Catad_tema Heartburn and GERD - articles

Gastroesophageal reflux disease: diagnosis, therapy and prevention

A. V. Kalinin
State Institute for Advanced Training of Physicians of the Ministry of Defense of the Russian Federation, Moscow

ABSTRACT

Gastroesophageal reflux disease: diagnosis, therapy and prevention

Gastroesophageal reflux disease (GERD) is a common disease. Until relatively recently, GERD seemed to practical doctors to be a harmless disease with a characteristic symptom - heartburn. In the last decade, GERD has received increased attention due to a clear trend towards an increase in the frequency of severe reflux esophagitis and an increase in cancer of the distal esophagus against the background of Barrett's esophagus. The established connection with GERD of pulmonary diseases, in particular bronchial asthma, allows for a new approach to their treatment. The adoption of a new classification of reflux esophagitis contributed to the unification of endoscopic findings. The introduction of 24-hour pH monitoring made it possible to diagnose the disease at an endoscopically negative stage. The widespread use of new drugs in clinical practice (H2 receptor blockers, PPIs, prokinetics) has significantly expanded the possibilities for treating GERD, incl. and during its severe course. The pure S-isomer of omeprazole, esomeprazole (Nexium), is considered as a promising treatment and prevention of GERD.

In the last decade, gastroesophageal reflux disease (GERD) has attracted increased attention due to the following circumstances. In developed countries of the world, there is a clear trend towards an increase in the incidence of GERD. Among the adult population of Europe and the USA, heartburn - a cardinal symptom of GERD - occurs in 20-40%. The significance of GERD is determined not only by its prevalence, but also by the severity of its course. Over the past ten years, severe reflux esophagitis (RE) has become 2-3 times more common. In 10-20% of patients with EC, a pathological condition described as “Barrett's esophagus” (BE) develops and is a precancerous disease. It has also been established that GERD occupies an important place in the genesis of a number of ENT and pulmonary diseases.

Significant progress has been made in the diagnosis and treatment of GERD. The introduction of 24-hour pH monitoring made it possible to diagnose the disease at an endoscopically negative stage. The widespread use in clinical practice of new drugs (H2-receptor blockers, proton pump inhibitors (PPIs), prokinetics) has significantly expanded the possibilities for treating even severe forms of GERD. Clear indications for surgical treatment of EC have been developed.

At the same time, practitioners and patients themselves underestimate the significance of this disease. In most cases, patients turn to a doctor late for medical help and, even with severe symptoms, treat themselves. Doctors, in turn, are poorly informed about this disease, underestimate its consequences, and carry out EC therapy irrationally. It is extremely rare for such a serious complication as BE to be diagnosed.

Definition of the concept of “gastroesophageal reflux disease”

Attempts to define the concept of “gastroesophageal reflux disease” face significant difficulties:

• in practically healthy individuals, reflux of gastric contents into the esophagus is observed;
• sufficiently prolonged acidification of the distal esophagus may not be accompanied by clinical symptoms and morphological signs of esophagitis;
• Often, with pronounced symptoms of GERD, there are no inflammatory changes in the esophagus.

As an independent nosological unit, GERD was officially recognized in the materials on the diagnosis and treatment of this disease, adopted in October 1997 at the interdisciplinary congress of gastroenterologists and endoscopists in Genval (Belgium). It has been proposed to distinguish between endoscopically positive and endoscopically negative GERD. The latter definition applies to those cases where a patient with manifestations of a disease that meets the clinical criteria for GERD does not have damage to the esophageal mucosa. Thus, GERD is not synonymous with reflux esophagitis; the concept is broader and includes both forms with damage to the esophageal mucosa and cases (more than 70%) with typical symptoms of GERD, in which there are no visible changes in the esophageal mucosa during endoscopic examination .

The term GERD is used by most clinicians and researchers to denote a chronic relapsing disease caused by spontaneous, regularly recurring retrograde entry of gastric and/or duodenal contents into the esophagus, leading to damage to the distal esophagus and/or the appearance of characteristic symptoms (heartburn, retrosternal pain, dysphagia).

Epidemiology

The true prevalence of GERD is poorly understood. This is due to the wide variability of clinical manifestations - from episodic heartburn, in which patients rarely see a doctor, to clear signs of complicated EC requiring hospital treatment.

As already noted, among the adult population of Europe and the United States, heartburn, a cardinal symptom of GERD, occurs in 20-40% of the population, but only 2% are treated for EC. EC is detected in 6-12% of people undergoing endoscopic examination.

Etiology and pathogenesis

GERD is a multifactorial disease. It is customary to identify a number of factors predisposing to its development: stress; work associated with an inclined position of the body, obesity, pregnancy, smoking, hiatal hernia, some medications (calcium antagonists, anticholinergic drugs, B-blockers, etc.), nutritional factors (fat, chocolate, coffee, fruit juices, alcohol, acute food).

The immediate cause of RE is prolonged contact of gastric (hydrochloric acid, pepsin) or duodenal (bile acids, lysolecithin) contents with the mucous membrane of the esophagus.

The following reasons leading to the development of GERD are identified:

• insufficiency of the obturator mechanism of the cardia;
• reflux of gastric and duodenal contents into the esophagus;
• decreased esophageal clearance;
• decreased resistance of the esophageal mucosa.

Insufficiency of the obturator mechanism of the cardia.

Since the pressure in the stomach is higher than in the chest cavity, reflux of gastric contents into the esophagus would be a constant phenomenon. However, due to the obturator mechanism of the cardia, it occurs rarely, for a short time (less than 5 minutes), and as a result is not considered a pathology. Normal pH values ​​in the esophagus are 5.5-7.0. Esophageal reflux should be considered pathological if the total number of its episodes during the day exceeds 50 or the total time of decrease in intraesophageal pH<4 в течение суток превышает 4 ч.

The mechanisms that support the functionality of the esophagogastric junction (cardia obturator mechanism) include:

• lower esophageal sphincter (LES);
• diaphragmatic-esophageal ligament;
• mucous “rosette”;
• acute angle of His, forming the Gubarev valve;
• intra-abdominal location of the lower esophageal sphincter;
• circular muscle fibers of the cardia of the stomach.

The occurrence of gastroesophageal reflux is the result of a relative or absolute insufficiency of the obturator mechanism of the cardia. A significant increase in intragastric pressure with a preserved obturator mechanism leads to relative insufficiency of the cardia. For example, intense contraction of the antrum of the stomach can cause gastroesophageal reflux even in individuals with normal function of the lower esophageal sphincter. Relative insufficiency of the cardiac valve occurs, according to A.L. Grebeneva and V.M. Nechaev (1995), in 9-13% of patients with GERD. Much more often there is absolute cardiac failure associated with a violation of the obturator mechanism of the cardia.

The main role in the locking mechanism is given to the state of the LES. In healthy individuals, the pressure in this zone is 20.8+3 mmHg. Art. In patients with GERD it decreases to 8.9+2.3 mmHg. Art.

The tone of the LES is influenced by a significant number of exogenous and endogenous factors. The pressure in it decreases under the influence of a number of gastrointestinal hormones: glucogon, somatostatin, cholecystokinin, secretin, vasoactive intestinal peptide, enkephalins. Some of the widely used medications also have a depressive effect on the obturator function of the cardia (cholinergic substances, sedatives and hypnotics, beta-blockers, nitrates, etc.). Finally, the tone of the LES is reduced by certain foods: fats, chocolate, citrus fruits, tomatoes, as well as alcohol and tobacco.

Direct damage to the muscle tissue of the LES (surgical interventions, prolonged presence of a nasogastric tube, bougienage of the esophagus, scleroderma) can also lead to gastroesophageal reflux.

Another important element of the obturator mechanism of the cardia is the angle of His. It represents the angle of transition of one side wall of the esophagus into the greater curvature of the stomach, while the other side wall smoothly passes into the lesser curvature. The air bubble of the stomach and intragastric pressure ensure that the folds of the mucous membrane, forming the angle of His, fit tightly to the right wall, thereby preventing the reflux of stomach contents into the esophagus (Gubarev valve).

Often retrograde entry of gastric or duodenal contents into the esophagus is observed in patients with hiatal hernia. Hernia is detected in 50% of subjects over the age of 50 years, and in 63-84% of such patients signs of ER are detected endoscopically.

Reflux due to hiatal hernia is due to a number of reasons:

• dystopia of the stomach into the chest cavity leads to the disappearance of the angle of His and disruption of the valve mechanism of the cardia (Gubarev valve);
• the presence of a hernia neutralizes the locking effect of the diaphragmatic crura in relation to the cardia;
• localization of the LES in the abdominal cavity implies the influence of positive intra-abdominal pressure on it, which significantly potentiates the obturator mechanism of the cardia.

The role of reflux of gastric and duodenal contents in GERD.

There is a positive relationship between the likelihood of EC and the level of acidification of the esophagus. Animal studies have demonstrated the damaging effects of hydrogen ions and pepsin, as well as bile acids and trypsin, on the protective mucosal barrier of the esophagus. However, the leading role is not given to the absolute indicators of aggressive components of gastric and duodenal contents entering the esophagus, but to a decrease in clearance and resistance of the esophageal mucosa.

Clearance and resistance of the esophageal mucosa.

The esophagus is equipped with an effective mechanism to eliminate shifts in the intraesophageal pH level to the acidic side. This protective mechanism is referred to as esophageal clearance and is defined as the rate of decrease of a chemical irritant from the esophageal cavity. Esophageal clearance is ensured due to active peristalsis of the organ, as well as the alkalizing properties of saliva and mucus. With GERD, esophageal clearance slows down, primarily due to weakened esophageal peristalsis and the antireflux barrier.

