peristalsis of the stomach depends on the nature of the food, its temperature, consistency, and the presence of components that irritate the mucous membranes. For example, fatty acids and fat reduce the intensity of peristaltic waves, leading to a decrease in stomach tone.

Achalasia

Insufficient relaxation (persistent spasm of the LES) is a chronic disease - achalasia. It also leads to violations of the patency of the esophagus and the expansion of certain parts of it. Progressive achalasia leads to the development of inflammation of the esophageal mucosa (esophagitis) and heartburn. heartburn in this case is not associated with GER, but with the formation of lactic acid as a result of the decomposition of food blocked in the esophagus.

Paradoxically, both insufficient and excessive relaxation of the LES causes similar symptoms:

• heartburn;
• rotten belching;
• chest pain;
• nausea;
• discomfort in the epigastric region;
• increased salivation.

Increased salivation

Increased salivation (hypersalivation) can cause inflammation in the oral cavity. But more often it is observed with reflex irritations of special secretory nerves by reflux products, it is a companion of inflammatory processes of the digestive tract, especially the abdominal organs.

Excessive salivation affects the formation of a bolus (a lump of food) and its impregnation with salivary mucus. A pathological increase in the amount of saliva neutralizes the acid reaction of gastric juice, reduces the intensity of gastric digestion, stimulates the development of fermentation, putrefaction, and further complicates the course of GERD.

Similar clinical symptoms: diagnostic difficulties

Chest pain in violation of the esophagus occurs in about half of the cases. It is associated with spasms of the muscular layer of the esophagus or pressure of voluminous food boluses in its expanded part. Sometimes pain is localized between the shoulder blades, simulating angina pectoris. Sometimes pain also radiates to the lower jaw and neck. The difference between chest pain associated with GERD and heart pain is that they depend on the position of the body, food intake and are copied by soda or alkaline mineral water.

Ischemic heart disease (CHD) occurs due to a lack of blood supply to the main heart muscle - the myocardium. One of the main symptoms is shortness of breath and chest pains of varying intensity and localization. The general innervation of the chest organs explains the similar nature of pain in GERD and coronary artery disease, complicates differential diagnosis, the choice of a therapeutic scheme and preventive measures.

The course of GERD may be accompanied by symptoms that at first glance are not associated with the gastrointestinal tract. Chronic (the so-called gastric) cough, discomfort when inhaling, dry wheezing in the lungs, shortness of breath and other respiratory disorders are a manifestation of the esophagotracheobronchial (for simplicity, let's call it a cough) reflex caused by the ingress of gastric contents into the respiratory tract.

Additional Information! Vagus receptors "react" to an irritant only in the presence of inflammatory changes in the mucosa, so the cough reflex and asthma attacks are not stimulated by physiological reflux.

To establish the cause of the cough and determine the method of treatment, the completeness of the anamnesis is of key importance. To date, two main causes of the cough reflex are known:

1. Irritation by gastric contents of special (vagal) receptors located in the lower esophagus. A cough of this etiology precedes the appearance of "classic" symptoms of GERD, it is dry, prolonged (up to several years) and greatly complicates the course of SARS.
2. Irritation of the receptors of the larynx, trachea and bronchi when reflux microparticles enter them (microaspiration). In this case, the typical symptoms of GERD occur more frequently and precede respiratory distress. As a result of irritation of the mucous membranes, signs of inflammation of the larynx, damage to the vocal cords appear: hoarseness, weakness of the voice, falsetto.

See a doctor immediately

The reason for a visit to the doctor is regular bouts of heartburn, pain, fetid belching, prolonged cough of an unknown nature, frequent pneumonia.

As well as coughing, vomiting blood, progressive weakness, weight loss, black stools.

The benign nature of the symptoms can only be assessed by a qualified specialist.

Note! Dysfunctions of the immune system sometimes provoke the development of eosinophilic esophagitis, similar in symptoms to GERD. Under these conditions, therapy with secretion-regulating drugs becomes ineffective.

The positive dynamics of the disease is caused by hormonal antiallergic drugs and a strict diet.

Treatment

Diagnosis of GERD involves antireflux therapy. The most informative and sensitive diagnostic method is daily pH-metry.

The main directions of drug therapy for GERD:

• restoration of esophageal motility (self-cleaning ability);
• decreased acidity reflux;
• protection of the esophageal mucosa (anti-inflammatory therapy);
• reduction in the number and duration of refluxes.

Drugs called histamine H 2 receptor blockers are not intended to prevent the phenomenon of reflux, but to reduce the acidity of the food mass at the time of its reflux into the esophagus. Before the advent of proton pump inhibitors (PPIs), they were the mainstay of treatment for GERD.

The most used blockers are cimetidine, ranitidine, nizatidine, famotidine. The effectiveness of drugs reduces their selective effect on one type of receptor, while acid production is stimulated by three of their varieties.

Attention! The abrupt cancellation of blockers can provoke a “recoil” - a jump in acidity.

Prokinetics are drugs that stimulate the motility of the esophagus and stomach. Domperidone, cisapride, metoclopramide are more effective in the initial stage of the disease, especially in combination with blockers.

Prolonged and effective suppression of gastric acidity is provided by PPIs, therefore they are the basis of the therapeutic regimen: these are rabeprazole, lansoprazole, omeprazole, esomeprazole (Nexium). The regimen and dosage depends on the set and severity of symptoms, but the first daily intake is indicated half an hour before meals. The drugs of this group retain a long-term therapeutic concentration in the blood, and the maximum therapeutic effect is achieved on the 2nd-3rd day of administration.

The mucosal protection function is performed by antacids (Maalox, Almagel, Phosphalugel), designed to quickly relieve the unpleasant symptoms of GERD in case of a diet or excessive physical exertion, to stop occasional attacks of heartburn.

To reduce the frequency and duration of GERD symptoms, alginic acid preparations - alginates are widely used. Reacting with stomach acid, alginates form a gel-like viscous mass that makes reflux impossible. It envelops the walls of the stomach and has a neutral reaction. One of the most popular drugs in this group is Gaviscon Forte.

When medical methods of treatment do not bring results, as well as in the event of complications that are life-threatening for the patient, surgical methods of treatment are used - gastric fundoplication (laparoscopic or open), as well as the elimination of anatomical defects in the form of hiatal hernia as the cause of GERD.

Prevention

Prevention of GERD, like its treatment, is long-term and requires an integrated approach. Long-term remission of the disease is possible only with strict adherence to the diet and a radical change in lifestyle: a complete cessation of smoking and reasonable physical activity are necessary. Losing weight reduces the risk of hiatal hernia.

A high-protein diet and minimal (about 45 g per day) fat intake is shown. Products that irritate the gastric mucosa and stimulate acidity should be excluded from the diet. These are alcohol, spices, chocolate, coffee, carbonated drinks, sour fruits.

Food should be taken in small portions and no later than 2 hours before bedtime.

Tight uncomfortable clothing, excessive physical activity after eating impede the motility of the gastrointestinal tract, reduce the function of the LES as one of the regulators of the balance of the digestive system.

Under gastroesophageal reflux disease, a number of conditions are combined in which there is a reflux of acidic gastric contents from the stomach into the esophagus. Contact with such an aggressive acidic content on the esophageal mucosa can lead to inflammation and swelling. This state is called esophagitis, and in some patients this occurs without a visible change in the state of the mucosa. The contents of the stomach thrown into the esophagus contain hydrochloric acid and pepsin, an enzyme produced by the stomach lining to break down and digest proteins. This fluid may also contain bile that enters the lumen of the stomach from the duodenum during reflux (pathological, reverse of the normal movement of food, throwing). Among the three components of the gastric "juice" the most aggressive and damaging to the mucosa of the esophagus is hydrochloric acid.

GERD is a chronic condition. This is due to the fact that as soon as it appears in a person, it immediately acquires a permanent character and follows the patient for the rest of his life with episodes of renewal and attenuation. The chronic variant of the course is still confirmed by the resumption of the condition several months after the end of treatment, despite its regular nature. In most cases, patients have to adhere to recommendations for drug treatment for the rest of their lives, although there is a category of patients in whom GERD is episodic and there are no signs of severe esophagitis. For such patients, gastroenterologists recommend performing appointments during an exacerbation of gastroesophageal reflux disease (GERD).

In principle, the reflux of the acidic contents of the stomach into the esophagus occurs and is normal. So one of the clinical studies revealed that the frequency of reflux of gastric juice into the esophagus is almost the same in healthy people and patients with gastroesophageal reflux. However, it was found that the content that entered the esophagus in patients with GERD contains a greater amount and concentration of hydrochloric acid, compared with healthy people, and this acid lingers longer in the lumen of the esophagus. In addition, it is known that there are various protective mechanisms against gastroesophageal reflux. Among them, the effect of gravity should be singled out, according to which during the daytime the fluid moves in the direction from the esophagus to the stomach, which makes it difficult to delay and accumulate aggressive contents in the esophagus.

Gastroesophageal reflux and heartburn (video animation)

The second mechanism is the constant swallowing of saliva, which recreates a kind of flowing version of the movement of liquids towards the stomach. The third defense mechanism implies that due to the content of bicarbonates in saliva, those small amounts of gastric acid contents that still enter the esophagus are neutralized. But it should be recalled that the action of these protective mechanisms applies only to the daytime, when a person is most of the time in an upright position. At night, during sleep, these factors somewhat lose their protective power, as a person moves from a vertical position to a horizontal one. This leads to the fact that the fluid from the stomach thrown into the esophagus has the prerequisites for a longer stay there, which accordingly makes damage to the esophageal mucosa more likely.

