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 path. 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.

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Treatment of gastroesophageal reflux disease

Causes of gastroesophageal reflux disease

The term "" (GERD) is a recent development and has to some extent replaced the previous names "reflux esophagitis" and "reflux disease". Although these terms are synonymous, the new name "gastroesophageal reflux disease" is more complete, since it includes a characteristic symptom complex due to the reflux of acidic gastric contents into the esophagus.

In this case, not only the casting itself is important, but also the ability of the esophagus to be released, to be cleansed of such an irritant. This phenomenon is called esophageal clearance. It is believed that with normal clearance of the esophagus, single casts do not lead to gastroesophageal (gastroesophageal) reflux disease. In the case of a decrease in the clearance of the esophagus in response to the periodic intake of the acidic contents of the stomach, its mucous membrane quickly becomes inflamed.

Of great importance is also a decrease in the tone of the lower esophageal closure muscle, which is due to the frequent development of gastrin insufficiency in this disease. Gastrin is an important hormone of the stomach, it performs a general trophic function, regulates the tone of the closure muscles, and gastric secretion. The mechanism of gasgrin formation is disturbed in peptic ulcer, and reflux esophagitis develops, as a rule, in many of these patients.

Now the mechanism of gastroesophageal reflux disease is being clarified, taking into account the role of nitric oxide. Most clinicians interpret gastroesophageal reflux disease as varying degrees of damage to the mucous membrane of the distal esophagus, accompanied by characteristic clinical symptoms and resulting from a constant pathological reflux (reflux) of gastric duodenal contents into the lumen of the esophagus.

According to modern concepts, gastroesophageal reflux disease is considered as a consequence of impaired motility of the esophagus and stomach. Of key importance in the development of gastroesophageal reflux disease is a decrease in the antireflux barrier, a decrease in the tone of the lower esophageal closure and esophageal clearance, an increase in episodes (number) of its relaxation and an increase in intragastric pressure. Additional factors that create conditions for the development of gastroesophageal reflux disease are aggressive components of the gastric content ( hydrochloric acid, pepsin, bile acids, pancreatic enzymes trypsin and phospholipase) against the background of a decrease in the resistance of the esophageal epithelium.

Gastroparesis, decreased saliva production (Sjögren's disease), impaired cholinergic innervation of the esophagus are important.

A special role in the development of gastroesophageal reflux disease is assigned to Helicobacter pylori microorganisms. Drinks containing caffeine (coffee, tea, cocoa, Coca-Cola and Pepsi-Cola), juices (especially from citrus fruits), alcohol, milk, tomatoes, horseradish, onions, garlic, peppers and other spices increase the acid-forming function of the stomach and reduce tone lower esophageal closure.

Gastroesophageal reflux disease should be distinguished from secondary reflux esophagitis, which is observed in peptic ulcer, slippery hiatal hernia after stomach surgery, scleroderma, esophageal cancer, etc.

The main symptoms of gastroesophageal reflux disease are heartburn and regurgitation (belching), they appear at least 2 times a week for 4-8 weeks or more. Patients also complain of a feeling of constriction in the epigastric region, which occurs 15-40 minutes after eating and is provoked by the use of foods that stimulate the synthesis of hydrochloric acid by the stomach and bile by the liver. such products include:

• fried food,
• spicy dishes,
• juices,
• alcohol,
• red dry wines,
• carbonated drinks such as Coca-Cola, Pepsi-Cola, Fanta,
• coffee,
• chocolate,
• cocoa,
• radish,
• oil in large quantities.

Often, patients with gastroesophageal reflux disease complain of chest pain radiating to the neck, lower jaw, left shoulder and arm, under the left shoulder blade. In the latter case, differential diagnosis with coronary heart disease (angina pectoris) should be carried out. Breast pain in gastroesophageal reflux disease is associated with:

• food intake, in particular overeating,
• low head position during sleep.