Resistance of the esophageal mucosa is caused by preepithelial, epithelial and postepithelial factors. Epithelial damage begins when hydrogen ions and pepsin or bile acids overcome the aqueous layer bathing the mucosa, the preepithelial protective mucus layer and active bicarbonate secretion. Cellular resistance to hydrogen ions depends on the normal level of intracellular pH (7.3-7.4). Necrosis occurs when this mechanism is exhausted and cell death occurs due to their sudden acidification. The formation of small superficial ulcerations is counteracted by an increase in cell turnover due to increased proliferation of basal cells of the esophageal mucosa. An effective postepithelial protective mechanism against acid aggression is the blood supply to the mucous membrane.

Classification

According to the International Classification of Diseases, 10th revision, GERD belongs to the category K21 and is divided into GERD with esophagitis (K21.0) and without esophagitis (K21.1).

For the classification of GERD, the degree of severity of RE is of fundamental importance.

In 1994, a classification was adopted in Los Angeles, which distinguished endoscopically positive and endoscopically negative stages of GERD. The term “damage to the mucous membrane of the esophagus” has replaced the concepts of “ulceration” and “erosion”. One of the advantages of this classification is its relative ease of use in everyday practice. The Los Angeles classification of EC was recommended to be used when assessing the results of endoscopic examination (Table 1).

The Los Angeles classification does not provide for characteristics of complications of ER (ulcers, strictures, metaplasia). Currently, the classification of Savary-Miller (1978) as modified by Carisson et al. is more widely used. (1996), presented in Table 2.

Of interest is the new clinical and endoscopic classification, which divides GERD into three groups:

• non-erosive, the most common form (60% of all cases of GERD), which includes GERD without signs of esophagitis and catarrhal ER;
• erosive-ulcerative form (34%), including its complications: ulcer and stricture of the esophagus;
• Barrett's esophagus (6%) - metaplasia of stratified squamous epithelium to cylindrical in the distal section as a consequence of GERD (the identification of this PB is due to the fact that this form of metaplasia is considered a precancerous condition).

Clinic and diagnostics

The first stage of diagnosis is interviewing the patient. Among the symptoms of GERD, the main ones are heartburn, sour belching, a burning sensation in the epigastrium and behind the sternum, which often occur after eating, when bending the body forward or at night. The second most common manifestation of this disease is retrosternal pain, which radiates to the interscapular region, neck, lower jaw, left half of the chest and can simulate angina. For differential diagnosis of the genesis of pain, it is important what provokes and relieves it. Esophageal pain is characterized by a connection with food intake, body position and relief by taking alkaline mineral waters and soda.

Extraesophageal manifestations of the disease include pulmonary (cough, shortness of breath, most often occurring in a lying position), otolaryngological (hoarseness, dry throat) and gastric (rapid satiety, bloating, nausea, vomiting) symptoms.

An X-ray examination of the esophagus can detect the penetration of contrast from the stomach into the esophagus, detect a hiatal hernia, ulcer, stricture and tumor of the esophagus.

To better identify gastroesophageal reflux and hiatal hernia, it is necessary to conduct a polypositional study with the patient bending forward with straining and coughing, as well as lying on his back while lowering the head end of the body.

A more reliable method for detecting gastroesophageal reflux is daily (24-hour) pH-metry of the esophagus, which allows you to assess the frequency, duration and severity of reflux, the influence of body position, food intake and medications on it. Studying daily changes in pH and esophageal clearance allows us to identify cases of reflux before the development of esophagitis.

In recent years, scintigraphy of the esophagus with a radioactive isotope of technetium has been used to assess esophageal clearance. A delay of the ingested isotope in the esophagus for more than 10 minutes indicates a slowdown in esophageal clearance.

Esophagomanometry - measuring pressure in the esophagus using special balloon probes - can provide valuable information about a decrease in pressure in the LES area, disturbances in peristalsis and tone of the esophagus. However, this method is rarely used in clinical practice.

The main method for diagnosing EC is endoscopic. Using endoscopy, you can confirm the presence of EC and assess its severity, monitor the healing of damage to the esophageal mucosa.

A biopsy of the esophagus followed by histological examination is performed mainly to confirm the presence of BE with a characteristic endoscopic picture, since BE can only be verified histologically.

Complications of reflux esophagitis

Peptic ulcers of the esophagus are observed in 2-7% of patients with GERD; in 15% of cases, ulcers are complicated by perforation, most often into the mediastinum. Acute and chronic blood loss of varying degrees occurs in almost all patients with peptic ulcers of the esophagus, with severe bleeding observed in half of them.

Table 1.
Los Angeles classification of RE

RE severity level	Characteristics of changes
Grade A	One or more lesions of the esophageal mucosa no more than 5 mm in length, limited to one fold of the mucous membrane
Grade B	One or more lesions of the esophageal mucosa more than 5 mm in length, limited by folds of the mucosa, and the lesions do not extend between two folds
Grade C	One or more lesions of the esophageal mucosa more than 5 mm in length, limited by folds of the mucosa, and the lesions extend between two folds but occupy less than 75% of the circumference of the esophagus
Grade D	Damage to the mucous membrane of the esophagus, covering 75% or more of its circumference

Table 2.
Classification of RE according to Savary-Miller as modified by Carisson et al.

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

A serious complication of GERD is Barrett's esophagus, which sharply (30-40 times) increases the risk of cancer. BE is detected by endoscopy in 8-20% of patients with GERD. The prevalence of PB in the general population is much lower and amounts to 350 per 100 thousand population. According to pathological statistics, for every known case there are 20 unrecognized ones. The cause of BE is the reflux of gastric contents, and therefore BE is considered as one of the manifestations of GERD.

The mechanism of PB formation can be represented as follows. With EC, the surface layers of the epithelium are first damaged, then a mucosal defect may form. Damage stimulates the local production of growth factors, which leads to increased proliferation and metaplasia of the epithelium.

Clinically, BE is manifested by general symptoms of RE and its complications. During endoscopic examination, BE should be suspected when the bright red metaplastic epithelium in the form of finger-like protrusions rises above the Z-line (anatomical transition of the esophagus to the cardia), displacing the pale pink squamous epithelium characteristic of the esophagus. Sometimes multiple inclusions of squamous epithelium may remain in the metaplastic mucosa - this is the so-called “island type” of metaplasia. The mucous membrane of the overlying sections may not be changed, or esophagitis of varying degrees of severity may occur.

Rice. 1
Diagnosis of atypical GERD with pulmonary manifestations

Endoscopically, there are two types of BE:

• short segment BE - the prevalence of metaplasia is less than 3 cm;
• long segment BE - the prevalence of metaplasia is more than 3 cm.

During a histological examination of the PB, elements of three types of glands are found in place of the stratified squamous epithelium: some are similar to the fundus, others to the cardiac, and others to the intestinal. It is the intestinal epithelium in the benign tumor that is associated with a high risk of malignant transformation. Currently, almost all researchers believe that we can talk about BE only in the presence of intestinal epithelium, the marker of which is goblet cells (a specialized type of intestinal epithelium).

Assessing the degree of dysplasia of metaplastic epithelium in BE and differentiating it from malignant transformation are difficult tasks. The final judgment about malignancy in diagnostically difficult cases can be made when a mutation in the tumor suppressive p53 gene is detected.

Extraesophageal manifestations of GERD

The following syndromes of extraesophageal manifestations of GERD can be distinguished.

1. Oropharyngeal symptoms include inflammation of the nasopharynx and sublingual tonsil, development of erosion of tooth enamel, caries, periodontitis, pharyngitis, sensation of a lump in the throat.
2. Otolaryngological symptoms are manifested by laryngitis, ulcers, granulomas and polyps of the vocal folds, otitis media, otalgia and rhinitis.
3. Bronchopulmonary symptoms are characterized by chronic recurrent bronchitis, the development of bronchiectasis, aspiration pneumonia, lung abscesses, paroxysmal night apnea and attacks of paroxysmal cough, as well as bronchial asthma.
4. Chest pain associated with heart disease is manifested by reflex angina when gastric contents reflux into the esophagus.
5. Chest pain not associated with heart disease (non-cardiac chest pain) is a common complication of GERD, requiring adequate therapy based on a careful differential diagnosis with cardiac pain.

Establishing a connection between bronchopulmonary diseases and GERD is of great clinical value, as it allows for a new approach to their treatment.

Figure 1 shows the diagnostic algorithm for atypical GERD with pulmonary manifestations, proposed by the American Gastroenterological Association. Its basis is a trial treatment with PPIs, and if a positive effect is achieved, then the connection between the chronic respiratory disease and GERD is considered proven. Further treatment should be aimed at preventing the reflux of gastric contents into the esophagus and further entry of refluxate into the bronchopulmonary system.

Great difficulties can arise in the differential diagnosis of chest pain associated with heart disease (angina, cardialgia) and other diseases that cause chest pain. The algorithm for differential diagnosis is presented in Figure 2. Daily monitoring of esophageal pH can help in recognizing chest pain associated with GERD (Figure 3).

Treatment

The goal of treatment for GERD is to eliminate complaints, improve quality of life, fight reflux, treat esophagitis, and prevent or eliminate complications. Treatment of GERD is often conservative rather than surgical.