A number of human conditions make him more susceptible to the damaging effects of gastric juice. For example, when an elevated level of hormones adversely affects the obturator function of the esophagogastric (between the esophagus and stomach) sphincter, as a result, a greater reflux of gastric contents. Plus, the positive pressure of the fetus on the stomach affects, which leads to an increase in pressure in its lumen, which also contributes to the movement of gastric juice into the esophagus. There are also diseases such as scleroderma or any other connective tissue pathology that leads to damage to the muscular layer of the esophagus and, accordingly, weakening the function of its lower valve. This again leads to an increase in the reflux of acidic contents up into the esophagus and the development of gastroesophageal reflux disease.

Fig.1 The mechanism of development of reflux disease

What causes the development of gastroesophageal reflux?

The reasons for the development of gastroesophageal reflux disease are different. Moreover, one patient may have several of them at once. In the majority of patients with GERD, the leading cause of its development is the production of excess amounts of gastric juice and hydrochloric acid. However, for a separate category of patients, this condition does not cause inconvenience and excess amounts of hydrochloric acid produced do not have significant effects. Among the factors that to some extent have a predisposing effect on the development of a condition characterized by gastroesophageal reflux, the following are distinguished: impaired activity of the lower esophageal sphincter, hernia of the esophageal opening of the diaphragm, impaired peristalsis of the muscular wall of the esophagus and impaired evacuation of food from the stomach.

Violation of the obturator function of the lower esophageal sphincter

The activity of the lower esophageal sphincter is considered to be a key protective mechanism to prevent the reflux of gastric contents into the esophagus. The esophagus is a hollow organ, the wall of which contains a large number of muscle fibers. The contraction of the muscular layer of the esophagus (in other words, peristalsis) allows you to move food (food bolus) from the pharynx to the stomach. In several places, the accumulation of muscle tissue in the wall of the esophagus forms special muscle sphincters, or otherwise muscle sphincters, often located at the transition sites of one section of the digestive tract to another. The lower esophageal sphincter is located at the junction of the esophagus to the stomach. This formation is constantly in a closed state, and only when passing through the sphincter of food, it relaxes for a few seconds, skipping the food lump, and closes again. It is the constant presence of the sphincter in a state of tone that prevents the reflux of aggressive gastric contents.

There are several different disorders of the activity of the lower esophageal sphincter, among which the most common are abnormally weak (incomplete) closure of the sphincter and the so-called transient (periodic) pathological relaxation of the sphincter for a long (up to several minutes) time. The first creates conditions for the constant reflux of gastric juice into the esophagus. The second violation leads to an increase in the time of exposure of gastric contents to the esophageal mucosa, and, as a rule, there is no correct ratio of the interaction of swallowing movements and the work of the sphincter. Such transient disturbances are associated with the overflow of the stomach with food.

hiatal hernia (hiatal hernia)

So far, the mechanism of the formation of gastroesophageal reflux in the presence of a hiatal hernia in a patient is not fully known. It is known that the majority of patients with GERD have a diagnosed hiatal hernia. However, its presence does not guarantee that the patient will definitely develop reflux disease.

Fig. 2 Hernia of the esophageal opening of the diaphragm

The lower esophageal sphincter is usually located just at the point of transition of the esophagus into the stomach from the chest to the abdominal cavity, through the diaphragmatic opening. The diaphragm is exactly that muscular formation that separates the chest from the abdomen. When a hiatal hernia occurs, the upper part of the stomach moves through an inconsistent, underdeveloped diaphragm into the chest. With this movement, the lower esophageal sphincter is also displaced, which is no longer in close contact with the diaphragm. Accordingly, their joint work to prevent the reflux of gastric contents into the esophagus is disconnected. They work separately, and this is a determining factor in the development of gastroesophageal reflux. There is a kind of division of one powerful barrier into two isolated and weaker ones, which significantly increases the likelihood of reflux of gastric masses.

The second point, which can also contribute to the development of GERD in diaphragmatic esophageal hernia, is the formation of a kind of hernial sac, limited on the one hand by the sphincter of the esophagus, and on the other hand by compression of the stomach moved into the chest by the diaphragm (see figure). At the same time, it turns into a kind of trap for gastric contents. As a result of the disconnected inconsistent work of the esophageal sphincter and the sphincter of the diaphragm, it is possible to throw gastric juice from this sac into the esophagus, which leads to the development of reflux esophagitis.

There is also a third mechanism, which is also considered important in terms of the development of reflux in hiatal hernia. With a normal structure, the esophagus passes into the stomach at a certain angle, while forming a kind of valve. It is an additional barrier. When a hernia occurs, this angle, and, accordingly, the protective sash disappear.

Violation of the peristalsis of the muscular wall of the esophagus

As mentioned earlier, the existence of swallowing movements and the movement of saliva through the esophagus is one of the protective mechanisms that allows you to passively remove physiologically (occurring under normal conditions) acid thrown into the esophagus. During swallowing, a wave of successive contractions of the muscular layer of the esophagus is formed, through which the food bolus or saliva moves from the upper parts of the esophagus to the lower parts, and further to the stomach. These muscle contractions are called peristalsis.

Violation of these peristaltic movements leads to a violation of the full evacuation (removal) of abandoned acid back into the stomach. There are two types of peristalsis disorders. In the first type, peristaltic movements die out before the food bolus or saliva reaches the stomach. In the second variant, peristalsis is too weak to carry out adequate movement of food through the esophagus. As a result, both of these disorders are an important predisposing factor to the development of severe gastroesophageal reflux disease. There is evidence of an adverse effect of smoking on esophageal motility. For example, scientists have found a decrease in the strength and intensity of peristaltic movements for at least 6 hours after smoking a cigarette.

Violation of the evacuation of food from the stomach

Most often during the day, the development of reflux occurs after eating. This reflux occurs due to a transient relaxation of the lower esophageal sphincter caused by overdistension (distension) of the overstuffed stomach. Approximately 20% of patients with GERD had impaired evacuation of food from the stomach into the duodenum. Accordingly, the more food is in the stomach, the greater the likelihood of reflux of gastric contents into the esophagus and the development of reflux esophagitis.

What are the symptoms of reflux esophagitis?

Signs of gastroesophageal reflux include primarily heartburn, belching (regurgitation - reverse reflux) and nausea. Other symptoms occurring in this disease are regarded as complications.

Heartburn

When acidic gastric contents enter the esophagus, irritation of the nerve fibers located in the mucosa occurs. This irritation forms a kind of pain impulse, similar to a burning sensation in the esophagus. It just bears the name of heartburn. Sometimes heartburn can be quite intense, and is characterized by sharp pain in the chest, usually behind the breastbone, or in the upper abdomen. In such a situation, doctors have to differentiate it from pain that occurs with cardiac pathology, for example, with angina pectoris.

Since the appearance of gastroesophageal reflux is typical after a meal, this time is most typical for the onset of heartburn. Especially often heartburn occurs when the patient takes a horizontal position after eating, which increases the time the acid stays in the esophagus. It happens that some patients wake up due to pain caused by heartburn at night.

Belching (regurgitation - reverse reflux)

Belching is the appearance in the oral cavity of the contents of the stomach, which arose there as a result of reflux. In most patients with reflux, reflux occurs to the level of the lower esophagus, and the contents are in them in small quantities. However, when more gastric contents are refluxed, sometimes even with food, reflux reaches the upper esophagus and oral cavity.

In the upper part of the esophagus is the upper esophageal sphincter, which is a muscular ring similar in function to the lower esophageal sphincter. It also prevents reflux of contents into the pharynx and oral cavity. But sometimes, if there is a violation of the coordination of peristaltic waves in the esophagus, this muscle pulp does not work correctly and small amounts of reflux fluid still enter the higher located departments. As a result, the taste buds of the oral cavity recognize the acidic environment of the content, which has a characteristic sour taste. Sometimes, with a pronounced reflux, a significant amount of abandoned liquid appears in the oral cavity, possibly even with an admixture of food masses. This condition usually occurs with a combination of causes that cause gastroesophageal reflux and with already expressed disorders.

Nausea

Nausea is not a typical symptom of GERD. However, in some patients, it can be a fairly frequent and pronounced manifestation of gastroesophageal reflux. Severe nausea can lead to vomiting. Symptoms such as unexplained nausea and vomiting are important conditions requiring further evaluation for gastroesophageal reflux disease.

What are the complications of gastroesophageal reflux disease?

Esophageal ulcers

Acidic gastric contents, getting into the esophagus, cause damage to its mucous membrane lining the inner lumen. The body responds to this damage with an inflammatory response in the form of esophagitis. The main goal of any inflammation is to neutralize the damaging agent and initiate the tissue healing process. If the damaging effect is too pronounced, then an ulcer or ulcerative defect of the esophageal mucosa is possible. It is a local (in a certain place) damage and destruction of the mucosa resulting from inflammation. However, further spread of the inflammatory process deep into the wall of the esophagus is possible, as a result, this ulcerative defect reaches and damages the walls of the vessels supplying the esophagus. This is fraught with the development of a rather formidable complication of ulcer formation - ulcer bleeding.

Sometimes the degree of this bleeding is very serious and may require the following measures:

• blood transfusions,
• performing an endoscopic stop of bleeding (a gastroduodenoscope is inserted into the lumen of the esophagus through the mouth, which allows you to identify the place of this bleeding, its intensity and take therapeutic measures to stop it), or
• even surgery.

Formation of strictures

Esophageal ulcers sometimes heal with formation scars(fibrosis, fibrous process, stricture). Over time, due to constant ulcer formation and subsequent cicatricial process, the lumen of the esophagus narrows, which is called a stricture. As a result of the narrowing of the lumen, the patency of the esophagus for food is disturbed, and this entails a number of unpleasant consequences. There is a need for endoscopic removal of stuck food, expansion of the lumen of the esophagus, etc. This creates significant discomfort for the patient. The only way to prevent the formation of esophageal stricture is the prevention and treatment of gastroesophageal reflux.