Usually stops after the use of antacids or alkaline mineral waters (Polyana Kvasova, Polyana Kupel, Luzhanska).

Such complaints are usually provoked by physical activity, frequent torso bending, overfilling of the stomach with liquid, fatty, sweet foods, alcohol, and are aggravated at night. The entry of the contents of the esophagus into the lumen of the bronchi can lead to bronchospasm, Mendelssohn's bronchoaspiration syndrome (for a fatal case, it is enough for 2-4 ml of acidic gastric juice to enter the bronchial tree).

How to treat gastroesophageal reflux disease?

Medical treatment of gastroesophageal reflux disease is divided into 2 phases: initial (initial) and secondary.

In the first phase, an inhibitor of the passage pump (lamprazole, pantoprazole) is prescribed, the purpose of which is the healing of erosive esophagitis and the complete overcoming of clinical manifestations. Initial treatment should last 4 weeks. Subsequently, a switch is made to a dose that maintains remission for the next 4 weeks. In erosive GERD, the duration of initial treatment should be 4-12 weeks, followed by the appointment of one of the long-term therapy regimens. The generally accepted strategy for treatment with antisecretory drugs is to initially give double doses of proton pump inhibitors for 4–8 weeks, followed by a transition to long-term treatment.

The second phase is a long-term treatment, the goal of which is to achieve remission. It is carried out in 3 versions:

1) long-term daily use of proton pump inhibitor in anti-relapse doses;

2) "on demand" therapy: the use of a proton pump inhibitor in a full dose in a short 3-5-day course in case of spreading symptoms;

3) "weekend" therapy: the use of a proton pump inhibitor in an anti-relapse dose.

If initial treatment fails within 2 weeks, esophagoscopy and pH monitoring should be performed. If monitoring indicates a nocturnal "breakthrough" of acidity, then the patient should be prescribed famogidin or renitidine in addition to a double dose of a proton pump inhibitor. If the reflux is bile, then ursodeoxycholic acid (ursosan) or a cytoprotector is indicated. To improve the resistance of the mucous membrane of the esophagus, a decoction of flax seeds (1/3 cup each), sucralfate (venier), maalox, phosphatugel, gelusil, gestal, pee-hoo are recommended.

The most effective is Maalox. These patients are prescribed prokinetics - cisapride or cerucal (metoclopramide), which increase the tone of the lower esophageal closure, reduce the severity of gastroesophageal reflux and reduce acidification of the esophagus.

Sea buckthorn and rosehip oils give positive results. The dose is selected individually - from 1 teaspoon at night to 1 teaspoon 3-4 times a day.

Endoscopic and surgical treatment of GERD is recommended for patients with:

• the need for long-term drug therapy;
• insufficient effect of "drug therapy;
• diaphragmatic hernia, large volume of reflux;
• complications - bleeding, stricture, Barrett's esophagus, cancer of the esophagus;
• patient's personal wishes.

Criteria for the effectiveness of treatment:

• healing of erosive lesions of the esophagus,
• disappearance of heartburn
• improving the quality of life.

The recurrence rate during the first year after successful completion of treatment is 39-65% for erosive GERD.

What diseases can be associated

The nature of gastroesophageal reflux disease is explained by impaired motility of the esophagus and stomach, the disease develops against the background of a reduced antireflux barrier, reduced tone of the lower esophageal closure and esophageal clearance.

An increased risk of experiencing the symptoms of gastroesophageal reflux disease is a violation in the production of digestive hormones (gastrin) and pancreatic enzymes against the background of a decrease in the resistance of the esophageal epithelium.

Treatment of gastroesophageal reflux disease at home

The most important condition treatment of gastroesophageal reflux disease is a lifestyle change:

• quitting smoking and drinking alcohol,
• weight loss,
• avoiding a horizontal position of the body after eating and during sleep,
• refusal to wear corsets, bandages, anything that increases intra-abdominal pressure.

