Extraesophageal manifestations of gerb in children. Symptoms and treatment of gerb

Burkov S.G.

Good afternoon, dear colleagues. In my report I will focus on extraesophageal manifestations of gastroesophageal reflux disease. So, gastroesophageal reflux disease is a disease with the development of characteristic symptoms of inflammatory damage to the distal part of the esophagus due to repeated reflux of gastric and/or duodenal contents into the esophagus. There are two variants of the disease: endoscopically positive or, in fact, gastroesophageal reflux disease and its endoscopically negative variant, which accounts for about 65% of cases. Reflux esophagitis and, in fact, GERD with damage to the esophagus of about 25% and complicated forms of GERD, Barrett's esophagus, which account for about 10% of cases. In 2006 in Montreal, 40 experts from 18 countries determined that there is a typical reflux syndrome, including heartburn, belching, epigastric pain, esophageal injury syndrome - reflux esophagitis, reflux stricture, Barrett's esophagus, esophageal adenocarcinoma. Extraesophageal syndromes were also identified. Experts agreed that a connection has been proven between gastroesophageal reflux disease and reflux cough syndrome, reflux laryngitis syndrome, reflux asthma, and reflux dental erosion syndrome. At the same time, experts have not reached a consensus and believe that a connection can be assumed between gastroesophageal reflux disease, pharyngitis, sinusitis, idiopathic pulmonary fibrosis and idiopathic recurrent otitis media. The prevalence of reflux disease is high. Thus, in Europe, about 50 million people suffer from GERD, in the USA this figure is close to 20 million, and in our country the prevalence in different regions ranges from 40% to 60%. At the same time, 67% of patients note the main symptom of GERD, heartburn, in the daytime, and 49% – both during the day and at night. More than 90% of patients rate the severity of disease symptoms as moderate to severe. Today we would like to present to you the results of our collaborative study, which included 592 patients of various ages–, from 18 to 80 years. Of these, 162 patients suffered bronchial asthma, 80 non-coronary chest pain. 350 patients with various forms of gastroesophageal reflux disease were examined and examined to assess the condition of the upper respiratory tract and the mucous membrane of the oral cavity and tongue. They underwent a full clinical and laboratory experimental examination, including special research methods - computer spirometry, pneumotachometry, pharyngoscopy, determination of taste sensitivity.