Barrett's esophagus

Prolonged and / or severe gastroesophageal reflux leads to a change in the structure of mucosal cells, as a result of which the cells lose their normal division pattern and this division becomes malignant. This condition is referred to in clinical medicine as Barrett's esophagus, is precancerous and occurs in approximately 10% of patients with gastroesophageal reflux disease. Type esophageal cancer directly associated with Barrett's esophagus is called adenocarcinoma. The truth is still not entirely clear why some patients with reflux develop cancer, while others do not.
The diagnosis of Barrett's esophagus is usually confirmed endoscopically and by microscopic evaluation of the cell structure of the esophageal mucosa. To do this, a biopsy of the mucosa is performed, which allows you to see precancerous changes and select the necessary preventive treatment that will not allow this condition to turn into cancer. For patients with Barrett's esophagus, this procedure is performed regularly to assess the dynamics of the process of changes in the mucosa. Of course, the main direction of this prevention is the selection of therapy necessary to suppress the effects of gastroesophageal reflux. Currently, the most effective treatment for Barrett's esophagus is surgery. However, the effectiveness of endoscopic methods for removing pathologically altered mucosa has recently been evaluated. For complete information about this disease, you can read the article Barrett's esophagus.

Cough and bronchial asthma

A large number of nerves adjoin the lower esophagus. So, for example, some of them, when stimulated by gastric contents thrown into the esophagus, lead to pain or heartburn. Irritation of other nerves can lead to the development of a cough. Thus, the backflow of gastric contents can provoke a cough without entering the pharynx or oral cavity. When the nerves innervating the bronchi are irritated, a reduction in the lumen of the small bronchi and the development of an attack may occur.

It happens that GERD is the cause of an unexplained cough. Also, gastroesophageal reflux can provoke an attack of bronchial asthma in a patient already suffering from this disease. The very mechanism of the irritating effect of reflux has not yet been fully understood, but the fact that it predisposes to the development chronic cough and asthma is a fact.

Inflammatory phenomena of the pharynx and larynx

They often result from the backflow of stomach contents past the upper esophageal sphincter, into the pharynx (pharynx) or larynx. This leads to constant irritation of the mucous membrane of these organs and the appearance of signs of inflammation, manifested by sore throat and hoarseness. However, finding a causal relationship between these conditions and GERD can be extremely difficult due to the many other factors that cause hoarseness (hoarseness).

Inflammation and infection of the lungs

The entry of reflux fluid into the larynx does not exclude the entry of its small amounts into the respiratory tract of the lungs. This process is called aspiration and can lead to coughing and choking. The adverse effect of aspiration masses on the mucosa of the trachea and bronchi leads to the appearance of inflammatory processes in the airways and the development of pneumonia. Aspiration pneumonia is one of the most dangerous types. pneumonia, since it very often proceeds with the development of rapidly progressive respiratory failure and requires immediate treatment in a hospital setting. This is also due to the high probability of infection due to the significant population of the gastrointestinal tract by various microorganisms. When persistent episodes of aspiration of small amounts of gastric contents into the respiratory tract occur, especially when they are not clinically manifest, slowly progressive sclerosis of the lung tissue occurs ( pulmonary fibrosis), which is often detected by X-ray examination. The most unpleasant thing is that an episode of aspiration can occur at night, when the mechanisms of passive protection of the lungs from getting into them of various pathological masses (cough reflex or relaxation of the upper esophageal sphincter) do not work or are poorly expressed.

Accumulation of pathological fluid in the sinuses and middle ear

The pharynx connects with various peripharyngeal cavity formations. These include the middle ear cavity, sinuses (maxillary, frontal). In its upper section, the pharynx is connected to the cavities of the middle ear by means of the Eustachian tubes. Under normal conditions, a certain amount of mucous secretion is secreted in these cavities, moisturizing the surface of the mucosa. At the point of departure of these tubes from the pharynx, the pharyngeal mucosa contains a significant amount of lymphatic tissue or the so-called adenoids. Contact with the mucous membrane of aggressive gastric contents leads to their increase. As a result of this enlargement, the adenoids block the opening of the Eustachian tube, which connects the middle ear to the pharynx, and this causes the accumulation of pathological fluid in the middle ear cavity. The same thing happens with the sinus cavities. This condition causes a feeling of discomfort and congestion in the sinuses and ears. More often abnormal accumulation of fluid in the middle ear and sinuses seen in children than in adults.

How is reflux esophagitis diagnosed?

Symptoms and effectiveness of therapeutic treatment

It is quite easy to suspect the existence of gastroesophageal reflux, the main complaint of patients is heartburn. It is described by patients as a burning sensation behind the sternum or upper abdomen, and appears after eating, as well as at night when a person moves to a horizontal position. To stop heartburn, patients themselves or on the recommendation of doctors take drugs that reduce the production of hydrochloric acid. This somewhat reduces the intensity of discomfort during heartburn, which can also be regarded as a diagnostic criterion indicating the presence of GERD. This approach to the treatment of reflux disease is absolutely wrong, despite the high efficiency of the therapy used in the relief of heartburn.

In this situation, "blind" treatment does not completely identify the cause of gastroesophageal reflux, and even more dangerous, you can miss such a condition as ulceration, and also not identify its cause. For example, it may be due to an infection called Helicobacter pylori(Helicobacter pylori), or taking non-steroidal anti-inflammatory drugs (for example, ibuprofen) that causes ulceration. Such findings somewhat change the tactics of treatment for gastroesophageal reflux.

Esophagogastroduodenoscopy (Endoscopy)

(EGDS, also called gastroscopy among the population) is one of the main methods for diagnosing gastroesophageal reflux disease. EGDS is the introduction into the lumen of the gastrointestinal tract of a special flexible optical system, which is called a gastroduodenoscope. As you progress, it is used to examine the mucosa of the esophagus, stomach and duodenum, and also evaluates a number of other parameters.

The esophagus, in most patients with clinical manifestations of gastroesophageal reflux, appears normal on endoscopy. However, sometimes the lining of the esophagus appears inflamed. This state is called esophagitis. In addition, if erosions (superficial defects of the esophageal mucosa) or ulcers (deeper mucosal defects) are detected, it is possible to speak with great confidence about the presence of gastroesophageal reflux disease in the patient. EGDS allows you to identify the complicated course of this disease, for example, the presence of ulcers, strictures of the esophagus or Barrett's esophagus. With such findings, it is necessary to supplement the study with a biopsy of the mucosa.

Esophagogastroduodenoscopy also makes it possible to diagnose and differentiate from GERD other pathologies of the gastrointestinal tract, such as cancerous neoplasms of the stomach or duodenum.

Fig. 3 Esophagogastroscopy with biopsy of the gastric mucosa

Biopsy

A biopsy of the esophageal mucosa, which is performed during esophagogastroduodenoscopy, is a fairly informative technique that evaluates the structure of the mucosa and detects damage to this membrane. However, its value in detecting esophagitis is not so significant. More often it is used to exclude or confirm oncological pathology of the esophagus, stomach or duodenum. Biopsy with endoscopy is the only way to confirm the diagnosis of Barrett's esophagus.

X-ray examination

Often before gastroscopy, an X-ray examination of the esophagus in GERD was performed earlier. When performing this study, patients were offered to drink a radiopaque preparation (barium mixture), which fills the lumen of the gastrointestinal tract, and the condition of the internal walls of the digestive tract, as well as its functional state, was assessed from the resulting picture. The disadvantage of X-ray contrast studies is the inability to positively diagnose gastroesophageal reflux with its help. It only allows to identify complications of this pathology, such as ulceration, strictures, or indirect signs that could indicate the possibility of reflux, for example, a violation of the evacuation of food from the stomach. Therefore, X-ray examination is a widely used method of additional examination of these patients.

Examination of the oral cavity, pharynx and larynx

As described above, the course of GERD can be complicated by the appearance of inflammation of the oropharynx and larynx, which forces patients to first contact an ENT doctor (otorhinolaryngologist) with complaints of cough, hoarseness, hoarseness, and frequent tonsillitis. The otorhinolaryngologist during examination reveals these inflammatory phenomena. Despite the fact that they are more often the cause of a respiratory infection, one should not forget about gastroesophageal reflux as one of the possible causes of infections of the oropharynx and upper respiratory tract. If the treatment prescribed by the ENT doctor is ineffective, you need to think about the reflux nature of the inflammation and redirect the patient to a gastroenterologist in a timely manner.

(pH - meter)

Study of the acidity of gastric juice or pH - meter considered the "gold standard" in the diagnosis of gastroesophageal reflux disease. As already mentioned, the appearance of reflux of gastric contents into the esophagus is also possible in healthy people. However, patients with gastroesophageal reflux often present with increased gastric acidity. Patients with GERD can be differentiated from healthy individuals by the time that this increased acidity persists in the lumen of the esophagus. Determining the residence time of gastric contents is possible thanks to a study called 24-hour esophageal pH-metry. During this study, a special catheter is placed in the lumen of the esophagus, at the tip of which there is a special sensor that measures the level of acidity. The other end of this catheter is connected to a recorder that records changes in acidity over time (usually 20-24 hours).

Sometimes there are problems with the interpretation of the data obtained, since it happens that in patients with clinical manifestations of GERD, there is no increased acidity or, conversely, in the absence of a clinical picture of the disease, increased acid production is determined. This situation requires a comparative analysis of changes in acidity with clinical manifestations and taking into account the effectiveness of ongoing drug therapy. So, if heartburn attacks correspond with an increase in acidity recorded with pH-metry, one can confidently assert the presence of gastroesophageal reflux disease.

pH-metry can also be used to evaluate the effectiveness of the treatment. With unsatisfactory results of treatment, this will allow you to correct the prescribed therapy or look for another reason for the onset of the symptoms of the disease. Thus, it is known that approximately 10-20% of patients do not respond with improvement in response to ongoing therapy. This requires an additional diagnostic search. Sometimes the lack of effect from the ongoing treatment is caused by advanced forms of the disease, in which it is necessary to resolve the issue of surgical correction of this pathology.