Changes in the mode and nature of nutrition are important:

• overeating should be avoided
• avoid eating at night
• Avoid lying down after eating
• Minimize high-fat foods in your diet
  • milk,
  • cream,
  • goose,
  • duck,
  • pork,
  • lamb,
  • coffee,
  • coca cola,
  • citrus fruits and juices from them,
  • tomatoes,
  • garlic,
  • red dry wines.

Dispensary observation is subject to patients with prolonged heartburn (10 years or more), erosive forms of GERD, Barrett's esophagus.

In the case of Barrett's esophagus with low-grade dysplasia, proton pump inhibitors should be prescribed at a double dose for at least 3 months, followed by a dose reduction to the standard dose. Endoscopic follow-up with biopsy should be performed annually. In high-grade dysplasia, another endoscopic examination with multiple biopsies from altered mucosal sites should be performed. For a patient with Barrett's syndrome and high-grade dysplasia, endoscopic mucosal resection or surgical esophagotomy is recommended.

What drugs are used to treat gastroesophageal reflux disease?

• - 20 mg 2 times a day or 40 mg 1 time per day at night, the course of treatment is 4 weeks; maintenance dose of 20 mg at night for the next 4 weeks;
• - 20 mg 2 times a day before breakfast and dinner;
• - 150 mg 2 times a day;
• - 500 mg 1-1.5 hours after meals 4 times a day;
• - 1-2 packets 3-4 times a day;
• - 10-20 mg 3-4 times a day.

Treatment of gastroesophageal reflux disease with folk methods

• decoction of flax seeds - 1 tsp flax seeds brew in a glass of boiling water, stand for 5 minutes on low heat, leave for another half an hour, strain; take three times a day before meals in a warm form for ⅓ cup;
• herbal collection - combine 4 parts of St. John's wort herb, 2 parts of calendula officinalis flowers, plantain leaves, licorice roots, calamus and 1 part of common tansy and peppermint flowers; 1 tsp the resulting collection pour a glass of boiling water, after half an hour strain and take three times a day before meals in a warm form for ⅓ cup;
• sea ​​buckthorn and rosehip oils - the dose is selected individually from 1 teaspoon at night to 1 teaspoon 3-4 times a day.

Treatment of gastroesophageal reflux disease during pregnancy

Treatment of gastroesophageal reflux disease in pregnant women should be carried out under the supervision of a specialist. If GERD manifested during pregnancy, then it is highly likely that the disease will be temporary, the symptoms will be reduced to zero after childbirth.

At the initial stage of GERD during pregnancy, the doctor will recommend lifestyle changes, then herbal medicine, and only with extremely uncomfortable symptoms, drug treatment is appropriate. Basically, the treatment of GERD in pregnant women is symptomatic, improving the quality of life, the well-being of the expectant mother.

Which doctors to contact if you have gastroesophageal reflux disease

When examining a patient with gastroesophageal reflux disease, dry mouth (xerostomia), hypertrophied fungiform papillae of the tongue (the result of gastric hypersecretion), positive left or right phrenicus symptom, signs of laryngitis (hoarseness) are revealed.

The diagnosis of gastroesophageal reflux disease is confirmed radiologically - in the presence of reverse flow (reflux) of the contrast agent from the stomach into the esophagus, the results of round-the-clock pH monitoring in the esophagus (at a pH of 5.5-7 pH in a patient with GERD for 5 minutes - 1 hour or more - less than 4).

However, the gold standard for diagnosing gastroesophageal reflux disease is the endoscopic examination method. Classification of lesions of the esophagus according to esophagoscopy:

• 0 degree - the mucous membrane of the esophagus is intact;
• I degree of severity - individual erosions that do not merge with each other and / or erythema of the mucous membrane of the distal esophagus;
• II degree of severity - erosion, which merge with each other, but do not extend to most of the mucous membrane of the lower third of the esophagus;
• III degree of severity - erosive lesions of the lower third of the esophagus, erosion merge and spread to the entire surface of the mucous membrane of the distal esophagus;
• IV degree of severity - erosive and ulcerative changes or complications (stricture of the esophagus, bleeding, metaplasia of the mucous membrane with the formation of an endoscopic picture of the "bridge" and the formation of Barrett's esophagus).