Conservative treatment includes:

• recommendations for maintaining a certain lifestyle and diet;
• drug therapy: antacids, antisecretory drugs (H2 receptor blockers and proton pump inhibitors), prokinetics.

The following basic rules have been developed that the patient must always follow, regardless of the severity of RE:

• after eating, avoid bending forward and not lying down;
• sleep with the head of the bed raised;
• do not wear tight clothes and tight belts, corsets, bandages, which lead to increased intra-abdominal pressure;
• avoid large meals; do not eat at night; limit the consumption of foods that cause a decrease in LES pressure and have an irritating effect (fats, alcohol, coffee, chocolate, citrus fruits);
• stop smoking;
• reduce body weight in case of obesity;
• Avoid taking medications that cause reflux (anticholinergics, antispasmodics, sedatives, tranquilizers, calcium channel inhibitors, β-blockers, theophylline, prostaglandins, nitrates).

Antacids.

The goal of antacid therapy is to reduce the acid-proteolytic aggression of gastric juice. By increasing the intragastric pH level, these drugs eliminate the pathogenic effect of hydrochloric acid and pepsin on the esophageal mucosa. The arsenal of modern antacids has reached impressive proportions. Currently, they are produced, as a rule, in the form of complex preparations, the basis of which is aluminum hydroxide, magnesium hydroxide or bicarbonate, which are not absorbed in the gastrointestinal tract. Antacids are prescribed 3 times a day 40-60 minutes after meals, when heartburn most often occurs, and at night. It is recommended to adhere to the following rule: every attack of pain and heartburn should be stopped, since these symptoms indicate progressive damage to the mucous membrane of the esophagus.

Antisecretory drugs.

Antisecretory therapy for GERD is carried out to reduce the damaging effect of acidic gastric contents on the mucous membrane of the esophagus during gastroesophageal reflux. H 2 receptor blockers (ranitidine, famotidine) have found widespread use in EC. When using these drugs, the aggressiveness of the refluxed gastric contents is significantly reduced, which helps to stop the inflammatory and erosive-ulcerative process in the mucous membrane of the esophagus. Ranitidine is prescribed once at night in a daily dose of 300 mg or 150 mg 2 times a day; famotidine is used once at a dose of 40 mg or 20 mg 2 times a day.

Rice. 2.
Differential diagnosis of chest pain

Rice. 3.
Episodes of recurrent chest pain correlate with episodes of pH reflux<4 (В. Д. Пасечников, 2000).

In recent years, fundamentally new antisecretory drugs have appeared - H + ,K + -ATPase inhibitors(PPIs - omeprazole, lansoprazole, rabeprazole, esomeprazole). By inhibiting the proton pump, they provide a pronounced and long-lasting suppression of acidic gastric secretion. PPIs are particularly effective for peptic erosive-ulcerative esophagitis, ensuring healing of the affected areas in 90-96% of cases after 6-8 weeks of treatment.

In our country, omeprazole has found the most widespread use. The antisecretory effect of this drug is superior to Hg receptor blockers. Omeprazole dosage: 20 mg 2 times a day or 40 mg in the evening.

In recent years, new PPIs, rabeprazole and esomeprazole (Nexium), have found widespread use in clinical practice.

Rabeprazole converts faster than other PPIs into the active (sulfonamide) form. Thanks to this, already on the first day of taking rabeprazole, such a clinical manifestation of GERD as heartburn decreases or completely disappears.

Of significant interest is a new PPI - esomeprazole (Nexium), which is a product of a special technology. As is known, stereoisomers (substances whose molecules have the same sequence of chemical bonds of atoms, but different locations of these atoms relative to each other in space) can differ in biological activity. Pairs of optical isomers, which are mirror images of each other) are designated as R (from the Latin rectus - straight or rota dexterior - right wheel, clockwise) and S (sinister - left or counterclockwise).

Esomeprazole (Nexium) is the S-isomer of omeprazole, the first and only PPI currently available that is a pure optical isomer. It is known that the S-isomers of other PPIs are superior in pharmacokinetic parameters to their R-isomers and, accordingly, racemic mixtures, which are the existing drugs of this group (omeprazole, lansoprazole, pantoprazole, rabeprazole). So far, it has been possible to create a stable S-isomer only for omeprazole. Studies in healthy volunteers have shown that esomeprazole is optically stable in any dosage form - both oral and intravenous.

The clearance of esomeprazole is lower than that of omeprazole and the R-isomer. The consequence of this is the higher bioavailability of esomeprazole compared to omeprazole. In other words, a large proportion of each dose of esomeprazole remains in the bloodstream after first-pass metabolism. Thus, the amount of the drug that inhibits the proton pump of the gastric parietal cell increases.

The antisecretory effect of esomeprazole is dose-dependent and increases during the first days of administration [11]. The effect of esomeprazole occurs 1 hour after oral administration at a dose of 20 or 40 mg. When taking the drug daily for 5 days at a dose of 20 mg once a day, the average maximum acid concentration after stimulation with pentagastrin is reduced by 90% (measurement was carried out 6-7 hours after taking the last dose of the drug). In patients with symptomatic GERD, the intragastric pH level during 24-hour monitoring after 5 days of esomeprazole in doses of 20 and 40 mg remained above 4 for an average of 13 and 17 hours, respectively. Among patients taking esomeprazole 20 mg per day, maintaining a pH level above 4 for 8, 12 and 16 hours was achieved in 76%, 54% and 24% of cases, respectively. For 40 mg esomeprazole, this ratio was 97%, 92% and 56%, respectively (p<0,0001) .

An important component that ensures the high stability of the antisecretory effect of esomeprazole is its extremely predictable metabolism. Esomeprazole provides 2 times greater stability of such an indicator as individual variability in the suppression of pentagastrin-stimulated gastric secretion than omeprazole at an equivalent dose.

The effectiveness of esomeprazole in GERD has been studied in several randomized, double-blind, multicenter studies. In two large studies that included more than 4000 GERD patients uninfected with H. pylori, esomeprazole at daily doses of 20 or 40 mg was significantly more effective in healing erosive esophagitis than omeprazole at a dose of 20 mg. In both studies, esomeprazole was significantly superior to omeprazole after both 4 and 8 weeks of treatment.

Complete relief of heartburn (absence for 7 consecutive days) in a group of 1960 patients with GERD was also achieved with esomeprazole 40 mg/day in more patients than with omeprazole on day 1 of taking the drugs (30% vs. 22% , R<0,001), так и к 28 дню (74% против 67%, р <0,001) . Аналогичные результаты были получены и в другом, большем по объему (п = 2425) исследовании (р <0,005) . В обоих исследованиях было показано преимущество эзомепразола над омепразолом (в эквивалентных дозах) как по среднему числу дней до наступления полного купирования изжоги, так и по суммарному проценту дней и ночей без изжоги в течение всего периода лечения. Еще в одном исследовании, включавшем 4736 больных эрозивным эзофагитом, эзомепразол в дозе 40 мг/сут достоверно превосходил омепразол в дозе 20 мг/сут по проценту ночей без изжоги (88,1%, доверительный интервал - 87,9-89,0; против 85,1%, доверительный интервал 84,2-85,9; р <0,0001) .Таким образом, наряду с известными клиническими показателями эффективности лечения ГЭРБ, указанные дополнительные критерии позволяют заключить, что эзомепразол объективно превосходит омепразол при лечении ГЭРБ. Столь высокая клиническая эффективность эзомепразола существенно повышает и его затратную эффективность. Так, например, среднее число дней до полного купирования изжоги при использовании эзомепразола в дозе 40 мг/сут составляло 5 дней, а оме-празола в дозе 20 мг/сут - 9 дней . При этом важно отметить, что омепразол в течение многих лет являлся золотым стандартом в лечении ГЭРБ, превосходя по клиническим критериям эффективности все другие ИПП, о чем свидетельствует анализ результатов более чем 150 сравнительных исследований .

Esomeprazole has also been studied as a maintenance drug for GERD. Two double-blind, placebo-controlled studies involving more than 300 patients with GERD with healed esophagitis assessed the effectiveness of three dosages of esomeprazole (10, 20, and 40 mg/day) given for 6 months.

At all doses studied, esomeprazole was significantly superior to placebo, but the best dose/efficacy ratio for maintenance therapy was 20 mg/day. There are published data on the effectiveness of a maintenance dose of esomeprazole 40 mg/day prescribed to 808 patients with GERD: remission after 6 and 12 months was maintained in 93% and 89.4% of patients, respectively.

The unique properties of esomeprazole have enabled the use of a completely new approach to long-term treatment of GERD - on-demand therapy, the effectiveness of which was studied in two 6-month blind, placebo-controlled studies, including 721 and 342 patients with GERD, respectively. Esomeprazole has been used in doses of 40 mg and 20 mg. If symptoms of the disease appeared, patients were allowed to use no more than one dose (tablet) per day, and if the symptoms did not stop, then they were allowed to take antacids. When summing up the results, it turned out that on average, patients took Esomeprazole (regardless of the dose) once every 3 days, while inadequate control over symptoms (heartburn) was noted by only 9% of patients receiving 40 mg of esomeprazole, 5% - 20 mg and 36 % - placebo (p<0,0001). Число больных, вынужденных дополнительно принимать антациды, оказалось в группе плацебо в 2 раза большим, чем в пациентов, получавших любую из дозировок эзомепразола .

Thus, clinical studies convincingly indicate that Esomeprazole is a promising treatment for GERD both in its most severe forms (erosive esophagitis) and in non-erosive reflux disease.

Prokinetics.