There are situations when patients with clinical manifestations, but the absence of confirmed gastroesophageal reflux, respond well to the treatment, and a placebo effect occurs (improvement in a non-existent pathology - the psychological effect of an imaginary improvement). It is especially important to identify this category of patients with the help of a study of gastric acidity before planning surgical treatment, since it is unlikely to be effective.
Relatively recently, a new method of long-term (up to 48 hours) measurement of acidity has appeared in clinical practice, which is the placement of a special wireless capsule in the lumen of the lower esophagus, the so-called capsule pH-metry. The capsule registers the level of acid in the esophagus and transmits this information to a receiver worn by the patient on the belt. After the scheduled study period, the information from the receiver is downloaded to a computer and analyzed by the examiner.

Of course, this research method has huge advantages over catheter pH-metry, mainly associated with the absence of discomfort caused by a catheter located in the nose and throat. In addition, it favorably reflects on the normal rhythm of human life. Another advantage is a longer recording period, which allows more reliable detection of changes in acidity.

However, there are several unresolved problems with the use of capsule pH metering, for example, sometimes there are problems associated with early detachment and migration of the capsule through the digestive tract or the lack of effective transmission of information to the receiver. Rarely there are unpleasant sensations, and even pain when swallowing. The solution of these technological problems will definitely make this study a key one in the diagnosis of diseases accompanied by gastroesophageal reflux and increased gastric acidity.

Examination of motility (peristalsis) of the esophagus

The study of the motility of the muscular layer of the esophagus, allows you to assess how well the muscles of the esophagus, in particular the muscles of the lower esophageal sphincter, work. To do this, a catheter is installed in the lumen of the esophagus, which registers the pressure exerted by the contraction of the sphincter on the sensor located at the end of the catheter. Registration is made at rest and with a sip of liquid. This allows you to evaluate the function of the esophageal sphincter at rest and when recreating peristaltic activity (reduction period).

First, such an assessment reveals those caused by abnormal function of the esophageal sphincter, clinically resembling the symptoms of GERD and not responding to ongoing treatment. Secondly, based on the results of this study, surgeons determine the indications for choosing one or another method of surgical treatment of gastroesophageal reflux disease.

Study of the evacuation function of the stomach

The study of the evacuation function of the stomach is a study that allows you to assess how timely the processed food comes from the stomach into the duodenum. Evacuation disorders are recorded in approximately 20% of patients with GERD. During this study, the patient is allowed to take food labeled with a radioactive, but absolutely harmless to the human body, substance, and the readings are recorded using a special estimating chamber in which the patient is placed. This camera captures how fast the radiopharmaceutical-labeled food bolus is evacuated from the stomach. The information obtained in the course of this study will make it possible to correct the prescribed treatment by prescribing drugs that improve food evacuation or to plan the course of surgical intervention, taking into account the identified violations.

Signs of nausea, vomiting, and regurgitation (reflux) are more likely to occur either in violation of evacuation or in gastroesophageal reflux. And it is precisely the evaluation of the evacuation function that will make it possible to distinguish these two violations from each other.

How is reflux esophagitis treated?

Lifestyle change

One of the simplest and most effective ways to treat GERD is to change your lifestyle and fight bad habits, especially those related to nutrition.

As mentioned earlier, the reflux of gastric juice into the esophagus occurs much more often at night than during the day. This is due to the sleep-wake mode, in other words, the transition of a person to a horizontal position during sleep. This transition is considered a predisposing factor in the development of gastroesophageal reflux. In addition, the absence of passive intake of abandoned contents back into the stomach suggests a longer stay in the esophagus. This condition can be corrected by taking an elevated position of the upper half of the body, for example by placing a pillow.

Elevated posture is recommended for all patients with reflux symptoms, however, some patients reflux during the daytime and for them changing body position is ineffective. An additional measure may be to change the side on which the person sleeps, so in the presence of symptoms of reflux, it is preferable to sleep on the left side, which purely anatomically reduces the possibility of reflux into the esophagus.

It is also necessary to change the mode of eating, its frequency and nature. Food should be fractional, little by little at short intervals and in small quantities. it is necessary to avoid eating in the evening and at night, that is, on the eve of sleep.

A number of foods affect the function of the lower esophageal sphincter, leading to its relaxation and thereby predisposing to the development of reflux. These products include:

• chocolate,
• mint,
• alcohol, And
• drinks containing caffeine.

This also includes fatty foods, which should be completely excluded, as well as such a factor as smoking that reduce the contractile activity of the esophageal sphincter.

It is important to exclude foods that provoke excessive production of hydrochloric acid by the stomach. The most typical representatives of these products are spices, products containing acid (for example, green apple or citrus juices), carbonated drinks and tomato juice.

A relatively new approach in the treatment of GERD is the use of chewing gum. Chewing it allows you to stimulate the production of large amounts of saliva rich in sodium bicarbonate and peristalsis by moving it along the esophagus. It is important to know that its use should be in a clear relationship with the diet (taken after meals).

Acid neutralizers

Despite the use of new modern drugs that suppress the production of hydrochloric acid by the stomach, the use of acid-neutralizing substances remains relevant. The main purpose of these drugs for GERD is to neutralize excess hydrochloric acid. Their only drawback is considered to be a short duration of action, since an hour after their application, gastric juice re-accumulates. The best way to use acid neutralizers is to take them about an hour after a meal or when the initial signs of reflux (heartburn) appear.
The composition of various drugs that neutralize the acid of gastric juice includes calcium, aluminum and magnesium. According to the predominant presence of one of these substances in the composition, they are divided into subgroups.

When using calcium-based substances (usually calcium carbonate), unlike other acid-neutralizing drugs, in addition to a positive effect, there is a stimulation of the production of gastrin (gastrin) by the stomach and duodenum. And gastrin, in turn, is a hormone that is responsible for the production of hydrochloric acid by the stomach. Therefore, when using calcium-containing preparations, a kind of vicious circle arises. Because of this effect, drugs of this group are used in practice less and less.

The use of aluminum-containing and magnesium-containing drugs is also accompanied by side effects. In the first case, when taking drugs, patients tend to constipation, when using drugs of the magnesium group - diarrhea. Therefore, when one or another condition appears, it is recommended to mutually replace these drugs with each other.

Histamine receptor blockers (histamine antagonists)

Due to the fact that drugs that neutralize hydrochloric acid have a short duration of action, drugs that suppress the release of hydrochloric acid from the stomach are more often used. The first drug used for this purpose was a histamine receptor blocker. tagamet(Tagamet). Histamine is the main substance responsible for the production of acid in the stomach. Histamine, produced by the walls of the stomach, acts as a stimulant on cells (more precisely, their histamine receptors) that produce hydrochloric acid of gastric juice. When these receptors are blocked, the production of acid by the stomach is turned off. More often, histamine receptor antagonists are referred to as H2 blockers, since they predominantly “turn off” histamine H2 receptors. For GERD, drugs in this class are usually recommended to be taken at night to suppress acidity at night, or 30 minutes before a meal, because excess acid formation occurs immediately after a meal. Currently, the most used H2 receptor blockers are tagamet (Tagamet), ranitidine(Zantac) nizatidine(Axid) and famotidine(Pepcid).

Proton pump blockers (proton pump inhibitors)

The second group of drugs developed to treat conditions with excess acid production, such as gastroesophageal reflux, are proton pump inhibitors, such as omeprazole(Prilosec). The main mechanism of action of these drugs is the blocking of the proton pump, which supplies the cell that produces hydrochloric acid with hydrogen protons (H +), necessary for its formation. The advantage of these drugs is that they turn off both basal (unstimulated, constant) and stimulated (occurring on a food stimulus) secretion of hydrochloric acid. H2 receptors block only stimulated secretion. This mechanism allows you to stop the production of gastric juice for a longer time and selectively (selectively) the production of hydrochloric acid.

Usually, proton pump inhibitors are prescribed in the absence of effects from histamine receptor blockers or in the complicated course of gastroesophageal reflux disease (erosion, ulcers, strictures and Barrett's esophagus). Here are the main of these drugs - omeprazole(Prilosec) lansoprazole(Prevacid) rabeprazole(Aciphex), pantoprazole(Protonix) and esomeprazole(Nexium). The latter consists of a combination of omeprazole and sodium bicarbonate (Zegerid). They are usually given an hour before a meal, which is when their blood concentrations reach their peak levels.

Stimulants of peristaltic activity

The mechanism of stimulation of these drugs is to stimulate the muscular layer of the gastrointestinal tract, including the esophagus, stomach, small intestine, and large intestine. The most commonly used drug in this group is metoclopramide(Reglan). Metoclopramide increases esophageal motility and stimulates contractile activity of the lower esophageal sphincter. However, this effect is temporary, so the use of this drug is most effective 30 minutes before a meal, which will increase the tone of the lower sphincter while food is in the stomach, and this will reduce the possibility of reflux of gastric contents and its amount into the esophagus.

When is surgical treatment of gastroesophageal reflux disease indicated?

In some situations, the previously described groups of medications lose their effectiveness. For example, despite the suppression of acidity and the disappearance of heartburn, regurgitation of gastric contents into the pharynx and upper respiratory tract can occur with the development of corresponding complications. In addition, it happens that significant financial resources are spent on the purchase of medications, and sometimes it is more economical and more competent to spend them on performing an operation than to be treated therapeutically. It also happens that this pathology is not amenable to medical treatment at all. In such a situation, there is a need for surgical treatment of GERD.