Diagnostic criteria for suspected GERD:

• typical clinical symptoms: heartburn and sour belching;
• test with a proton pump inhibitor: the effectiveness of a 5-7-day course of use of modern proton pump inhibitors, such as esomeprazole (rabeprazole, pantolrazole);
• endoscopic confirmation of esophagitis;
• positive results of 24-hour esophageal pH monitoring (pH less than 4, duration not less than 5 minutes in a row).

Methods of additional diagnostics:

• general blood test and biochemical blood test;
• test for Helicobacter pylori (breath test);
• biopsy - is indicated if intestinal metaplasia is suspected during endoscopy, in patients with ulcerative lesions of the esophagus and / or its stenosis, if a non-reflux etiology of esophagitis is suspected).

Treatment of other diseases with the letter - g

Treatment of sinusitis

Treatment of galactorrhea

Treatment of lung hamartoma

Treatment of gangrene of the lung

Treatment of gastritis

Treatment of hemolytic leukopenia

Treatment of hemorrhagic stroke

Treatment of hemorrhoids

Treatment of pulmonary hemothorax

Treatment of hemophilia

Treatment of hemochromatosis

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 eating, 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 and 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. With irritation of the nerves innervating the bronchi, 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. Its chewing allows you to stimulate the production of large amounts of saliva rich in sodium bicarbonate and peristalsis by moving it through 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) is one of the most common diseases of the digestive tract, which is reflected in the postulate "The 20th century is the century of peptic ulcer disease, and the 21st century is the century of GERD", put forward at the VI Joint Gastroenterological Week (Birmingham, 1997). According to epidemiological studies, the prevalence of GERD in the adult population of Western Europe and North America reaches 10-20%, in Moscow - 23.6%.

GERD is considered as a condition that develops when the reflux of stomach contents causes symptoms and / or complications that disturb the patient. Heartburn and regurgitation are recognized as the most characteristic symptoms of the disease, and reflux esophagitis is the most common complication. Regurgitation (sour eructation, regurgitation) is the entry of stomach contents due to reflux into the oral cavity or lower pharynx. Heartburn is a burning sensation behind the sternum and / or “in the pit of the stomach”, spreading from bottom to top, individually occurring in a sitting, standing, lying position or when bending forward, sometimes accompanied by a feeling of acid and / or bitterness in the throat and mouth, often associated with a feeling of fullness in the epigastrium that occurs on an empty stomach or after the consumption of any kind of solid or liquid food, alcoholic or non-alcoholic beverages, or the act of smoking.

The leading pathogenetic mechanism of the onset of the disease is pathological gastroesophageal reflux (GER). Since intra-abdominal pressure exceeds intra-thoracic pressure, a pressure gradient acts to promote the reflux of stomach contents into the esophagus, which is opposed by the lower esophageal sphincter (LES). The failure of the latter leads to the development of pathological GER, the result of which impact on the mucosa of the esophagus is determined by its composition (hydrochloric acid, pepsin, bile acids, etc.), the duration of exposure and the intrinsic resistance of the mucosa. In addition to the ineffectiveness of NPS, the occurrence of GER is facilitated by an increase in intra-abdominal (for example, with obesity, pregnancy, constipation) or intragastric pressure (with gastric or duodenal stasis of a functional or organic nature).