Representatives of this group of drugs have an antireflux effect and also enhance the release of acetylcholine in the gastrointestinal tract, stimulating the motility of the stomach, small intestine and esophagus. They increase the tone of the LES, accelerate gastric emptying, have a positive effect on esophageal clearance and weaken gastroesophageal reflux.

Domperidone, which is an antagonist of peripheral dopamine receptors, is usually used as a prokinetic agent for EC. Domperidone is prescribed 10 mg (1 tablet) 3 times a day 15-20 minutes before meals.

In case of EC caused by reflux of duodenal contents (primarily bile acids) into the esophagus, which is usually observed in gallstone disease, a good effect is achieved by taking non-toxic ursode-oxycholic bile acid at a dose of 5 mg/kg per day for 6-8 months .

Choice of treatment tactics.

When choosing treatment for GERD in the stage of erosive-ulcerative RE, it should be remembered that in these cases therapy is not an easy task. On average, healing of a mucosal defect occurs:

• 3-4 weeks for duodenal ulcer;
• 4-6 weeks for stomach ulcers;
• for 8-12 weeks for erosive and ulcerative lesions of the esophagus.

Currently, a step-by-step treatment scheme has been developed depending on the severity of EC. According to this scheme, already in grades 0 and 1 EC, it is recommended to begin treatment with a full dose of PPI, although the use of H 2 blockers in combination with prokinetics is also allowed (Fig. 4).

The treatment regimen for patients with severe EC (stage II-III) is presented in Figure 5. The peculiarity of this regimen is longer treatment cycles and the prescription (if necessary) of high doses of PPIs. In the absence of effect from conservative treatment in patients in this category, it is often necessary to raise the question of antireflux surgery. The advisability of surgical treatment should also be discussed for complications of EC that are not amenable to drug therapy.

Surgery.

The goal of operations aimed at eliminating reflux is to restore normal function of the cardia.

Indications for surgical treatment: 1) failure of conservative treatment; 2) complications of GERD (strictures, recurrent bleeding); 3) frequent aspiration pneumonia; 4) PB (due to the risk of malignancy). Especially often, indications for surgery arise when GERD is combined with a hiatal hernia.

The main type of surgery for reflux esophagitis is Nissen fundoplication. Currently, methods of fundoplication performed through a laparoscope are being developed and implemented. The advantages of laparoscopic fundoplication include significantly lower rates of postoperative mortality and rapid rehabilitation of patients.

Currently, in case of BE, the following endoscopic techniques are used to influence foci of incomplete intestinal metaplasia and severe epithelial dysplasia:

• laser destruction, coagulation with argon plasma;
• multipolar electrocoagulation;
• photodynamic destruction (photo-sensitizing drugs are administered 48-72 hours before the procedure, then treated with a laser);
• endoscopic local resection of the esophageal mucosa.

All of the listed methods of influencing the foci of metaplasia are used against the background of the use of PPIs that suppress secretion and prokinetics that reduce gastroesophageal reflux.

Prevention and medical examination

Due to the widespread prevalence of GERD, which leads to a decrease in the quality of life, and the danger of complications in severe forms of EC, the prevention of this disease is a very urgent task.

The goal of primary prevention of GERD is to prevent the development of the disease. Primary prevention includes compliance with the following recommendations:

• maintaining a healthy lifestyle (no smoking and drinking strong alcoholic beverages);
• rational nutrition (avoid large meals, do not eat at night, limit the consumption of very spicy and hot foods;
• weight loss in obesity;
• Only according to strict indications, take medications that cause reflux (anticholinergic, antispasmodic, sedatives, tranquilizers, calcium channel inhibitors, b-blockers, prostaglandins, nitrates) and damage the mucous membrane (non-steroidal anti-inflammatory drugs).

Rice. 4.
Choice of treatment for patients with endoscopically negative or mild (0-1) degrees of reflux esophagitis

Rice. 5.
Choice of treatment for patients with severe (II-III) degrees of reflux esophagitis

The goal of secondary prevention of GERD is to reduce the frequency of relapses and prevent progression of the disease. An obligatory component of secondary prevention is compliance with the above recommendations for primary prevention. Secondary drug prevention largely depends on the severity of EC.

“On-demand therapy” is used to prevent exacerbations in the absence of esophagitis or mild esophagitis (grade 0-1 ER). Each attack of pain and heartburn should be stopped, since this is a signal of pathological acidification of the esophagus, which contributes to progressive damage to its mucous membrane. Severe esophagitis (especially grade III-IV EC) requires long-term, sometimes constant maintenance therapy with PPIs or H2 receptor blockers in combination with prokinetics.

The criteria for successful secondary prevention are considered to be a reduction in the number of exacerbations of the disease, absence of progression, reduction in the severity of EC and prevention of the development of complications.

Patients with GERD in the presence of endoscopic signs of ER require clinical observation with endoscopic control at least once every 2-3 years.

Patients who have been diagnosed with BE should be included in a special group. It is advisable to carry out endoscopic monitoring with targeted biopsy of the esophageal mucosa from the area of ​​visually altered epithelium annually (but at least once a year), if there was no dysplasia during the previous study. If the latter is detected, endoscopic monitoring should be carried out more often so as not to miss the moment of malignancy. The presence of low-grade dysplasia in BE requires endoscopy with a biopsy every 6 months, and severe dysplasia - after 3 months. In patients with confirmed severe dysplasia, the question of surgical treatment should be raised.

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Gastroesophageal reflux disease

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

ICD-10

K21.0 Gastroesophageal reflux with esophagitis

K21.9 Gastroesophageal reflux without esophagitis.

EXAMPLE OF FORMULATION OF DIAGNOSIS

EPIDEMIOLOGY

The true prevalence of the disease is unknown, due to the wide variability of clinical symptoms. Symptoms of GERD, upon careful questioning, are found in 20–50% of the adult population, and endoscopic signs in more than 7–10% of the population. In the United States, heartburn, the main symptom of GERD, is experienced weekly by 10–20% of adults. There is no comprehensive epidemiological picture for Russia.

The true prevalence of GERD is much higher than statistical data, including because only less than 1/3 of GERD patients consult a doctor.

Women and men get sick equally often.

CLASSIFICATION

Currently, there are two forms of GERD.

■ Endoscopically negative reflux disease, or non-erosive reflux disease, 60–65% of cases.

■ Reflux esophagitis - 30–35% of patients.

■ Complications of GERD: peptic stricture, esophageal bleeding, Berrett's esophagus, esophageal adenocarcinoma.

Table 4-2. Los Angeles classification of reflux esophagitis

DIAGNOSTICS

The diagnosis of GERD should be assumed if the patient has characteristic symptoms: heartburn, belching, regurgitation; in some cases, extraesophageal symptoms are observed.

HISTORY AND PHYSICAL EXAMINATION

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

The intensity of clinical manifestations of GERD depends on the concentration of hydrochloric acid in the refluxate, the frequency and duration of its contact with the mucous membrane of the esophagus, and the hypersensitivity of the esophagus.

ESOPHAGUEAL SYMPTOMS OF GERD

■ Heartburn is a burning sensation of varying intensity that occurs behind the breastbone (in the lower third of the esophagus) and/or in the epigastric region. Heartburn occurs in at least 75% of patients and occurs due to prolonged contact of the acidic contents of the stomach (pH less than 4) with the mucous membrane of the esophagus. The severity of heartburn does not correlate with the severity of esophagitis. It is characterized by intensification after eating, drinking carbonated drinks, alcohol, during physical stress, bending over and in a horizontal position.

■ Sour belching usually increases after eating or drinking carbonated drinks. Regurgitation of food, observed in some patients, increases with physical activity and a position that promotes regurgitation.

■ Dysphagia and odynophagia (pain when swallowing) are observed less frequently. The appearance of persistent dysphagia indicates the development of esophageal stricture. Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma.

■ Pain behind the sternum can radiate to the interscapular region, neck, lower jaw, left half of the chest; often imitate angina pectoris. Esophageal pain is characterized by a connection with food intake, body position and its relief by taking alkaline mineral waters and antacids.

EXTRA-ESOURCAL SYMPTOMS OF GERD:

■ bronchopulmonary - cough, asthma attacks;

■ dental - caries, erosion of tooth enamel.

LABORATORY EXAMINATION

There are no laboratory symptoms pathognomonic for GERD.

INSTRUMENTAL RESEARCH

MANDATORY INVESTIGATION METHODS

SINGLE STUDIES

■ FEGDS: allows you to differentiate non-erosive reflux disease and reflux esophagitis, and identify the presence of complications.

■ X-ray examination of the esophagus and stomach: if a hiatal hernia, stricture, or adenocarcinoma of the esophagus is suspected.

STUDIES CONDUCTED IN DYNAMICS

■ FEGDS: can not be repeated for non-erosive reflux disease.

■ Biopsy of the esophageal mucosa for complicated GERD: ulcers, strictures, Berrett’s esophagus.

ADDITIONAL INVESTIGATION METHODS

SINGLE STUDIES

■ 24-hour intraesophageal pH-metry: increase in total reflux time (pH less than 4.0 more than 5% during the day) and duration of the reflux episode (more than 5 minutes). The method allows you to evaluate the pH in the esophagus and stomach, the effectiveness of drugs; the value of the method is especially high in the presence of extraesophageal manifestations and the absence of effect from therapy.

■ Intraesophageal manometry: carried out to assess the functioning of the lower esophageal sphincter, the motor function of the esophagus.