Fig. 4 Stage of exposure of the fundus of the stomach during laparoscopic fundoplication

Surgery to prevent backflow (reflux) of stomach contents into the esophagus is called fundoplication also called anti-reflux surgery. During this operation, from the part of the stomach called the fundus (from the Latin fundus - bottom, plica - fold), a fold or sleeve is formed around the lower part of the esophagus, enveloping it and forming a kind of artificial valve. This operation is performed through open access by laparotomy or through the use of laparoscopic technology. During the operation, manipulations on the lower esophagus and stomach, as well as other abdominal organs, are performed through small percutaneous accesses. The main advantage of this procedure is the absence of the need for a major traumatic operation.

Fig.5 Final view of the esophageal-gastric junction after the fundoplication operation

Surgical treatment has long proved to be highly effective in the treatment of clinical manifestations and complications of GERD. Thus, approximately 80% of operated patients have good results and no recurrence of disease signs within 10 years after surgery. The rest have to continue taking the drugs, and it is not yet completely clear whether this is caused by the re-development of reflux or due to manifestations of some other pathology.

Laparoscopic Nissen fundoplication (video)

Of course, endoscopic interventions have a number of advantages, mainly associated with the absence of the need for surgical treatment and hospitalization. However, it has not yet been fully determined how effective and long-term these procedures are, and this requires further clinical research.

Fig.6 Laparoscopic fundoplication

Endoscopic treatment

Endoscopic methods of treatment of this pathology have appeared relatively recently. There are three main types of endoscopic interventions on the esophagus for gastroesophageal reflux. The first is the imposition of a circular louse on the lower esophagus in the area where its sphincter is located, as a result of which it shrinks somewhat and restores its obturator function. In the second type of intervention, the sphincter of the esophagus is intentionally damaged by radiofrequency waves, which leads to its scarring and narrowing of the lumen. This procedure is called radiofrequency ablation. The third category of endoscopic operations on the esophagus is the injection of materials, often of a polymeric structure, into the area of ​​​​the sphincter, which caused its compression and reduction of the lumen, and, accordingly, the reflux of gastric contents.

What issues of diagnosis and treatment of reflux esophagitis remain unresolved?

Mechanism of heartburn and mucosal damage

One of the unresolved problems in the diagnosis and treatment of GERD remains the cause of the discrepancy between the appearance of reflux, heartburn and damage to the esophageal mucosa.

• Why isn't every episode of gastroesophageal reflux accompanied by heartburn?
• Why do some patients with a certain degree of reflux develop heartburn, while others with the same degree of reflux do not?
• Why does heartburn occur in the esophagus without visible signs of mucosal damage or esophagitis?
• Why is heartburn intensity lower in some patients with severe mucosal damage than in patients without mucosal damage?
• What is more due to the appearance of heartburn, esophagitis, or the penetration of acid through the expanded intercellular spaces of the mucosa?

Modern medicine has enough knowledge to confirm the relationship between reflux and mucosal damage, and about the mechanisms that provoke heartburn. However, the development of the problem of the causes of heartburn formation remains relevant and in the future will allow the development of new directions in the treatment of this condition.

One of the rather interesting theories of the origin of heartburn suggests that reflux causes irritation of nerve endings located directly under the mucous membrane and is not associated with inflammation. In another theory, an opinion is expressed about the appearance of pain, which is the equivalent of heartburn with excessive pathological contraction of the muscles of the lower esophagus in response to irritation of the mucous membrane with gastric juice, more precisely, this contraction is of a long-term irreversible nature.

Treating a condition called Barrett's esophagus

It is known that 10% of patients with GERD have features of Barrett's esophagus. These patients are usually recommended to have regular gastroduodenoscopy due to concern about the possible development of esophageal cancer. However, a number of researchers believe that such frequent endoscopic examinations are inappropriate, and significantly increase the cost of treatment. Another study confirmed that esophageal cancer is more likely to develop in patients with frequent and prolonged episodes of heartburn, respectively, only this category of patients should be subjected to regular examinations.

A number of authors believe that only earlier (timely) and radical elimination of gastroesophageal reflux in Barrett's esophagus will prevent progression to cancer. Additionally, new endoscopic methods for destroying the mucosa altered in Barrett's esophagus, such as laser removal or electrocautery (cauterization), are being evaluated.
A new direction in diagnosing the condition of the esophageal mucosa in this pathology and predicting the possible development of cancer is DNA diagnostics of altered mucosal cells.

Undoubtedly, the leading method of treating early cancerous changes in the esophageal mucosa remains surgical treatment, more often it is the surgical removal of a part of the esophagus or esophagectomy. Other methods, such as photodynamic therapy or endoscopic mucosal excision, are in clinical trials.

Gastroesophageal reflux disease (GERD), which can be treated by various methods, is a pathology of the digestive system, when the acidic contents of the stomach are thrown into the esophagus, as a result of which its walls become inflamed. The main symptoms of GERD are heartburn and sour belching. The diagnosis and treatment of the disease is carried out by a gastroenterologist. If a person has GERD, the treatment will be to take medications that reduce the acidity of the stomach and protect the lining of the esophagus from the action of acid. Good results are obtained by following a certain diet. Features of the course of GERD, symptoms, treatment will be considered in this article.

Causes of the disease

Often, reflux disease occurs due to a decrease in the tone of the lower esophageal sphincter, and this, in turn, occurs with the use of caffeine and alcohol, smoking, in case of pregnancy under the influence of hormonal factors. What other reasons could there be for the development of GERD? Treatment of any ailments with antispasmodics, analgesics, calcium antagonists can lead to gastroesophageal reflux disease. Also, its occurrence is possible against the background of an increase in intra-abdominal pressure due to ascites, obesity, flatulence. Conditions for reflux are created with diaphragmatic hernia, when the pressure on the lower region of the esophagus in the chest is reduced.

An increase in intragastric pressure and the reflux of stomach contents into the esophagus can occur with abundant and hasty food intake, since then a lot of air is swallowed along with it. The presence in the diet in excess of products containing peppermint, rich in animal fats, hot spices, fried foods, carbonated water leads to the same consequences. A duodenal ulcer can also cause GERD.

Symptoms

Treatment of reflux disease is desirable to start as early as possible, otherwise its manifestations can cause a lot of problems. When the contents of the stomach (and this is food, and digestive enzymes, and hydrochloric acid) enter the esophagus, irritation of its mucosa occurs, inflammation begins and GERD occurs. Symptoms, treatment in this case are typical for many esophageal disorders. So, the symptoms of the disease are usually the following:

In addition to esophageal signs, GERD also manifests itself as extraesophageal. These are digestive disorders (flatulence, abdominal pain, nausea); pathology of the pharynx and oral cavity (caries, tonsillitis, destruction of tooth enamel); damage to the ENT organs (polyps of the vocal cords, rhinitis, laryngitis, otitis media); damage to the respiratory system (pneumonia, bronchial asthma, bronchitis, emphysema, bronchiectasis); ailments of the cardiovascular system (angina pectoris, arrhythmia, arterial hypertension).

Diagnostics

Until GERD is diagnosed by a gastroenterologist, it is pointless to start treatment, because the methods of therapy should be selected based on the characteristics of the pathological process. To identify reflux disease and determine the mechanism of its development, the following methods are used:

• X-ray of the esophagus. With such a study, erosion, strictures, ulcers, hernias can be detected.
• Endoscopy of the esophagus. This procedure also allows you to identify inflammatory changes.
• Radioactive technetium scintigraphy. The study involves taking ten milliliters of egg white with Tc11: the patient takes a sip of this remedy every twenty seconds, and at this time a picture is taken on the halocamera every second for four minutes. This method makes it possible to assess esophageal clearance.
• Manometric study of the sphincters of the esophagus. This procedure allows you to detect a change in the tone of the sphincters.
• Monitoring pH in the lower esophagus. Such a study is necessary in order to select individual therapy and monitor the effectiveness of medications.

GERD: treatment

The goal of therapeutic measures for this disease is to eliminate its symptoms, combat reflux and esophagitis, improve the quality of life, and prevent complications. Conservative therapy is most often used, surgical treatment of GERD is indicated only in extreme cases. Let's take a closer look at ways to deal with the disease. The set of activities includes:

• adherence to a diet and a certain lifestyle;
• taking antacids, antisecretory drugs and prokinetics.

Regardless of the stage and severity of GERD, treatment implies the constant observance of certain rules:

• Do not lie down or lean forward after eating.
• Do not wear tight clothes, corsets, tight belts, bandages - this leads to an increase in intra-abdominal pressure.
• Sleep on a bed with the part where the head is raised.
• Do not eat at night, avoid large meals, do not eat too hot food.
• Give up alcohol and smoking.
• Limit the consumption of fats, chocolate, coffee and citrus fruits, as they are irritating and reduce LES pressure.
• Lose weight if you are obese.
• Refuse to take medications that cause reflux. These include antispasmodics, β-blockers, prostaglandins, anticholinergics, tranquilizers, nitrates, sedatives, calcium channel inhibitors.

Medicines for reflux disease. Antacids and alginates

Such drugs for the treatment of GERD are used when the manifestations of the disease are moderate and infrequent. Antacids should be taken after each meal (after one and a half to two hours) and at night. The main drug from this group is Almagel.

Alginates create a thick foam on the surface of the contents of the stomach and, due to this, return to the esophagus with each episode of reflux, thereby providing a therapeutic effect. Due to the content of antacids, alginates produce an acid-neutralizing effect, at the same time they form a protective film in the esophagus, which creates a pH gradient between its lumen and the mucosa and thus protects the mucosa from the negative effects of gastric juice.