Mechanisms for the formation of heartburn sensation remain not fully understood. Most often, heartburn is the result of pathological GER (both acid and duodenal contents). In addition, the sensation of heartburn may be associated with impaired motility of the esophagus, increased sensitivity of its mucosa due to disorders of the central and peripheral innervation, changes in psychological status. Accounting and correct assessment of these mechanisms largely determines the success of therapy. Its main goals are to relieve symptoms, improve well-being (quality of life), as well as treat and prevent complications, primarily reflux esophagitis. Based on the pathogenesis of the disease, this can be achieved by reducing the volume and modifying the composition of the refluxant, increasing the antireflux function of the LES, reducing the pressure gradient directed from the stomach to the esophagus, increasing the clearance of the esophagus, and protecting the esophageal mucosa from the damaging effects of the refluxant. In the presence of motor disorders, hypersensitivity of the esophagus and changes in the psycho-emotional status, their correction is required.

The main directions in the treatment of GERD include recommendations for changing lifestyle and diet, pharmacotherapy (antisecretory drugs, prokinetics, alginates, antacids), with the ineffectiveness of which they resort to surgical treatment (laparoscopic fundoplication, etc.). Two pharmacotherapy strategies are considered as alternatives. The first of them, “increasing in stages”, provides for a change in lifestyle at the initial stage of treatment, the use of alginates or antacids. If they were ineffective, a transition was made to the second (histamine H2-receptor blockers and/or prokinetics) or immediately to the third stage (proton pump inhibitors (PPIs)). In the second strategy, "gradually decreasing", PPIs are prescribed, and only after achieving a clinical and endoscopic effect, patients are gradually transferred to maintenance doses of PPIs or on-demand therapy, including taking alginates or antacids.

The "phasing down" strategy is recommended primarily for patients with reflux esophagitis, as it significantly reduces the healing time of esophageal mucosal erosions. For the relief of symptoms of uncomplicated (endoscopically negative) GERD, “gradually increasing” therapy is relevant, and already at the first step, the appointment of alginates. Previous studies have demonstrated the safety and efficacy of alginates in suppressing the symptoms of GERD and alleviating the manifestations of reflux esophagitis.

The source of alginic acid (from lat. alga - sea grass, algae) are brown algae, mainly Laminaria hyperborea. Alginic acids are polysaccharides, the molecules of which are built from residues of D-mannuronic and L-guluronic acids. The mannuronic acid blocks impart viscosity to alginate solutions. When the blocks of guluronic acid are associated with the participation of calcium cations, gelation occurs.

Gaviscon is a suspension for oral administration, which includes active substances: sodium alginate, sodium bicarbonate, calcium carbonate. When taken orally, Gaviscon reacts with acid in the gastric lumen to form a non-absorbable alginate gel barrier. Due to the carbon dioxide formed during the interaction of sodium bicarbonate with hydrochloric acid, the "alginate raft" floats on the surface of the contents of the stomach and mechanically prevents the occurrence of GER. If reflux does occur, however, the alginate gel is the first to enter the esophagus and exerts a protective effect.

The aim of our work was to evaluate the clinical efficacy of Gaviscon suspension in patients with GERD.

Research objectives:

1. Evaluate the effectiveness of a 10-day intake of Gaviscon suspension in relieving GERD symptoms (heartburn, regurgitation, etc.).

2. Determine the dynamics of intraesophageal pH monitoring after taking Gaviscon suspension.

Material and research methods

We examined 30 patients (mean age 46.2 ± 15.0 years, women 50%) with non-erosive form of GERD who were hospitalized at the Central Research Institute of Gastroenterology. 46.7% of patients had a normal body mass index, and 53.3% had an excess body mass index. The duration of GERD symptoms ranged from 1 to 30 years, on average 6.0 ± 8.7 years.

For 10 days, patients received a suspension of Gaviscon 20 ml 4 times a day 30-40 minutes after the three main meals and at bedtime. GERD symptoms were assessed daily using a 5-point Likert rating scale, where 1 is no symptoms at all and 5 is severe symptoms that significantly affect the patient's quality of life. Before prescribing the drug, esophagogastroduodenoscopy (EGDS) and daily pH monitoring (Gastroscan-24) were performed. In 10 patients, an acute pharmacological test was performed under the control of pH monitoring with a 1-fold or 4-fold intake of Gaviscon 20 ml. Before and after treatment with Gaviscon, the state of health was assessed using a visual analogue scale (VAS). Taking into account the possible role of psychoemotional disorders in the formation of complaints in patients with GERD, especially its endoscopically negative form, the psychological status was assessed using the SMOL questionnaire and the type of attitude to the disease was determined using the LOBI questionnaire. The safety of the therapy was assessed based on the presence/absence of side effects.