■ Ultrasound of the abdominal organs: if GERD is unchanged, it is performed to identify concomitant pathology of the abdominal organs.

■ ECG, bicycle ergometry: used for differential diagnosis with ischemic heart disease; no changes are detected with GERD.

■ Proton pump inhibitor test: relief of clinical symptoms (heartburn) while taking proton pump inhibitors.

DIFFERENTIAL DIAGNOSTICS

With a typical clinical picture of the disease, differential diagnosis is usually not difficult. In the presence of extraesophageal symptoms, it should be differentiated from ischemic heart disease, bronchopulmonary pathology (bronchial asthma, etc.). For differential diagnosis of GERD with esophagitis of other etiologies, a histological examination of biopsy specimens is performed.

INDICATIONS FOR CONSULTATION WITH OTHER SPECIALISTS

The patient should be referred for consultation to specialists if the diagnosis is uncertain, if there are atypical or extraesophageal symptoms, or if complications are suspected. You may need to consult a cardiologist, pulmonologist, or otorhinolaryngologist (for example, a cardiologist if you have chest pain that is not relieved by taking proton pump inhibitors).

TREATMENT

GOALS OF THERAPY

■ Relief of clinical symptoms.

■ Healing of erosions.

■ Improving quality of life.

■ Preventing or managing complications.

■ Prevention of relapse.

INDICATIONS FOR HOSPITALIZATION

■ Carrying out antireflux treatment in case of complicated course of the disease, as well as in case of ineffectiveness of adequate drug therapy.

■ Carrying out surgical intervention (fundoplication) if drug therapy and endoscopic or surgical interventions are ineffective in the presence of complications of esophagitis: stricture, Berrett's esophagus, bleeding.

NON-DRUG TREATMENT

✧Avoid large meals.

✧Limit the consumption of foods that reduce the pressure of the lower esophageal sphincter and have an irritating effect on the mucous membrane of the esophagus: foods rich in fat (whole milk, cream, cakes, pastries), fatty fish and meat (goose, duck, as well as pork, lamb, fatty beef), alcohol, drinks containing caffeine (coffee, cola, strong tea, chocolate), citrus fruits, tomatoes, onions, garlic, fried foods, avoid carbonated drinks.

✧After eating, avoid bending forward and horizontal position; The last meal is no later than 3 hours before bedtime.

✧Sleep with the head end of the bed raised.

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

✧Quit smoking.

✧Maintain normal body weight.

■ Do not take drugs that promote reflux (sedatives and tranquilizers, calcium channel inhibitors, β-blockers, theophylline, prostaglandins, nitrates).

DRUG THERAPY

Duration of treatment for GERD: 4–6 weeks for non-erosive reflux disease and at least 8–12 weeks for reflux esophagitis, followed by maintenance therapy for 26–52 weeks.

Drug therapy includes the prescription of prokinetics, antacids and antisecretory agents.

■ Prokinetics: domperidone 10 mg 4 times a day.

■ The goal of antisecretory therapy for GERD is to reduce the damaging effect of acidic gastric contents on the esophageal mucosa during gastroesophageal reflux. The drugs of choice are proton pump inhibitors (omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole).

✧GERD with esophagitis (8–12 weeks):

-omeprazole 20 mg 2 times a day, or

–lansoprazole 30 mg 2 times a day, or

–esomeprazole 40 mg/day, or

–rabeprazole 20 mg/day.

Relief of symptoms and healing of erosions. If the standard dose of proton pump inhibitors is ineffective, the dose should be doubled.

✧Non-erosive reflux disease (4–6 weeks):

–omeprazole 20 mg/day, or

–lansoprazole 30 mg/day, or

–esomeprazole 20 mg/day, or

–rabeprazole 10–20 mg/day.

Treatment effectiveness criterion- permanent relief of symptoms.

■ Taking histamine H2 receptor blockers as antisecretory drugs is possible, but their effect is lower than that of proton pump inhibitors.

■ Antacids can be used as a symptomatic treatment for infrequent heartburn, but in this case, preference should be given to taking proton pump inhibitors “on demand”. Antacids are usually prescribed 3 times a day 40–60 minutes after meals, when heartburn and chest pain most often occur, and also at night.

■ For reflux esophagitis caused by the reflux of duodenal contents (primarily bile acids) into the esophagus, which is usually observed with cholelithiasis, a good effect is achieved by taking ursodeoxycholic acid at a dose of 250–350 mg/day. In this case, it is advisable to combine ursodeoxycholic acid with prokinetics in the usual dose.

Maintenance therapy is usually carried out with proton pump inhibitors according to one of the following regimens.

■ Continuous use of proton pump inhibitors in a standard or half dose (omeprazole, esomeprazole - 10 or 20 mg/day, rabeprazole - 10 mg/day).

■ On-demand therapy - taking proton pump inhibitors when symptoms appear (on average once every 3 days) for endoscopically negative reflux disease.

SURGERY

The goal of operations aimed at eliminating reflux (fundoplications, including endoscopic ones) is to restore normal function of the cardia.

Indications for surgical treatment:

■ ineffectiveness of adequate drug therapy;

■ complications of GERD (esophageal strictures, repeated bleeding);

■ Berrett's esophagus with high-grade epithelial dysplasia due to the risk of malignancy.

APPROXIMATE DURATION OF TEMPORARY DISABILITY

They are determined by the relief of clinical symptoms and healing of erosions during control FEGDS.

FURTHER MANAGEMENT OF THE PATIENT

In the case of non-erosive reflux disease with complete relief of clinical symptoms, a control FEGDS is not necessary. Remission of reflux esophagitis should be confirmed endoscopically. When the clinical picture changes, FEGDS is performed in some cases.

Maintenance therapy is mandatory, since without it the disease recurs in 90% of patients within 6 months.

Dynamic monitoring of the patient is carried out to monitor complications, identify Berrett's esophagus and drug control of symptoms of the disease.

Symptoms suggestive of complications should be monitored:

■ dysphagia and odynophagia;

■ bleeding;

■ loss of body weight;

■ early feeling of satiety;

■ chest pain;

■ frequent vomiting.

If all these signs are present, consultation with specialists and further diagnostic examination are indicated.

Intestinal epithelial metaplasia serves as the morphological substrate of asymptomatic Berrett's esophagus. Risk factors for Berrett's esophagus:

■ heartburn more than 2 times a week;

■ male gender;

■ duration of symptoms more than 5 years.

If a diagnosis of Berrett's esophagus is established, endoscopic examinations with biopsies should be performed annually during continuous maintenance therapy with a full dose of proton pump inhibitors. If low-grade dysplasia is detected, repeat FEGDS with biopsy and histological examination of the biopsy specimen is carried out after 6 months. If low-grade dysplasia persists, it is recommended to perform a repeat histological examination after 6 months. If low-grade dysplasia persists, repeated histological examinations are carried out annually. If high-grade dysplasia is detected, the result of histological examination is assessed independently by two morphologists. Once the diagnosis is confirmed, the issue of endoscopic or surgical treatment of Berrett's esophagus is decided.

EDUCATION OF THE PATIENT

The patient should be explained that GERD is a chronic condition that usually requires long-term maintenance therapy with proton pump inhibitors to prevent complications.

The patient should be informed about the possible complications of GERD and recommended to consult a doctor if symptoms of complications occur (see section “Further management of the patient”).

Patients with long-term uncontrolled reflux symptoms should be explained the need for endoscopic examination to identify complications (such as Berrett's esophagus), and in the presence of complications, the need for periodic FEGDS with taking a biopsy sample.

FORECAST

With non-erosive reflux disease and mild reflux esophagitis, the prognosis is generally favorable. Patients remain able to work for a long time. The disease does not affect life expectancy, but significantly reduces its quality during exacerbation. Early diagnosis and timely treatment prevent the development of complications and maintain ability to work. The prognosis worsens with a long duration of the disease in combination with frequent long-term relapses, with complicated forms of GERD, especially with the development of Berrett's esophagus, due to the increased risk of developing adenocarcinoma of the esophagus.

Gastroesophageal reflux disease is a pathological process that results from deterioration of the motor function of the upper gastrointestinal tract. It occurs as a result of reflux - a regularly repeated reflux of stomach or duodenal contents into the esophagus, resulting in damage to the mucous membrane of the esophagus, and damage to overlying organs (larynx, pharynx, trachea, bronchi) can also occur. What kind of disease is this, what are the causes and symptoms, as well as the treatment of GERD - we will look at this in this article.

GERD - what is it?

GERD (gastroesophageal reflux disease) 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. This is a normal physiological phenomenon if it occurs occasionally after eating and is not accompanied by unpleasant subjective sensations.

But if there are many such reflux and they are accompanied by inflammation or damage to the mucous membrane of the esophagus, and extra-esophageal symptoms, then this is already a disease.

GERD occurs in all age groups, in both sexes, including children; the incidence increases with age.

Classification

There are two main forms of gastroesophageal reflux disease:

• non-erosive (endoscopically negative) reflux disease (NERD) - occurs in 70% of cases;
• (RE) - the incidence rate is about 30% of the total number of GERD diagnoses.

Experts distinguish four degrees of reflux damage to the esophagus:

1. Linear defeat– individual areas of inflammation of the mucous membrane and foci of erosion on its surface are observed.
2. Drain lesion– the negative process spreads over a large surface due to the merging of several foci into continuous inflamed areas, but not the entire area of ​​the mucous membrane is yet covered by the lesion.
3. Circular lesion– zones of inflammation and foci of erosion cover the entire inner surface of the esophagus.
4. Stenosing lesion– against the background of complete damage to the inner surface of the esophagus, complications are already occurring.