Prokinetics

These drugs restore the normal physiological state of the esophagus by increasing the tone of the lower sphincter, improving clearance and increasing peristalsis. The main means of pathogenetic therapy for GERD is the prokinetic drug "Motilium". It normalizes the motor activity of the upper digestive tract, restores the active peristalsis of the stomach and improves antroduodenal coordination. "Motilium" is well tolerated if long-term therapy is necessary, reduces the percentage of relapses of the disease.

proton pump inhibitors

If GERD with esophagitis is diagnosed, treatment with prokinetics is carried out in combination with proton pump inhibitors. As a rule, a new generation drug "Pariet" is used. Due to its use, the secretion of acid decreases, there is a positive trend in the clinical manifestations of the disease. Patients talk about a decrease in the intensity or even the complete disappearance of heartburn, a decrease in pain.

With GERD, the treatment regimen with prokinetics and proton pump inhibitors is used as follows: 20 milligrams of Pariet and 40 milligrams of Motilium are prescribed per day.

Therapy in young children

In babies, reflux causes frequent spitting up. Treatment consists of several stages:

Therapy in older children

Of great importance in the treatment of reflux disease is the correction of the child's lifestyle.

• You should raise the end of the bed where the head is located by at least fifteen centimeters. Such a simple measure can reduce the duration of acidification of the esophagus.
• It is necessary to introduce dietary restrictions for the child: reduce the fat content in the diet and increase the protein content, reduce the amount of food consumed, exclude irritating foods (citrus juices, chocolate, tomatoes).
• It is necessary to develop a habit in the child not to eat at night, not to lie down after eating.
• It is required to ensure that the child does not wear tight clothes, does not sit for a long time, bent over.

As a medical treatment, as in adults, antacids are used, usually in the form of a suspension or gel (Almagel, Phosphalugel, Maalox, Gaviscon), prokinetic agents (Motilak, Motilium , "Tserukal"). The choice of a specific medication and the determination of the dosage is carried out by the attending physician.

Surgical intervention

Sometimes, to restore the normal function of the cardia, it is necessary to resort to surgery aimed at eliminating reflux. Indications for surgical treatment are as follows:

• complications of GERD (repeated bleeding, strictures);
• ineffectiveness of conservative therapy;
• frequent aspiration pneumonia;
• diagnosing Barrett's syndrome with high-grade dysplasia;
• the need for young patients with GERD for long-term antireflux therapy.

Reflux is often removed by fundoplication. However, this method is not without drawbacks. So, the result of the operation depends entirely on the experience of the surgeon, sometimes after surgery there is a need for medical treatment, there is a risk of death.

Currently, various endoscopic techniques have been used to influence metaplasia foci: electrocoagulation, laser destruction, photodynamic destruction, argon plasma coagulation, endoscopic local resection of the esophageal mucosa.

Therapy with folk remedies

In the initial stages of GERD, alternative treatment can be very helpful. In general, at these stages, you can cope with the disease simply by observing the antireflux regimen and changing your lifestyle. If the disease is mild, instead of antacids, various traditional medicines can be used to relieve heartburn, which strengthen and protect the esophageal mucosa, improve sphincter tone and reduce the acidity of gastric juice. With a severe course of the pathological process, it will not be possible to do without drug therapy, and in the presence of complications, surgical intervention is generally required. Therefore, the treatment of GERD with folk remedies is rather an auxiliary and preventive method. It can be used as an adjunct to highly effective drug therapy regimens.

Phytotherapy is very popular among people. Here are some traditional medicine recipes for the treatment of reflux disease.

Treatment of GERD with folk remedies involves not only herbal medicine, but also the use of mineral waters. They should be used at the final stage of the fight against the disease or during remissions in order to consolidate the results. With reflux disease, alkaline low-mineralized waters, such as Borjomi, Smirnovskaya, Slavyanovskaya, are effective. You need to drink them, slightly warmed up, since gas is released during the heating process. However, the temperature should not exceed 40 degrees, otherwise the salts will precipitate. Drink warm degassed mineral water should be forty minutes before meals in a glass for one month. After drinking water, it is recommended to lie down for twenty minutes.

We would like to preface the discussion of therapeutic options in gastroesophageal reflux disease (GERD) with brief information on the mechanisms of development and diagnosis of this pathology. The possibilities of surgical treatment of GERD will not be discussed in this article.

Definition

So, A.S. Trukhmanov defines GERD as the occurrence of characteristic symptoms and (or) an inflammatory lesion of the distal parts of the esophagus due to repeated reflux of gastric contents into the esophagus. .

According to the definition of the International Working Group, the term "gastro-esophageal reflux disease" should be applied to all individuals at risk of physical complications of gastro-oesophageal reflux, or experiencing a significant deterioration in health-related well-being (quality of life), as a result of reflux symptoms, after adequate belief in benign nature of symptoms .

The term "endoscopically negative reflux disease" should be used in individuals who meet the definition of gastroesophageal reflux disease but lack both Barrett's esophagus and no visible mucosal defects (erosions or ulcers) on endoscopic examination. .

Development mechanisms

Without dwelling on the pathogenetic mechanisms of the development of this disease, we will only say that it is based on the effect of acid and pepsin on the esophageal mucosa due to a combination (in various proportions) of pathological reflux of gastric contents into the esophagus with a violation of its clearance. Pathological reflux of the contents, in turn, is caused by a dysfunction of the lower esophageal sphincter (either as a result of a decrease in its tone or an increase in the frequency of spontaneous relaxation, or due to its anatomical defect, for example, with a hernia of the pod). The violation of esophageal clearance may be based on a decrease in saliva production or a violation of esophageal motility. As a result of all of the above, there is an imbalance between the factors of aggression and the factors of protection, which leads, but not necessarily, to the occurrence of reflux esophagitis.

Epidemiology

According to S.I. Pimanova occasionally GERD symptoms are observed in half of the adult population, and the endoscopic picture of esophagitis is observed in 2-10% of the examined people . It must be remembered that GERD is not always accompanied by esophagitis. Up to 50-70% of patients with heartburn present with endoscopically negative GERD at the time of seeking medical attention. . The attitude of a number of practitioners towards endoscopically negative GERD as the mildest degree of this disease that does not require intensive drug therapy is fundamentally wrong. A number of studies have demonstrated that the quality of life in patients with endoscopically positive and negative GERD is impaired to almost the same extent. . Studies have shown that endoscopically negative GERD very rarely turns into reflux esophagitis, which in turn rarely progresses to more severe forms over time. .

Diagnostics

Since the diagnosis of GERD is widely described in many manuals, we will dwell only on some of its points. The main symptom of GERD observed in at least 75% of patients is heartburn. . There may also be pain or a burning sensation in the sternum, belching, etc. Most often, GERD symptoms occur after eating.

Diagnosis of erosive esophagitis is based on endoscopic examination. Barium radiography has a fairly high sensitivity in severe (98.7%) and moderate (81.6%) esophagitis, but insensitive (24.6%) in its mild degree. . Endoscopy with biopsy is the only reliable method for diagnosing Barrett's esophagus. The severity of erosive reflux esophagitis on the endoscopic picture is divided into 4 degrees A, B, C and D (according to the Los Angeles classification).

pH monitoring is a sensitive and specific diagnostic test and is particularly important for the detection of endoscopically negative GERD. More than 50 episodes of pH drop below 4 is considered as a diagnostic criterion for GERD . In a number of patients, a less significant decrease in the pH of the esophagus occurs, but if most episodes of such a decrease coincide with the moments of the onset of symptoms, it allows us to speak of a "hypersensitive esophagus".

Among the provocative tests, the Bernstein test plays a certain role (the onset of typical symptoms after the introduction of a weak solution of hydrochloric acid into the esophagus and their disappearance after the introduction of saline). Determining the pressure of the lower esophageal sphincter is useful in deciding on surgical treatment.

Treatment

Before proceeding to the consideration of individual aspects of the treatment of GERD, it is necessary to emphasize the fact that its main task is to get rid of the symptoms that disturb patients as soon as possible. The disappearance of symptoms usually correlates well with the healing of mucosal defects in erosive esophagitis. .

Life style change.

Although according to the GERD Working Group, lifestyle factors do not play a decisive role in the development of GERD recommendations aimed at eliminating factors contributing to reflux or impairing esophageal clearance should be given.

Diet. It is necessary to stop taking reflux-inducing foods (fatty foods, chocolate and excessive amounts of alcohol, onions and garlic, coffee, carbonated drinks, especially various types of colas) and drugs with a low pH (orange and pineapple juice, red wine). However, an attempt to drastically restrict the diet of a patient (especially a young one) is rarely possible in practice, your recommendations simply will not be followed. It is wiser to identify which products cause the appearance or exacerbation of symptoms in this particular patient and try to refuse at least them. The patient should be informed that overeating should be avoided. After eating, it is advisable not to take a horizontal position and not to work in an inclination. The last meal should be 3 hours before bedtime.

Weight control. Losing weight does not always lead to resolution of symptoms, but weight loss may reduce the risk of hiatal hernia. However, giving advice to lose weight is much easier than doing it. Fat people sometimes try to hide the lack of a waist by overtightening the waist belt, which leads to increased intra-abdominal pressure and the development of reflux (as well as wearing too tight clothes).

Smoking is a contributing factor to GERD by both relaxing the sphincter and reducing salivation and should therefore be stopped. . Although smoking cessation has minimal benefit in GERD according to some studies .

Elevating the head end of the bed is important in patients with nocturnal or laryngeal symptoms (which constitute a small proportion of patients with GERD), but is questionable in other cases.

A number of drugs such as antispasmodics, beta blockers, hypnotics and sedatives, nitrates and calcium antagonists can contribute to the development of reflux.

Antacids.