Research results and discussion

The most frequent complaints were heartburn, sour eructation, belching with air, dysphagia and odynophagia were less common (Table 1). Reduction of symptoms on the first day of therapy occurred in 26 (86.7%) patients. Two patients did not note the positive effect of Gaviscon and refused to continue taking the drug by 4-5 days. One patient developed an allergic reaction in the form of urticaria on the 3rd day of treatment. Thus, 3 patients dropped out of the study, and their data were not taken into account when assessing the effectiveness of therapy. In the majority of the remaining patients, complete elimination of symptoms occurred within 1 to 7 days (Table 2). It should be emphasized that inpatients are a more severe group of patients with GERD and the longest periods of relief of symptoms were in patients with overweight and with changes in psychoemotional status.

During therapy, patients felt better, which was reflected in an increase in the VAS score from 41.8 ± 15.3 before treatment to 60.2 ± 16.8 mm on the 10th day of taking Gaviscon.

Conducted in 10 patients under the control of pH monitoring, an acute pharmacological test with Gaviscon demonstrated its antireflux effect lasting from 1.5 to 3.5 hours. At the same time, the generalized De Meester indicator normalized or significantly decreased. The average pH in the stomach in 3 patients did not change, in 7 patients a moderate antacid effect was observed, due to the bicarbonates that make up the drug.

Tolerability of treatment in the vast majority of patients was good, 1 patient noted a short-term increase in burning sensation along the esophagus after taking the drug, 1 patient noted the appearance of flatulence. In 1 patient, on the 3rd day of treatment, an allergic reaction in the form of urticaria was noted. After discontinuation of the drug, the allergy symptoms disappeared on their own.

Two patients refused to take Gaviscon on the 4th-5th day of treatment without noting a clinical effect. The diagnosis in both patients was established on the basis of clinical manifestations of the disease: they were worried about heartburn. At the same time, according to the EGDS data, there were no changes in the esophageal mucosa, pH monitoring did not reveal pathological GER. During the psychological examination (questionnaires SMOL and LOBI), both patients revealed severe disorders of mental adaptation. Probably, the mechanism of formation of heartburn sensation in these patients was not pathological GER, but hypersensitivity of the esophagus against the background of changes in psychological status. An indirect confirmation of this is the inefficiency of Gaviscon, which relieves heartburn only in patients whose mechanism of formation is pathological GER.

Conclusion

Gaviscon Suspension has an anti-reflux effect by preventing stomach contents, both acidic and mixed, from entering the esophagus by creating an "alginate raft".

The duration of the antireflux effect of a single dose of Gaviscon suspension ranged from 1.5 to 3.5 hours.

The reason for the ineffectiveness of Gaviscon suspension may be non-reflux mechanisms of heartburn formation.

Gaviscon suspension is an effective and safe drug for the relief of GERD symptoms and can be recommended in the practice of gastroenterologists and therapists.

For literature inquiries, please contact the editor.

D. S. Bordin, Candidate of Medical Sciences
A. A. Masharova, Candidate of Medical Sciences, Associate Professor
T. S. Kozhurina
Central Research Institute of Gastroenterology, Moscow

Gastroesophageal reflux disease (GERD) in questions and answers

The International Foundation for Functional Gastrointestinal Diseases (IFFGD), USA, has prepared a series of materials for patients and their families regarding functional disorders of the gastrointestinal tract. This material is devoted to gastroesophageal reflux disease.

First draft writers: Joel Richter , Philip O. Katz and J. Patrick Waring , editor William F. Norton . In 2010, an updated version was prepared by Ronnie Fass.