Causes

The main pathogenetic substrate for the development of gastroesophageal reflux disease is gastroesophageal reflux itself, that is, retrograde reflux of stomach contents into the esophagus. Reflux most often develops due to incompetence of the sphincter located at the border of the esophagus and stomach.

The following factors contribute to the development of the disease:

• Decreased functional ability of the lower esophageal sphincter (for example, due to destructuring of the esophagus due to hiatal hernia);
• Damaging properties of gastrointestinal contents (due to the content of hydrochloric acid, as well as pepsin, bile acids);
• Gastric emptying disorders;
• Increased intra-abdominal pressure;
• Pregnancy;
• Smoking;
• Overweight;
• Decreased clearance of the esophagus (for example, due to a decrease in the neutralizing effect of saliva, as well as bicarbonates of esophageal mucus);
• Taking medications that reduce smooth muscle tone (calcium channel blockers, beta-agonists, antispasmodics, nitrates, M-anticholinergics, bile-containing enzyme preparations).

Factors contributing to the development of GERD are:

• disorders of motor functions of the upper digestive tract,
• hyperacidotic conditions,
• reduced protective function of the esophageal mucosa.

Symptoms of gastroesophageal reflux disease

Once in the esophagus, the contents of the stomach (food, hydrochloric acid, digestive enzymes) irritate the mucous membrane, leading to the development of inflammation.

The main symptoms of gastroesophageal reflux are as follows:

• heartburn;
• belching acid and gas;
• acute sore throat;
• discomfort in the pit of the stomach;
• pressure that occurs after eating, which increases after eating food that promotes the production of bile and acid.

In addition, acid from the stomach, entering the esophagus, has a negative effect on local tissue immunity, affecting not only the esophagus, but also the nasopharynx. A person suffering from GERD often complains of chronic pharyngitis.

GERD often occurs with atypical clinical manifestations:

• chest pain (usually after eating, worse when bending over),
• heaviness in the stomach after eating,
• hypersalivation (increased salivation) during sleep,
• bad breath,
• hoarseness.

Symptoms appear and intensify after eating, physical activity, in a horizontal position, and decrease in a vertical position, after drinking alkaline mineral waters.

Signs of GERD with esophagitis

Reflux disease in the esophagus can cause the following reactions:

• inflammatory process,
• damage to the walls in the form of ulcers,
• modification of the lining layer in contact with the refluxate into a form unusual for a healthy organ;
• narrowing of the lower esophagus.

If the above symptoms occur more than 2 times a week for 2 months, you should consult a doctor for examination.

GERD in children

The main reason for the development of reflux disease in children is the immaturity of the lower sphincter, which prevents the evacuation of food from the stomach back into the esophagus.

Other causes that contribute to the development of GERD in childhood include:

• functional insufficiency of the esophagus;
• narrowing of the gastric outflow tract;
• recovery period after surgery on the esophagus;
• operations for gastric resection;
• consequences of serious injuries;
• oncological processes;
• difficult childbirth;
• high intracranial pressure.

Common symptoms of GERD in a child are as follows:

• frequent burping or burping;
• poor appetite;
• pain in the stomach;
• the child is excessively capricious during feeding;
• frequent vomiting or retching;
• hiccups;
• labored breathing;
• frequent cough, especially at night.

Treatment for gastroesophageal reflux disease in children will depend on symptoms, age, and overall health. In order to prevent the development of this disease in a child, parents should closely monitor his diet.

Complications

Gastroesophageal reflux disease can cause the following complications in the body:

• esophageal stricture;
• ulcerative lesions of the esophageal mucosa;
• bleeding;
• the formation of Barrett's syndrome - complete replacement (metaplasia) of the stratified squamous epithelium of the esophagus with columnar gastric epithelium (the risk of esophageal cancer with epithelial metaplasia increases 30-40 times);
• malignant degeneration of esophagitis.

Diagnostics

In addition to the diagnostic methods described, it is important to visit the following specialists:

• cardiologist;
• pulmonologist;
• otorhinolaryngologist;
• surgeon, his consultation is necessary in case of ineffectiveness of the ongoing drug treatment, the presence of large diaphragmatic hernias, or in the event of complications.

To diagnose gastroesophageal reflux, the following methods are used:

• endoscopic examination of the esophagus, which allows to identify inflammatory changes, erosions, ulcers and other pathologies;
• daily monitoring of acidity (pH) in the lower part of the esophagus. Normal level pH should be between 4 and 7, changes in evidence may indicate the cause of the disease;
• radiography - allows you to detect ulcers, erosions, etc.;
• manometric examination of the esophageal sphincters - performed to assess their tone;
• scintigraphy using radioactive substances - performed to assess esophageal clearance;
• biopsy - performed if Barrett's esophagus is suspected;
• ECG and daily ECG monitoring; Ultrasound examination of the abdominal organs.

Of course, not all methods are used for accurate diagnosis. Most often, the doctor only needs the data obtained during the examination and interview of the patient, as well as the conclusion of the FEGDS.

Treatment of reflux disease

Treatment of gastroesophageal reflux disease can be medication or surgery. Regardless of the stage and severity of GERD, during therapy it is necessary to constantly adhere to certain rules:

1. Do not lie down or lean forward after eating.
2. Do not wear tight clothes, corsets, tight belts, bandages - this leads to an increase in intra-abdominal pressure.
3. Sleep on a bed in which the part where the head is located is raised.
4. Do not eat at night, avoid large meals, do not eat too hot food.
5. Quit alcohol and smoking.
6. Limit consumption of fats, chocolate, coffee and citrus fruits, as they are irritating and reduce LES pressure.
7. Lose weight if you are obese.
8. Stop taking medications that cause reflux. These include antispasmodics, β-blockers, prostaglandins, anticholinergic drugs, tranquilizers, nitrates, sedatives, calcium channel inhibitors.

Medications for GERD

Drug treatment of gastroesophageal reflux disease is carried out by a gastroenterologist. Therapy takes from 5 to 8 weeks (sometimes the course of treatment lasts up to 26 weeks) and is carried out using the following groups of drugs:

1. Antisecretory agents (antacids) have the function of reducing the negative effect of hydrochloric acid on the surface of the esophagus. The most common are: Maalox, Gaviscon, Almagel.
2. As a prokinetic Motilium is used. The course of treatment for catarrhal or endoscopically negative esophagitis lasts about 4 weeks, for erosive esophagitis 6-8 weeks, if there is no effect, treatment can be continued up to 12 weeks or more.
3. Taking vitamin preparations, including vitamin B5 and U in order to restore the mucous membrane of the esophagus and generally strengthen the body.

GERD can also be caused by an unbalanced diet. Therefore, drug treatment must be supported by proper nutrition.

With timely identification and compliance with lifestyle recommendations (non-drug treatment measures for GERD), the prognosis is favorable. In the case of a prolonged, often relapsing course with regular refluxes, the development of complications, and the formation of Barrett's esophagus, the prognosis noticeably worsens.

The criterion for recovery is the disappearance of clinical symptoms and endoscopic findings. To prevent complications and relapses of the disease, monitor the effectiveness of treatment, it is necessary to regularly visit a doctor, therapist or gastroenterologist, at least once every 6 months, especially in the fall and spring, and undergo examinations.

Surgical treatment (operation)

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

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 of young patients with GERD for long-term antireflux therapy.

Diet for GERD

Diet for gastroesophageal reflux disease is one of the main areas of effective treatment. Patients suffering from esophagitis should adhere to the following dietary recommendations:

1. Eliminate fatty foods from your diet.
2. To stay healthy, avoid fried and spicy foods.
3. If you are ill, it is not recommended to drink coffee or strong tea on an empty stomach.
4. People prone to esophageal diseases are not recommended to consume chocolate, tomatoes, onions, garlic, mint: these products reduce the tone of the lower sphincter.

Thus, the approximate daily diet of a patient with GERD is as follows (see daily menu):

Some doctors believe that for patients diagnosed with gastroesophageal reflux disease, these dietary rules and a healthy lifestyle are more important than the foods from which the menu is composed. You should also remember that you need to approach your diet taking into account your own feelings.

Folk remedies

Alternative medicine involves a large number of recipes; the choice of a specific one depends on the individual characteristics of the human body. But folk remedies cannot act as a separate therapy; they are included in the general complex of therapeutic measures.

1. Sea buckthorn or rosehip oil: take one teaspoon up to three times a day;
2. The home medicine cabinet of a patient with reflux disease should contain the following dried herbs: birch bark, lemon balm, flax seeds, oregano, St. John's wort. You can prepare a decoction by pouring a couple of tablespoons of the herb with boiling water in a thermos and letting it sit for at least an hour, or by adding a handful of the medicinal plant to boiling water, remove the pan from the stove, cover with a lid and let it brew.
3. Crushed plantain leaves(2 tbsp.), St. John's wort (1 tbsp.) Place in an enamel container, pour boiling water (500 ml). After half an hour, the tea is ready to drink. You can take the drink for a long time, half a glass in the morning.
4. 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.

Prevention

In order to never encounter an unpleasant disease, it is important to always pay attention to your diet: do not overeat, limit the consumption of unhealthy foods, and monitor your body weight.

If these requirements are met, the risk of GERD will be minimized. Timely diagnosis and systematic treatment can prevent the progression of the disease and the development of life-threatening complications.