Discussing the use of antacids, of which there are a great many in our time (almagel, phosphalugel, maalox, rutacid, etc.), I would like to emphasize that, in our opinion, antacids do not play an independent role in the treatment of GERD and can only be used as a short-term remedy. symptom control. The low effectiveness of antacids is based on the short duration of pH control achieved by their use. Evidence from many authors supports a minimal effect of antacids (even in combination with lifestyle changes) in reflux esophagitis, although it is superior to the placebo effect. . We suggest that patients (treated for GERD) use antacids as a method of rapidly controlling symptoms, usually following a diet or exercise disorder, and those with infrequent (less than 4 per month) episodes of heartburn without endoscopic evidence of esophagitis.

Antisecretory drugs.

The most effective treatment for GERD is to reduce stomach acid production with H2 blockers or proton pump inhibitors. The goal of this therapy is to increase the pH of the gastric juice to 4 and during the period of the greatest likelihood of reflux, i.e. not the prevention of reflux as such, but the elimination of the pathological effects of the components of gastric juice on the esophagus. H2 blockers. Prior to the advent of H2 proton pump inhibitors, blockers were the drug of choice in the treatment of GERD. In practice, 4 H2 histamine receptor blockers are currently used (cimetidine, ranitidine, famotidine and nizatidine). The mechanism of action of drugs is to block gastric secretion stimulated by histamine. However, two other stimulation pathways, acetylcholine and gastrin, remain open. It is with this fact that the degree of suppression of secretion is lower than that of proton pump inhibitors (PPI) and the degree of inhibition of gastric secretion is gradually reduced with prolonged use of H2 blockers, when stimulation of acid production begins to be increasingly carried out through other mediators (mainly gastrin).

Cimetidine (H2 blocker of the first generation). Apply 200 mg 3-4 times a day and 400 mg at night. The maximum daily dose is 12 grams.

Ranitidine (second generation) is used at a dosage of 150 mg 2 times a day, which can, if necessary, reach 300 mg 2 times a day (maximum dose of 9 grams per day). For nocturnal symptoms - 150-300 mg at night. Maintenance therapy - 150 mg at night.

Famotidine (third generation) is used at a dose of 20 mg twice daily, with a maximum daily dose of 480 mg. For nocturnal symptoms 20-40 mg at night, maintenance therapy 20 mg at night.

Nizatidite (fourth generation) is taken at 150 mg twice daily or 300 mg at bedtime.

Due to a very wide range of side effects (from androgenic effects to blockade of respiratory enzymes) and inconvenient dosage, cimetidine is not currently used in practice. Of all the other H2 blockers, we prefer famotidine (as the drug with the least common side effects). It must be remembered that all H2 blockers are canceled gradually in order to prevent the "recoil" syndrome - a sharp increase in acidity after stopping treatment.

Based on 33 randomized trials (involving 3000 people), the following data were obtained: placebo led to symptomatic relief of GERD in 27% of patients, H2 blockers in 60% and PPI in 83% . Esophagitis stopped in 24%, 50% and 78% of cases, respectively. These figures allow us to conclude that the effectiveness of H2 blockers in the treatment of GERD, which, however, is significantly inferior to that of PPI. H2 blockers retain a role in the treatment of GERD. They are effective as a therapy for nighttime reflux. , even if you continue to take PPI and as on-demand therapy.

Proton pump blockers.

Their action is based on blocking the ATP-ase of the brothel pump (due to the formation of an irreversible bond with the cystine residue of the enzyme). It must be remembered that PPI blocks only the currently active proton pump. The drugs of this group are absorbed in the form of inactive compounds, passing into the active active substance directly in the tubular systems of secretory cells. All PPIs except esomeprazole have a short half-life (30 - 120 minutes). The destruction of PPI occurs in the liver, and there are two ways of their destruction - fast and slow. The destruction process is stereodependent. The dextrorotatory isomer decays along the fast path, the left-handed isomer decays along the slow one. All PPIs, again except for esomeprazole (only the levorotatory isomer), are represented by the right and levorotatory isomers. This fact explains the longer maintenance of the minimum therapeutic concentration of esomeprazole compared to other PPIs.

PPIs are prescribed before meals (usually 30 minutes before breakfast, with a single dose), so that the action occurs at the time of the presence of the maximum number of active proton pumps - 70 - 80% of their total number. The next dose of PPI again blocks 70-80% of the receptors (remaining and regenerated), so the peak of the antisecretory effect occurs on the 2nd-3rd day (slightly faster when using esomeprazole). PPIs are practically ineffective as on-demand therapy (the onset of heartburn symptoms indicates an acid rush has already occurred, followed by a decrease in the number of active pumps, and therefore no target for PPI).

When analyzing the comparative efficacy of various PPIs, it can be concluded that there are no significant advantages between omeprazole, rabeprazole, lansoprazole and pantoprazole. The effectiveness of esomeprazole (nexium) is slightly higher. When comparing the duration of maintenance of intragastric pH > 4 using various PPIs, data were obtained on better control of gastric secretion when using Nexium (Fig. 1).

Although it should be noted that when using 40 mg of omeprazole, the difference is not so noticeable. The benefits of Nexium are more pronounced in severe forms of esophagitis (grade D) . Omeprazole is used at a dose of 20 - 40 mg per day (either a single dose in the morning or twice a day). In severe cases, the dose can reach 60 mg per day. Lansoprazole is used at 30 mg/day, pantoprazole at 40 mg/day, rabeprazole at 20 mg/day and Nexium at 40 mg/day. Cancellation of the drug should also be gradual.

prokinetic drugs.

Prokinetic drugs (domperidone, metoclopramide, and cisapride) may increase lower esophageal sphincter pressure, improve esophageal clearance, and accelerate gastric emptying. Cisapride is only available for limited use in the US due to concerns about cardiac arrhythmias (see below). Metoclopamid in 20-50% of cases causes weakness, restlessness, tremor, parkinsonism or tardive dyskinesia. It is used 10 mg 3-4 times a day. The maximum single dose is 20 mg, daily 60 mg.

Cisapride. Although cisapride has generally been considered practically safe, its recent widespread use in the United States has been associated with cardiac arrhythmias. Most often they developed when taking cisapride in combination with drugs that inhibit cytochrome P-450 and increase the level of cisapride. As a result, the manufacturer partially restricted the use of this drug in the United States. Studies comparing the efficacy of cisapride 910 mg four times a day) with H2 receptor antagonists (ranitidine 150 mg twice a day) and cimetidine (400 mg four times a day) demonstrated their superiority over placebo and similar efficacy in relieving symptoms of GERD and curing esophagitis . The combination of H2 blockers with cisapride gives a better effect than either drug alone, but is inferior to omeprazole .

Domperidone (motilium) is similar in mechanism of action to metoclopramide, but does not penetrate the blood-brain barrier and therefore does not cause central side effects, but increases the level of prolactin in the blood. Applied 10 mg 3-4 times a day. None of the drugs did not give a good therapeutic effect in severe degrees of esophagitis.

The role of HP infection.

At present, the role of Hp infection in GERD remains debatable. Although GERD is an indication for eradication therapy according to the Maastrican Accords, not all authors agree with this. A number of studies have shown that Hp eradication does not lead to a cure for reflux esophagitis, nor does it have a preventive role in terms of its recurrence. . The fact that Hp infection can cause both an increase and a decrease in gastric secretion makes its role in the development of GERD even more debatable. The data of some authors even point to the protective role of Hp infection in GERD. , due to the alkalizing action, and in the further development of mucosal atrophy.

Almost the only factor justifying eradication therapy for GERD is that chronic use of PPI, against the background of an existing Hp infection, contributes to the development of atrophic gastritis and metaplasia. . According to Kuipers EJ comparing the likelihood of developing atrophic gastritis in groups of patients with GERD and Hp infection who received omeprazole or underwent fundoplication, it developed in 31% and 5% of patients, respectively. Although another study found no such pattern . In turn, eradication therapy does not cause exacerbation or aggravation of GERD. .

In our practice, we test for the presence of Hp and carry out eradication of patients with GERD only if they have a concomitant disease of the upper gastrointestinal tract, the relationship of which with Hp infection has been established (for example, peptic ulcer) or when planning chronic (more than a year) continuous use of proton pump inhibitors.

New directions of pharmacotherapy.

According to Ciccaglione et al, the drug baclofen, which reduces the number of spontaneous relaxations of the lower esophageal sphincter, at a dosage of 10 mg 3 times a day for a month, showed a significant superiority over placebo, improved esophageal pH monitoring data and reduced the severity of GERD symptoms. . It was also noted to be well tolerated. The drug inhibits 34-60% of spontaneous relaxation of the lower esophageal sphincter and increases its basal pressure. . However, there is still insufficient evidence to justify the widespread use of baclofen in the treatment of GERD.

Therapeutic modes.

Currently, there are two main tactical approaches to the treatment of GERD, the so-called step-up and step-down. The first use of the weakest measures (lifestyle modification, antacids) as the first stage of treatment with the gradual use of increasingly powerful drugs in case of ineffectiveness (H2 blockers, then their combination with prokinetics, and only then PPI). The second option of therapy involves the appointment of the most effective treatment (PPI), which allows you to quickly stop the symptoms, and then reduce the dose of drugs and possibly switch to weaker drugs.

In our practice, we only follow step-down therapy. We believe that the patient comes to us for the fastest relief of his disturbing symptoms, which should be achieved by prescribing a group of drugs from which the best effect can be expected. You should not forget lifestyle advice, but in combination with a standard dose of PPI. As for starting treatment with H2 blockers, then switching to PPI if necessary - you won't be judged for that, but does it make sense? H2 blockers have no fewer possible side effects, their price is not significantly lower. Leave them for on-demand therapy and nocturnal episodes of reflux. True, there is a very small group of patients with reflux esophagitis refractory to proton pump inhibitor therapy in whom sufficient pH control can be achieved using high doses of H2 blockers. .