Even a little knowledge can make a big difference

Introduction

Gastroesophageal reflux disease, abbreviated as GERD, is a very common disease that affects at least 20% of adult men and women in the United States. It is also common in children. GERD often goes unrecognized because its symptoms can be misunderstood and this is unfortunate because GERD is usually treatable and serious complications can occur if left untreated.

The purpose of this publication is to gain a deeper understanding of issues such as the nature of GERD, its definition and its treatment. Heartburn is the most common, but not the only, symptom of GERD. (The disease can even be asymptomatic). Heartburn is not specific to GERD and may result from other diseases of the esophagus or other organs. GERD is often treated on its own, without consulting a specialist, or treated incorrectly.

GERD is a chronic disease. Her treatment should be on a long-term basis, even after her symptoms are under control. It is necessary to pay due attention to changing habits in daily life and to long-term medication. This can be done through dispensary observation and patient education.

GERD is often characterized by painful symptoms that can significantly impair a person's quality of life. Treatments for GERD are effective in a variety of ways, ranging from lifestyle changes to drugs and surgery. For patients suffering from chronic and recurrent symptoms of GERD, it is important to establish an accurate diagnosis and receive the most effective treatment available.

What is GERD?

Gastroesophageal reflux disease or GERD is a very common condition. Gastroesophageal means that it is related to both the stomach and the esophagus. Reflux- that there is a backflow of acidic or non-acidic stomach contents into the esophagus. GERD is characterized by its own symptoms and can develop with or without damage to the tissues of the esophagus resulting from repeated or prolonged exposure of the esophageal mucosa to acidic or non-acidic stomach contents. If tissue damage is present, the patient is said to have esophagitis or erosive GERD. The presence of symptoms without visible tissue damage is called non-erosive GERD.

GERD is often accompanied by symptoms such as heartburn and sour belching. But sometimes GERD occurs without visible symptoms and is detected only after complications become apparent.

What causes reflux?

After swallowing, food passes down the esophagus. Once in the stomach, it stimulates the cells that produce acid and pepsin (an enzyme), which are necessary for the digestion process. A bundle of muscles at the bottom of the esophagus, called the lower esophageal sphincter (LES), acts as a barrier to prevent backflow (reflux) of stomach contents into the esophagus. To allow the swallowed portion of food to pass into the stomach, the LES relaxes. When this barrier relaxes at the wrong time, when it is weak, or when it is otherwise not effective enough, reflux can occur. Factors such as bloating, delayed gastric emptying, significant hiatal hernia, or too much acid in the stomach can also trigger acid reflux.

What causes GERD?

It is not known if there is a single cause of GERD. Failure of esophageal protective equipment to resist aggressive gastric contents entering the esophagus during reflux can lead to damage to the tissues of the esophagus. GERD can also occur without damage to the esophagus (approximately 50-70% of patients have this form of the disease).

Surgery . Surgical treatment may be indicated in the following cases:

• the patient is not interested in long-term drug therapy;
• symptoms cannot be controlled by methods other than surgery;
• symptoms return despite treatment;
• serious complications develop.

When choosing a surgical treatment, a thorough analysis of all circumstances with the participation of a gastroenterologist and a surgeon is recommended.

How long do you need to take medication to keep GERD from getting out of control?

GERD is a chronic disease, and most patients require long-term therapy to keep its symptoms under effective control. Just as patients with high blood pressure or chronic headaches also require regular treatment. Even after the symptoms are brought under control, the underlying disease remains. It is possible that in order to control GERD, drugs will have to be taken for the rest of your life. Unless new drugs and treatments are developed during this time.

Is long-term medication for GERD harmful?

Long-term use of any medication should be carried out only under the direction of a doctor. This applies to both prescription and over-the-counter drugs. Side effects are rare, however, any drug can potentially have unwanted side effects.