Gastroesophageal reflux disease (GERD) a disease characterized by the development of specific symptoms and/or inflammatory lesions of the distal part of the esophagus due to repeated, retrograde entry of gastric and/or duodenal contents into the esophagus.

The pathogenesis is based on insufficiency of the lower esophageal sphincter (circular smooth muscle, which is in a state of tonic contraction in a healthy person and separates the esophagus and stomach), which contributes to the reflux of stomach contents into the esophagus (reflux).

Long-term reflux leads to esophagitis and sometimes to tumors of the esophagus. Typical (heartburn, belching, dysphagia) and atypical (cough, chest pain, wheezing) manifestations of the disease occur.

Pathological changes in the respiratory system (pneumonia, bronchospasm, idiopathic pulmonary fibrosis), vocal cords (hoarseness, laryngitis, laryngeal cancer), hearing organ (otitis media), teeth (enamel defects), may be additional signs indicating reflux .

The diagnosis is made based on a clinical assessment of the symptoms of the disease, the results of endoscopic studies, and pH-metry data (monitoring pH in the esophagus).

Treatment consists of lifestyle changes and taking medications that reduce gastric acidity (proton pump inhibitors). In some cases, surgical treatment methods may be used.

• Classification of GERD

  First of all, the classification divides gastroesophageal reflux disease into 2 categories: GERD with esophagitis and GERD without esophagitis.

  • GERD with esophagitis (endoscopically positive reflux disease)

    Reflux esophagitis is damage to the mucous membrane of the esophagus, visible during endoscopy, an inflammatory process in the distal (lower) part of the esophagus caused by the action of gastric juice, bile, pancreatic and intestinal secretions on the mucous membrane of the esophagus. It is observed in 30-45% of patients with GERD.

    Complications of reflux esophagitis are:

    • Esophageal strictures.
    • Erosion and ulcers of the esophagus, accompanied by bleeding.
    • Barrett's esophagus.
    • Adenocarcinoma of the esophagus.

    The condition of the esophageal mucosa is assessed endoscopically according to the M.Savary-J.Miller classification, or according to the Los Angeles (1994) classification.

    • Classification by M.Savary-J.Miller as modified by Carrison et al.
      • Grade 0 – there are no signs of reflux esophagitis.
      • I degree – non-confluent erosions against the background of mucosal hyperemia, occupying less than 10% of the circumference of the distal esophagus.
      • Grade II - confluent erosive lesions occupying 10-50% of the circumference of the distal esophagus.
      • III degree – multiple, circular erosive and ulcerative lesions of the esophagus, occupying the entire circumference of the distal esophagus.
      • IV degree – complications: deep ulcers, strictures, Barrett’s esophagus.
    • The Los Angeles classification is used only for erosive forms of GERD.
      • Grade A - one or more defects of the esophageal mucosa no more than 5 mm long, none of which extends to more than 2 folds of the mucous membrane.
      • Grade B – one or more mucosal defects more than 5 mm in length, none of which extends to more than 2 folds of the mucous membrane.
      • Grade C – defects of the esophageal mucosa that extend to 2 or more folds of the mucosa, which together occupy less than 75% of the circumference of the esophagus.
      • Grade D – defects of the esophageal mucosa, occupying at least 75% of the circumference of the esophagus.
  • GERD without esophagitis (endoscopically negative reflux disease, or non-erosive reflux disease)

    GERD without esophagitis (endoscopically negative reflux disease, or non-erosive reflux disease) is damage to the esophageal mucosa that is not detected by endoscopic examination. Occurs in more than 50% of cases.

    The severity of subjective symptoms and duration of the disease do not correlate with the endoscopic picture. With endoscopically negative GERD, quality of life suffers in the same way as with reflux esophagitis, and pH measurements characteristic of the disease are observed.

• Epidemiology of GERD

  The incidence of GERD is often underestimated, since only 25% of patients consult a doctor. Many people do not complain because they manage the symptoms of the disease with over-the-counter medications. The occurrence of the disease is promoted by a diet containing excess amounts of fat.

  If we evaluate the prevalence of GERD by the frequency of heartburn, then 21-40% of residents of Western Europe, up to 20-45% of residents of the USA and about 15% of residents of Russia complain about it. The likelihood of having GERD is high if you experience heartburn at least twice a week. In 7-10% of patients it occurs daily. However, even with more rare heartburn, the presence of GERD cannot be excluded.

  The incidence of GERD in men and women of any age is (2-3):1. Incidence rates of GERD increase in people over 40 years of age. However, Barrett's esophagitis and adenocarcinoma are approximately 10 times more common in men.

• ICD 10 code K21.

For bronchospasms, the differential diagnosis is between GERD and bronchial asthma, chronic bronchitis. Such patients undergo pulmonary function testing, radiography and CT scan of the chest. In some cases, there is a combination of GERD and bronchial asthma. This is due, on the one hand, to the esophagobronchial reflex, which causes bronchospasm. On the other hand, the use of beta-agonists, aminophylline, reduces the pressure of the lower esophageal sphincter, promoting reflux. The combination of these diseases causes their more severe course.

In 5-10% of cases of GERD, drug therapy is ineffective.

Indications for surgical treatment methods:

• For complications of GERD.
• If conservative treatment is ineffective.
• When treating patients under 60 years of age with a hiatal hernia of 3-4 degrees.
• With grade V reflux esophagitis.

Before starting treatment, it is necessary to assess the patient's risk of complications. Patients who are at high risk of developing complications should undergo surgical treatment instead of prescribing medications.

The effectiveness of antireflux surgery and maintenance therapy with proton pump inhibitors is the same. However, surgical treatment has disadvantages. Its results depend on the experience of the surgeon, and there is a risk of death. In some cases, after surgery there remains a need for drug therapy.

Options for surgical treatment of the esophagus are: endoscopic plication, radiofrequency ablation of the esophagus, laparoscopic Nissen fundoplication.

Rice. Endoscopic plication (reducing the size of a hollow organ by placing gathered sutures on the wall) using the EndoCinch device.

Radiofrequency ablation of the esophagus (Stretta procedure) involves applying thermal radiofrequency energy to the muscle of the lower esophageal sphincter and cardia.

Stages of radiofrequency ablation of the esophagus.

Radiofrequency energy is delivered through a special device consisting of a bougie (currently conducted through a conductor wire), a basket balloon and four needle electrodes placed around the balloon.

The balloon is inflated and needles are inserted into the muscle under endoscopic guidance.

The installation is confirmed by measuring the tissue impedance and then a high-frequency current is applied to the ends of the needles while cooling the mucosa by applying water.

The tool is rotated to create additional “damage spots” at different levels and usually 12-15 groups of such spots are applied.

The antireflux effect of the Stretta procedure is associated with two mechanisms. One mechanism is to "tighten" the treated area, which becomes less sensitive to the effects of gastric distension after eating, in addition to creating a mechanical barrier to reflux. Another mechanism is disruption of the afferent vagal pathways from the cardia, involved in the mechanism of transient relaxation of the lower esophageal sphincter.

After laparoscopic Nissen fundoplication, 92% of patients experience complete disappearance of symptoms of the disease.

Rice. Laparoscopic Nissen fundoplication

• Treatment of complications of GERD
  • Strictures (narrowings) of the esophagus.

    Endoscopic dilatation is used in the treatment of patients with esophageal strictures. If, after a successful procedure, symptoms recur within the first 4 weeks, carcinoma must be excluded.

  • Esophageal ulcers.

    For treatment, you can use antisecretory drugs, in particular, rabeprazole (Pariet) - 20 mg 2 times a day for 6 weeks or more. During the course of treatment, control endoscopic examinations with biopsy, cytology and histology are carried out every 2 weeks. If a histological examination reveals high-grade dysplasia, or, despite 6-week treatment with omeprazole, the ulcerative defect remains the same size, then consultation with a surgeon is necessary.

    The criteria for the effectiveness of treatment for endoscopically negative GERD (GERD without esophagitis) is the disappearance of symptoms. Pain often resolves on the first day of taking proton pump inhibitors.

Gastroesophageal reflux disease (GERD) is common but rarely detected and therefore untreated or self-treated and inappropriately treated, which is undesirable since GERD usually responds well to treatment.

GERD is treated gradually. The doctor will help you choose the necessary course of treatment. If the disease is mild, the patient will only need to follow a certain diet and avoid certain activities and take over-the-counter medications. In cases where symptoms are more persistent (daily heartburn, symptoms that occur at night), prescription medications may be required. Surgery is a reasonable alternative to constant medication, especially if the disease is acquired at an early age.

Surgery is also indicated if medications do not work. However, today there is a new generation of drugs that can effectively control gastroesophageal reflux.

If you are still experiencing discomfort after taking strong medications, your symptoms may not be caused by GERD. Many gastroenterologists and surgeons do not recommend surgery in this situation, since symptoms still continue to appear after it.

Lifestyle changes.

Treatment of gastroesophageal reflux begins with lifestyle changes. First you need to understand what influences the occurrence of symptoms.