What about endoscopically negative GERD? Yes, exactly the same. As mentioned above, the degree of morphological changes in the esophagus does not correlate well with the severity of symptoms. . Moreover, in this group of patients, there is often a less pronounced effect of antisecretory therapy with longer persistence of symptoms. . It must also be remembered that the effectiveness of H2 blockers in endoscopically negative GERD does not exceed that in erosive reflux esophagitis. .

In severe reflux esophagitis (C, D), therapy with the most potent PPI (Nexium) or the maximum dose of other proton pump inhibitors is rational.

For nocturnal episodes of heartburn, despite the use of PPI, it is rational to add a single evening dose of an H2 blocker. Antacids can be used as an on-demand, patient-controlled therapy.

So, we adhere to a knowledgeable management strategy when a new patient with GERD appears.

• Proton pump inhibitors at a standard dose (within 2-4 weeks for endoscopically negative reflux esophagitis and grade A, B erosive esophagitis and within 8 weeks for its more severe forms).
• With ineffectiveness (defined by the persistence of symptoms after 7-10 days of treatment or the preservation of the endoscopic picture of esophagitis), increase the dose of PPI to the maximum or switch to a potentially more effective PPI - Nexium.
• In case of inefficiency - pH monitoring during treatment. An attempt to switch to high doses of H2 blockers in combination with prokinetics? Antireflux surgery?
• With effectiveness - a gradual decrease in dosage until the drug is discontinued. If the symptoms recur - taking the minimum effective dose of the drug (possible therapy every other day or weekend therapy), discussing the possibility of antireflux surgery.

supportive therapy.

Due to the chronic nature of GERD, there is a need for maintenance therapy. Reducing the dose of a drug or attempting maintenance therapy with a less potent drug than the drug used for treatment often results in a high relapse rate. Only in about 20% of patients after a course of treatment, lifestyle changes and periodic antacid intake are sufficient to maintain remission. H2 blockers and prokinetics are ineffective in maintaining remission in patients who achieved it using PPI. . Therapy with low doses of PPI is most effective. The effectiveness of weekend therapy and taking drugs every other day is debatable.

Conclusion.

Medical therapy remains the mainstay of GERD treatment. PPIs are the drugs of choice in treatment and long-term maintenance therapy. The role of Hp infection in the development and natural course of GERD, as well as its effect on the outcome of treatment, is not completely clear. The development of new drugs and comparison of the effectiveness of various schemes for their use is a promising direction for further improving the quality of treatment of this pathology.

Literature

1. Pimanov I.S. Esophagitis, gastritis and peptic ulcer. N. Novgorod 2000.
2. Antonson CW, Robinson MG, Hawkins TM, et al. High doses of histamine antagonists do not prevent relapses of peptic esophagitis following therapy with a proton pump inhibitor. Gastroenterology 1990;98:A16.
3. Berstad AE, Hatlebakk FG, Maartmann-Moe H, et al. Helicobacter pylori, gastritis and epithelial cell proliferation in patients with reflux oesophagitis after treatment with omeprazole. Gut 1997;41:735-739
4. Castell DO, Kahrilas PJ, Richter JE, Vakil NB, Johnson DA, Zuckerman S et al. Esomeprazole (40 mg) compared with lansoprazole (30 mg) on ​​the treatment of erosive esophagitis. Am J Gastroenterol 2002;97:575-83.
5. Ciccaglione AF, Bartolacci S, Marzio L. Effects of one month treatment with GABA agonist baclofen on gastro-esophageal reflux and symptoms in patients with gastro-esophageal reflux disease. gastroenterology. 2002;122:A-196.
6. Dent J, et al. An evidence-based appraisal of reflux disease management the Genval Workshop Report. Gut 1998;44(Suppl 2):S1-S16 (April).
7. DeVault K, Castell D and The Practice Parameters Committee of the American College of Gastroenterology. Updated Guidelines for the Diagnosis and Treatment of Gastroesophageal Reflux Disease. Am J Gastroenterol 1999;94:1434-1442.
8. Fass R. Epidemiology and pathophysiology of symptomatic gastroesophageal reflux disease. Am J Gastroenterol.
9. Galmiche JP, Fraitag B, Filoche B, et al. Double-blind comparison of cisapride and cimetidine in treatment of reflux esophagitis. Dig Dis Sci 1990;35:649-55.
10. Haruma K, Mihara M, Kawaguchi H, et al. Low prevalence of Helicobacter pylori infection in patients with reflux oesophagitis. Gastroenterology 1996;110:A130.
11. Holloway RH. GABA-B receptors and control of gastrointestinal motility. In: AGA Research Symposium: GABA-B receptor agonists as novel treatments of reflux disorders. Program and abstracts of Digestive Disease Week 2002; May 19-22, 2002; San Francisco, California.
12. Koehler RE, Weymean PJ, Oakley HF. Single- and double-contrast techniques in esophagitis. AJR 1980;135:15-9.
13. Kuipers EJ, Lundell L, Klinkenberg-Knoll EC, et al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux oesophagitis treated with omeprazole or fundoplication. N Engl J Med 1996;334:1018-1022.
14. Labenz J, Malfertheiner P. Helicobacter pylori in gastro-oesophageal reflux disease: causal agent, independent or protective factor? Gut 1997;41:277-280.
15. Laine L; Sugg J Effect of Helicobacter pylori eradication on development of erosive esophagitis and gastroesophageal reflux disease symptoms: a post hoc analysis of eight double blind prospective studies. Am J Gastroenterol 2002 Dec;97(12):2992-7 (ISSN: 0002-9270).
16. Lamberts R, Creutzfeldt W, Struber HG, et al. Long term omeprazole therapy in peptic ulcer disease: gastrin, endocrine cell growth and gastritis. Gastroenterology 1993;104:1356-1370.
17. Leite LP, Just RJ, Castell DO, et al. Control of gastric acid with high dose H2-receptor antagonists after omeprazole failure: Report of two cases. Am J Gastroenterol 195;90:1874-7.
18. Lepoutre L, Van der Spek P, Vanderlinden I, et al. Healing of grade II and III oesophagitis through motility stimulation with cisapride. Digestion 1990;45:109-14.
19. Lind T, Rydberg L, Kylebäck A, Jonsson A, Andersson T, Hasselgren G et al. Esomeprazole provides improved acid control vs. omeprazole in patients with symptoms of gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2000;14:861-7.
20. Lundell L, Havu N, Andersson A, et al. Gastric atrophy development and acid suppression therapy revisited. Result of a randomized clinical study with long term follow up . Gastroenterology 1997;112:A28.
21. Mann SG, Murakami A, McCarroll K, et al. Low dose famotidine in the prevention of sleep disturbance caused by heartburn after an evening meal. Aliment Pharmacol Ther 1995;9:395-401.
22. Ott DJ, Wu WC, Gelfand DW. Reflux esophagitis revisited: Prospective analysis of radiological accuracy. Gastrointest Radiol 1981;6:1-7. Koehler RE, Weymean PJ, Oakley HF. Single- and double-contrast techniques in esophagitis. AJR 1980;135:15-9.
23. Ott DJ, Chen YM, Gelfand DW, et al. Analysis of a multiphasic radiographic examination for detecting reflux esophagitis. Gastrointest Radiol 1986;11:1-6.
24. Richter JE, Long JF. Cisapride for gastroesophageal reflux disease: A placebo-controlled, double-blind study. Am J Gastroenterol 1995;90:423-30.
25. Robinson M, Yale J Biol Med 1999 Mar-Jun;72(2-3):169-72 (ISSN: 0044-0086).
26. Rohss K, Hasselgren G, Hedenström H. Effect of esomeprazole 40 mg vs omeprazole 40 mg on 24-hour intragastric pH in patients with symptoms of gastroesophageal reflux disease. Dig Dis Sci 2002;47:954-8.
27. Saco LS, Orlando RC, Levinson SL, et al. Double-blind controlled trial of bethanecol and antacid versus placebo and antacid in the treatment of erosive esophagitis. Gastroenterology 1982;82:1369-73.
28. Sehiguchi T, Shirota T, Horikoshi T, et al. Helicobacter pylori infection and severity of reflux oesophagitis. Gastroenterology 1996;110:A755.
29. Tew S, Jamieson GG, Pilowski I, et al. The illness behavior of patients with gastroesophageal reflux disease with and without endoscopic esophagitis. Dis Esophagus 1997;10:9-15.
30. Vicari JJ, Peek RM, Falk GW, et al. The seroprevalence of cag A-positive Helicobacter pylori strains in the spectrum of gastro-oesophageal reflux disease. Gastroenterology 1998;115:50-57.
31. Vigneri S, Termini R, Leandro G, et al. A comparison of five maintenance therapies for reflux esophagitis. N Engl J Med 1995;333:1106-10.
32. Werdmuller BFM, Loffeld RJLF. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci 1997;42:103-105. 135.
33. Wilder-Smith C, Röchss K, Lundin C, Rydholm H. Esomeprazole 40 mg provides more effective acid control than pantoprazole 40 mg. J Gastroenterol Hepatol 2002;17 Suppl:A784.
34. Wilder-Smith C, Rohss K, Claar-Nilsson C, Lundin C. Esomeprazole 40 mg provides faster and more effective acid control than lansoprazole 30 mg in patients with symptoms of gastroesophageal reflux disease. Gastroenterology 2002;122 4 Suppl 1:A200.
35. Wilder-Smith C, Claar-Nilsson C, Hasselgren G, Rohss K. Esomeprazole 40 mg provides faster and more effective acid control than rabeprazole 20 mg in patients with symptoms of GERD. J Gastroenterol Hepatol 2002;17 Suppl:A612.