Bronchial asthma. The outstanding English physician William Osler wrote about the relationship between bronchospasms and gastroesophageal reflux back in 1892, who described an attack of suffocation that occurred after eating. He was the first to suggest the development of bronchospasm as a result of stimulation of the vagal receptors of the distal part of the esophagus. Later, in 1946, Mendelssohn described a case of bronchospasm caused by aspiration of gastric contents. Thus, today there are two theories for the development of bronchospasm in GERD: reflex and microaspiration. That is, if there is a high reflux of stomach contents, acidic gastric contents, microaspiration of this contents into the trachea and bronchi is possible and then the development of symptoms from the respiratory system. In the event that there is distal reflux, that is, the acid is not thrown up high, then we can talk about reflex bronchospasm. Apparently, both cases occur in life, and it is necessary to differentiate where in pure form there is proximal reflux and microaspiration, but where there is only reflex bronchoconstriction, apparently, this is not possible. What factors may indicate the likely role of gastroesophageal reflux in the development and aggravation of symptoms of bronchial asthma? First of all, this is a late onset of bronchial asthma; this is a worsening of asthma symptoms after eating, lying down, or bending over; increased asthma symptoms at night, after taking sleeping pills; and the coincidence of cough, wheezing, dyspnea with reflux symptoms. We examined 162, as mentioned above, patients suffering from bronchial asthma. Of these, 86 were also diagnosed with gastroesophageal reflux disease and 76 patients were without reflux disease. Please note that the vast majority of patients had moderate bronchial asthma, and in the group of patients who suffered in parallel with gastroesophageal reflux disease and bronchial asthma, patients with nocturnal asthma predominated. The main symptom in these patients was heartburn, in 95% of cases, and was also noted here correlation connection between the severity and severity of heartburn and the severity of bronchial asthma. In cases where heartburn did not cause any particular concern in patients, there were no cases of severe bronchial asthma. In cases of severe damage, erosive damage to the esophagus, we also observed severe cases of bronchial asthma. According to the results of endoscopic examination, the majority of patients suffered from a non-erosive form of reflux disease. The patients were conditionally divided into three groups. The first group, in addition to basic anti-asthmatic treatment, received antisecretory therapy with proton pump inhibitors, the second group of patients, in addition to treatment of bronchial asthma, received symptomatic treatment with antacid drugs, and the third group of patients, without symptoms of gastroesophageal reflux disease, were treated only with bronchial asthma. The main group of drugs that are used to treat acid-related diseases and, of course, gastroesophageal reflux disease are proton pump inhibitors, which, by eliminating the effect of aggressive hydrochloric acid on the esophageal mucosa, lead to the elimination of symptoms, cure reflux esophagitis and, thus, improve quality of life of the patient. But among the huge number of drugs in this series, I would like to draw your attention to the following fact. According to the American Generic Drugs Association, in 2004 the share of generics in the US market was 30%. 63% of prescriptions written by US doctors in 2006 were for generics. According to experts, by 2011 the share of generics in the US market will reach 70%. And the advantage of a high-quality generic is that its price is about 30, and even 80% lower than original drug, which makes the drug more accessible to the population. And in this regard, I would like to draw your attention to a relatively new drug on our market, Lansoprozole (Lanzoptol), the effectiveness of which has been proven by numerous clinical studies, and here is one of them. The study included 170 patients suffering from reflux disease, and after a four-week course of therapy, the disease was cured in 82% of cases. It should be noted that Lansoprozole (Lansoptol) is the fastest-acting proton pump inhibitor, and therefore, if we want to achieve the fastest effect, we may need to think about using this drug. The high quality of Lanzoptol is also evidenced by the fact that, according to the results of the bioequivalence analysis, it is completely consistent and identical to the original Lansoprozole, and the original technique that was proposed by the developers, in which the active drug is presented in the form of microgranules collected into one large granule. This makes it possible to more effectively protect the drug, the active substance of the drug, from aggressive gastric juice, and this form of the drug is more active. So, we treated a group of patients suffering from bronchial asthma; they were prescribed a proton pump inhibitor, basic anti-inflammatory therapy, hormonal/non-hormonal, and traditional bronchodilator therapy with sympathomimetics and anticholinergics. When therapy was prescribed, heartburn was relieved almost on the first day in the vast majority of patients, and by the control period, by the 28th day, heartburn was relieved in almost 90% of patients. During therapy with a proton pump inhibitor, the need for bronchodilators decreased, the number of daytime attacks decreased, and the number of night attacks significantly decreased, that is, there was a sharply positive trend in the treatment of bronchial asthma. Again, I would like to show that the more severe the manifestations of reflux esophagitis, the more good results were achieved. That is, in patients with reflux esophagitis with an erosive form, the number of daytime attacks, night attacks and, accordingly, the consumption of bronchodilators decreased to a greater extent than in patients with NERD.

Speaking about laryngopharyngeal manifestations of reflux disease, it should be said that changes in the mucous membrane of the pharynx and larynx occur in patients with GERD 1.5-2 times more often than in patients without it. And the most common form of lesion is laryngitis posterior, the so-called “posterior laryngitis,” in which laryngoscopically, swelling, hyperemia, erosions and inflammatory granulomas are detected in the area of ​​the posterior third of the vocal cords. We examined 262 patients suffering from gastroesophageal reflux disease. The erosive form of reflux disease was identified in 27% of patients and the non-erosive form - in 72% of patients. Pathology of the ENT organs was detected in a total of 67% of patients. Please note that most often we detected chronic pharyngitis - in 33% of cases. In the total number of patients with chronic pharyngitis, patients with the hypertrophic form of the disease predominated. And by carrying out treatment with proton pump inhibitors - here is a long-term treatment, for 12 weeks - we were able to reduce the manifestations of chronic pharyngitis, and especially its hypertrophic form.

When we talk about the dental manifestations of reflux disease, the effect of various chemical substances on the oral cavity is widely known, however, hydrochloric acid has been recognized as a cause of pathological changes in the oral cavity relatively recently. Only in 1971, G. Howden first described pathological changes in the oral cavity in patients with hiatal hernia.