If you are experiencing symptoms of GERD, try the following tips:

• Avoid foods and drinks that stimulate the lower esophageal sphincter to relax, such as mint-flavored foods, chocolate and alcohol.
• Lose weight if you are overweight. Obesity can contribute to the development of GERD. Because excess weight increases pressure on the stomach and lower esophageal sphincter, acid reflux occurs.
• Do not lie down for at least two or three hours after eating. After eating it is good to take a walk. This not only prevents the symptoms of GERD, but also burns excess calories.
• Avoid known GERD triggers. Avoid fatty or fried foods (fried chicken), creamy sauces, mayonnaise or ice cream. Other foods that may cause complications include coffee, tea, soda, tomatoes, and citrus fruits. After consuming such products, the lower esophageal sphincter relaxes and the stomach contents return into the esophagus or irritation of the esophageal mucosa.
• Quit smoking. Smoking disrupts the functioning of the digestive system and, according to some studies, relaxes the lower esophageal sphincter. Smoking also reduces the bicarbonate content of saliva and reduces its ability to protect the esophagus from stomach acid. Some types of nicotine replacement therapy (nicotine patch, nicotine gum) may cause indigestion, abdominal pain, and vomiting. Before use, discuss possible side effects of these products with your doctor.
• Avoid wearing clothes that put pressure on your stomach, such as belts, skinny jeans, and elastic waistbands, which can put more pressure on your stomach and lower esophageal sphincter.
• Raise the head of the bed 15-20cm or use a wedge-shaped pillow so that gravity allows acid to flow into the stomach.
• Don't bend over after eating. If you need to pick something up from the floor, it’s better to sit down with your knees bent and try not to bend at the waist. Don't exercise after eating.
• Check the medications you are taking. Due to the use of certain medications, symptoms may worsen. These drugs include theophylline, calcium channel blockers, alpha blockers and beta blockers, anticholinergics that may be present in drugs used to treat Parkinson's disease, asthma, and some over-the-counter cold and cough medications. If you think that the drug you are taking is affecting your symptoms, discuss with your doctor what alternatives can be used instead. Do not stop your prescribed treatment without consulting your doctor.

Drug treatment of gastroesophageal reflux.

Your doctor may prescribe medication to treat GERD. Because GERD is often a chronic condition, you will need to take medications for the rest of your life. In some cases, long-term treatment is not required.

Be patient, it takes time to find the right drug and dosage. If symptoms do not go away even after taking the medications, or if they return immediately after completing the course, consult your doctor. If symptoms of GERD occur during pregnancy, contact your obstetrician before starting medication.

Below is information about medications that are commonly prescribed to treat GERD:

Over-the-counter antacids.

Such remedies help with mild and rarely manifested symptoms. Their action is to neutralize stomach acid. Most often, antacids act quickly and can be taken as needed. Because they do not last long, they do not prevent heartburn and are less effective for symptoms that occur frequently.

Most antacids contain calcium carbonate (Maalox) or magnesium hydroxide. Sodium bicarbonate, or baking soda, helps relieve heartburn and indigestion. It should be mixed with at least 120 ml of water and taken one to two hours after meals so as not to overload a full stomach. Talk to your doctor about the need for such treatment. Do not use this method for more than two weeks and use it only in extreme cases, since soda can lead to metabolic disorders and the formation of erosions. Before using it on children under 12 years of age, consult a doctor.

Another type of antacid contains alginate or alginic acid (for example, Gaviscon). The advantage of this antacid is that it prevents fluid from leaking back into the esophagus.

Antacids may interfere with your body's ability to absorb other medications, so if you are taking other medications, check with your healthcare provider before taking antacids.

Ideally, you should take antacids at least 2-4 hours after taking other medications to minimize the chance of misabsorption. People with high blood pressure should avoid taking high sodium antacids (Gaviscon).

Finally, antacids are not a reliable treatment for erosive esophagitis, a disease that must be treated with other medications.

Antiulcer drugs.

These medications reduce the amount of acid produced by the stomach and are available with or without a prescription. Usually the same drugs are available by prescription, but in higher dosages. They can help those who don't respond to over-the-counter medications. Most patients feel better if they take anti-ulcer medications and make lifestyle changes.

There are two types of these drugs: H2 blockers and proton pump inhibitors. Most likely, the doctor will first recommend taking the drug at a standard dose for several weeks, and then, if the desired effect cannot be achieved, he will prescribe a drug with a higher dosage.

Traditional H2 blockers include:

• nizatidine (“Axid AR” Axid AR)
• famotidine (“Pepcid AC” Pepcid AC)
• cimetidine ("Tagamet HB" Tagamet HB)
• ranitidine (Zantac 75 Zantac 75)

Pepcid Complete is a combination of famotidine, calcium carbonate and magnesium hydroxide found in antacids.

Proton pump inhibitors also reduce acidity, but are more powerful than H2 blockers. Proton pump inhibitors are most often prescribed to treat heartburn and acid reflux.

These drugs block the secretion of acid by the cells of the gastric mucosa, and significantly reduce the amount of stomach acid. They do not work as quickly as antacids, but can relieve reflux symptoms for many hours.

These drugs are also used to treat inflammation of the esophagus (esophagitis) and erosions of the esophagus. Studies have shown that most esophagitis patients who took such drugs recovered within 6-8 weeks. Your doctor will likely re-evaluate your health after 8 weeks of taking proton pump inhibitors and reduce your dosage or stop treatment based on the results. If symptoms do not return within three months, you will only need to take medication occasionally. Traditional proton pump inhibitors include:

• lanzoprazole (Prevacid)
• omeprazole (Prilosec, Prilosec)
• rabeprazole (“AcipHex”, AcipHex)
• pantoprazole (“Protonix” Protonix)
• esomeprazole (Nexium, Nexium)
• omeprazole + sodium bicarbonate (Zegerid)
• dexlansoprazole (Dexilant)

People with liver disease should consult their doctor before taking these medications.

Prokinetics.

Prokinetics, for example, metoclopramide (Cerucal, Reglan, Metozolv), increase the tone of the lower esophageal sphincter, so that acid does not enter the esophagus. They also increase the contractions of the esophagus and stomach to some extent, so that the stomach is emptied more quickly. These medications may be used as adjunctive treatment for people with GERD.

Surgical treatment of gastroesophageal reflux.

Surgery is an alternative to conservative treatment of GERD. Surgery is most often reserved for young patients (since they would otherwise require long-term treatment) with typical GERD symptoms (heartburn and belching) who benefit from medication but are looking for an alternative to daily medication.

For patients with atypical symptoms or patients who do not respond to drug treatment, surgery is indicated only if there is no doubt about the diagnosis of GERD and the relationship between the symptoms and reflux is confirmed by the results of the examinations.

In most cases, fundoplication is used. During this operation, the upper part of the stomach is wrapped around the lower esophageal sphincter, thereby increasing its tone. Nowadays, instead of traditional “open” surgery, minimally invasive (laparoscopic) technologies are usually used. One of the benefits of a fundoplication is that a hiatal hernia can also be repaired during the operation.

The surgery is not always effective, and some patients still have to take medications after it is performed. The results of this surgery are usually positive, but complications may occur, such as difficulty swallowing, bloating and gas, difficulty recovering from surgery, and diarrhea, which occurs due to damage to the nerve endings that surround the stomach and intestines.

Prevention of gastroesophageal reflux.

First of all, it is necessary to pay attention to lifestyle and avoid activities that can trigger the onset of the disease.

Remember that GERD occurs when stomach acid backs up into the esophagus, the long muscular tube that connects the throat to the stomach.

To ensure that the lower esophageal sphincter functions properly, follow these guidelines:

• Do not bend over or do other physical exercises that increase pressure on the abdominal cavity. Don't exercise on a full stomach.
• Avoid wearing clothes that fit tightly around the waist, such as elastic waistbands and belts, which can increase pressure on the stomach.
• Don't lie down after eating. If you lie down on your back after eating a large meal, it will be easier for stomach contents to enter the esophagus. For a similar reason, don't eat before bed. The head of the bed should be raised 15-20cm so that gravity allows the acid to remain in the stomach, where it should be while you sleep.
• Don't overeat. Due to the fact that there is a large amount of food in the stomach, pressure on the lower esophageal sphincter increases, causing it to open.

To keep the lower esophageal sphincter and esophagus functioning properly, follow these tips:

• Stop smoking and do not use products containing tobacco. Smoking relaxes the lower esophageal sphincter, reduces the amount of acid-neutralizing saliva in the mouth and throat, and damages the esophagus.
• Avoid foods that aggravate symptoms, such as tomato sauces, mints, citrus fruits, onions, coffee, fried foods, and carbonated drinks.
• Do not drink alcoholic beverages. Alcohol causes the lower esophageal sphincter to relax and the esophagus to contract unevenly, causing acid to back up into the esophagus and cause heartburn.
• Check the medications you are taking. Due to the use of certain medications, symptoms may worsen. Do not interrupt the prescribed treatment without consulting your doctor. Drugs that have this effect include medications for asthma and emphysema (such as theophylline), anticholinergics for Parkinson's disease and asthma, sometimes found in over-the-counter medications, some calcium channel blockers, alpha blockers, and beta blockers to treat heart disease or high blood pressure, some drugs that affect the nervous system, iron supplements.

Although some medications worsen the symptoms of GERD, others can cause drug-induced esophagitis, a condition that causes the same symptoms as GERD, but not due to reflux. Drug-induced esophagitis occurs when a pill is swallowed but does not reach the stomach because it sticks to the wall of the esophagus. Because of this, the mucous membrane of the esophagus is corroded, causing chest pain, ulcers of the esophagus and painful sensations during swallowing. Drugs that cause drug-induced esophagitis include aspirin, non-hormonal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Motrin, Aleve), alendronate (Fosamax), potassium, and some antibiotics (especially tetracycline and doxycycline). .

You can obtain more detailed information about the symptoms of gastroesophageal reflux disease from gastroenterologists at the Health 365 clinic in Yekaterinburg.