H2 blockers have been used to treat reflux disease since the mid-1970s. Since 1995, they have been available in reduced doses over the counter for the treatment of rare heartburn. They have been shown to be safe, although they sometimes cause side effects such as headache and diarrhea.

The proton pump inhibitors omeprazole and lansoprazole have been regularly used by GERD patients for many years (omeprazole was approved in the US in 1989 and worldwide a few years later). Side effects from these drugs are rare and mainly include occasional diarrhea, headache, or upset stomach. These side effects are generally no more common than with placebo and usually occur at the start of use. If none of these side effects have appeared after several months or years of taking proton pump inhibitors, it is unlikely that they will appear later.

Patients with heart disease who are taking clopidogrel (Plavix) should avoid taking proton pump inhibitors such as omeprazole and esomeprazole. In addition, recent studies have shown that long-term use of PPIs, especially more than once a day, can cause osteoporosis, bone fractures, pneumonia, gastroenteritis, and nosocomial colitis. Patients should discuss this with their healthcare provider.

When is surgery an alternative to medical treatment for GERD?

Medication helps control symptoms as long as the medication is taken correctly. Surgery is usually an alternative when long-term treatment is either ineffective or undesirable, or when there are serious complications of GERD.


The most common surgical procedure for the treatment of GERD is the Nissen fundoplication. It can be performed laparoscopically by an experienced surgeon. The purpose of the operation is to increase pressure in the lower esophageal sphincter to prevent reflux. When performed by an experienced surgeon (who has performed at least 30-50 laparoscopic procedures), its success approaches that of a well-planned and carefully administered therapeutic treatment with proton pump inhibitors.

Side effects or complications associated with surgery occur in 5-20% of cases. The most common is dysphagia, or difficulty swallowing. It is usually temporary and goes away in 3-6 months. Another problem that some patients have is their inability to burp or vomit. This is because the operation creates a physical barrier to any type of backflow of any stomach contents. The consequence of the impossibility of effective belching is the "gas-bloat" syndrome - bloating and discomfort in the abdomen.

A surgically created anti-reflux barrier can "break" in much the same way as a hernia penetrates other parts of the body. The recurrence rate has not been determined, but may be in the range of 10-30% up to 20 years after surgery. Factors that can contribute to this "breakdown" include: weightlifting, strenuous sports activities, drastic changes in weight, severe vomiting. Any of these factors can increase pressure, which can lead to weakening or disruption of the antireflux barrier created as a result of the operation.

In some patients, even after surgery, GERD symptoms may persist and medication may need to be continued.

Living with GERD

It is important to recognize that GERD is a disease that should not be ignored or self-medicated. Heartburn, the most common symptom, is so common that its importance is often underestimated. It may be overlooked and not associated with GERD.

It is important to understand that GERD can have serious consequences. The complications that can occur, as well as the discomfort or pain of acid reflux, can affect every aspect of a person's daily life—emotional, social, and professional.

Studies that measure the emotional state of people with untreated GERD often report worse scores than those with other chronic diseases such as diabetes, high blood pressure, peptic ulcers, or angina pectoris. However, nearly half of acid reflux sufferers do not recognize it as a disease.

GERD is a disease. It is not the result of a wrong lifestyle. It is usually accompanied by obvious symptoms, but may occur in the absence of any. Their ignoring or improper treatment can lead to more serious complications.

Most people with GERD have a mild form of the disease that can be controlled with lifestyle changes and medications. If you suspect you have GERD, the first step is to see a doctor for an accurate diagnosis. Recognized GERD is usually treatable. Working in partnership with your doctor, you will be able to develop the best treatment strategy available to you.

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The opinions of the authors do not necessarily reflect those of the International Foundation for Functional Gastrointestinal Diseases (IFFGD). IFFGD does not warrant or endorse any of the products in this publication, or any claim by the author, and accepts no liability in respect of such matters.

This brochure is in no way intended to replace the advice of a physician. We recommend visiting a doctor if a health problem requires an expert opinion.