All changes in the oral cavity with GERD can be divided into damage to soft tissues (red border of the lips, mucous membrane, tongue, periodontal tissue) and hard tissues of the tooth, as well as changes in the composition oral fluid. In total, we examined 88 patients suffering from gastroesophageal reflux disease. Erosive GERD was diagnosed in almost 73 percent of cases, and in 24% there was a non-erosive form of the disease. Let me present a few of our observations. Swelling of the tongue, scalloping of the lateral surfaces of the tongue, desquamation on the back of the tongue, erosion of the hard tissues of the teeth due to repeated injections of hydrochloric acid. The administration of proton pump inhibitors led to positive dynamics of both the condition of the oral mucosa and the dynamics of the condition of the tongue. In conclusion, I would like to give one small clinical observation of ours. A 70-year-old patient has been suffering from moderately severe infectious-allergic bronchial asthma for ten years. Over the past six months, he has had nighttime asthma attacks. Therapy with becotide and ventolin was carried out, and during the last three months the patient noted periodic heartburn and pain in the epigastric region. At the height of heartburn, the patient independently took baking soda and liquid antacids. The patient was prescribed proton pump inhibitor therapy. During therapy, heartburn stopped, the number of daytime attacks decreased and night attacks almost completely stopped, and the condition stabilized. The patient goes to a sanatorium and takes his entire traditional set of medications for the treatment of bronchial asthma with him, but Lanzoptol, considering that the heartburn has gone away and everything is fine, he does not take it with him. The aftereffect persists for some time, but then heartburn reappears in the patient, nocturnal attacks reappear, symptoms of bronchial obstruction intensify, the frequency of daytime attacks increases, and the need for bronchodilators increases. Three days later, after the patient resumed taking the proton pump inhibitor, the heartburn subsided, the daytime attacks subsided, the night attacks stopped, and the need for bronchodilators decreased.

Thus, the results of the study indicate the need for a thorough examination of patients suffering from gastroesophageal reflux disease by doctors of various specialties - pulmonologists, cardiologists, otolaryngologists and dentists for timely diagnosis and adequate treatment of extraesophageal manifestations of gastroesophageal reflux disease. Thank you for attention!

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Symptoms	Reflux-induced pathology	Pathogenetic mechanisms
Cadial: Pain in the left chest; Heart rhythm disturbances	Attacks of angina and heart rhythm disturbances; Esophageal motility disorders	Heart rhythm disturbances resulting from esophageal-cardiac reflux; Reflux leads to a decrease in coronary blood flow and provokes attacks of angina pectoris and heart rhythm disturbances; Reflux leads to hypermotility of the esophagus
Pulmonary: Chronic cough; Attacks of suffocation	Bronchial asthma; Chronical bronchitis; Repeated pneumonia; Idiopathic pulmonary fibrosis	Stimulation of the vagal receptors of the distal part of the esophagus by refluxate induces bronchospasm due to the vagovagal reflex effect on the bronchi; Micro- and macroaspiration of gastric contents into the bronchial tree
Otorhinolaryngeal: Chronic hoarseness; Feeling of a lump in the throat	Chronic laryngitis; Laryngeal croup; Chronic pharyngitis; Chronic rhinitis; Otalgia	Proximal refluxes lead to inflammation predominantly of the posterior wall of the larynx and the area of ​​the aryepiglottic fold, pronounced hyperkeratosis is detected with a tendency to form crusts and desquamations, so-called singing nodules, Rhine's edema, contact ulcers and granulomas, laryngeal stenosis and laryngospasm can be detected; Hypertonicity of the upper esophageal sphincter
Dental: Burning tongue, cheeks; Impaired sense of taste; Damage to hard dental tissues	Caries with subsequent development of halitosis; Dental erosions	Acidification of salivary fluid with a decrease in salivary pH below 7.0, which has a damaging effect on the oral mucosa and promotes demineralization
Symptoms of anemia: Weakness, fatigue, etc.	Hypochromic iron deficiency anemia	Microbleeding and erosion
Gastric: Distention and fullness of the stomach	Gastroparesis	Disorder of gastric accommodation in response to food intake due to incompetence of the lower esophageal sphincter (LES)

4.5. Diagnosis of gerb

The main methods for diagnosing GERD, most often used in practice, include:

esophagogastroduodenoscopy with biopsy;

omeprazole test (therapeutic test with one of the proton pump inhibitors);

daily monitoring of pH in the esophagus;

Less commonly used when examining patients:

X-ray examination;

Bernstein test;

esophagomanometry;

scintigraphy;

bilimetrics;

chromoendoscopy.

Endoscopic examination

Esophagoscopy makes it possible not only to examine the esophageal tube, but, if necessary, to perform a biopsy, remove a foreign body, cauterize the bleeding area, etc., that is, it can be both a diagnostic and a therapeutic procedure.

Esophagoscopy should be performed after an ECG study (especially in older people).

An endoscopic examination with a biopsy of the mucous membrane is a mandatory component to assess the severity of esophagitis and determine treatment tactics. At the same time, in patients with endoscopically positive GERD, endoscopic examination often reveals hyperemia and swelling of the mucous membrane of the esophagus (with catarrhal reflux esophagitis), erosive and ulcerative defects, which, depending on the severity, occupy a different surface area of ​​the distal esophagus (with erosive reflux esophagitis). esophagitis).

Degrees of gastroesophageal reflux disease:

0 degree – endoscopically negative gastroesophageal reflux disease: typical complaints, the presence of “pathological reflux”, according to 24-hour pH monitoring;

I degree – endoscopically positive gastroesophageal reflux disease: erythema, hyperemia and swelling of the mucous membrane of the distal esophagus, possible single erosions of less than 5 mm, occupying no more than 10% of the circumference;

II degree - superficial erosions or ulcerations, occupying 10-50% of the mucous membrane of the lumen of the distal esophagus;

III degree – deep ulcerations or confluent erosions occupying more than 50% of the mucous membrane of the distal esophagus;

IV degree - stage of development of complications - stricture of the esophagus, development of foci of small intestinal metaplasia (Barrett's esophagus).

In the case of endoscopically negative GERD, there are no endoscopic signs of reflux esophagitis. If a tumor lesion is suspected, it is advisable to conduct endoscopic ultrasonography, which will assess the condition of the submucosal layer of the esophagus and regional lymph nodes.

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Gastroesophageal reflux disease: extraesophageal manifestations, methods of diagnosis and correction

Zhukova T.V.,

Candidate of Medical Sciences, Associate Professor of the Department of Medical Examination and Rehabilitation of the Belarusian Medical Academy of Postgraduate Education

Belarusian Medical Academy of Post-Graduate Education, Minsk

Gastroesophageal reflux disease: extraesophageal manifestations, diagnosis and correction

Summary. Epidemiological studies in recent years have shown that in terms of prevalence, gastroesophageal reflux disease (GERD) takes a leading position among other gastroenterological diseases. The closest attention is currently paid to extraesophageal symptoms of GERD, which require timely diagnosis and correction. Keywords: gastroesophageal reflux disease, gastroenterological diseases, extraesophageal symptoms of GERD.

Medical news. - 2013. - No. 11. - P.4-8. Summary. Epidemiological studies of recent years have shown that on the frequency and prevalence of gastroesophageal reflux disease leaves on leading positions in a number of other gastroenterogycal diseases. Last years the tendency to increase in prevalence of gastroesophageal reflux disease is observed. Currently the closest attention extraesophageal GERD symptoms that require prompt diagnosis and correction. Keywords: gastroesophageal reflux disease, gastroesophageal reflux disease, extraesophageal GERD symptoms. Meditsinskie news. - 2013. - N 11. - P.4-8.

Gastroesophageal reflux disease (GERD) is a chronic relapsing disease caused by a violation of the motor-evacuation function of the gastroesophageal zone and characterized by spontaneous or regularly repeated reflux of gastric and/or duodenal contents into the esophagus, with the development of characteristic symptoms, regardless of whether they arise in this case morphological changes in the mucous membrane of the esophagus.

It is customary to distinguish endoscopically negative reflux disease (NERD), erosive GERD and Barrett's esophagus (Barrett's metaplasia). The division of GERD into endoscopically negative and positive variants is largely due to significant differences in the course and prognosis of these variants of the disease. Although in 5-12% of cases, insufficiently effectively corrected NERD can progress to reflux esophagitis, in most cases this form of the disease is characterized by a relatively stable non-progressive course, a good prognosis, the absence of any complications and requires other approaches to treatment.

boron of treatment and diagnostic tactics than erosive GERD.

The relevance of the problem of GERD is determined by a number of circumstances. Thus, epidemiological studies in recent years have shown that, in terms of prevalence, GERD takes a leading position among other gastroenterological diseases. Every day, the main symptom of GERD - heartburn - is experienced by 7-11% of the adult population of the USA and Canada, at least once a week - 12%, once a month - 40-50%. The prevalence of GERD in Russia among the adult population is 40-60%, and esophagitis is detected in 45-80% of people. However, it can be assumed that the prevalence of GERD in the population is significantly higher than statistical data. This may be due to the existing limitations and difficulties in using the diagnostic research methods used and the fact that not all patients seek medical help.

The great clinical significance should be emphasized of this disease. Studies show that GERD patients themselves evaluate the quality

of their life is lower than patients with coronary heart disease.

Clinically, esophageal and extraesophageal symptoms of GERD are distinguished. Such characteristic symptoms, such as heartburn, belching, regurgitation, dysphagia (difficulty swallowing), odynophagia (pain when swallowing), a feeling of bitterness in the mouth, pain in the epigastric region and esophagus, hiccups, vomiting, a feeling of a lump behind the sternum, significantly worsen the quality of life and reduce performance patients.

The closest attention is currently paid to the “extraesophageal” symptoms of GERD, in particular its cardiac variant. In 50% of cases, the cause of pain in the left half of the chest that is not associated with heart damage (non-cardiac chest pain) is GERD.

Retrosternal pain is a syndrome that causes increased attention from both the doctor and the patient. Patient complaints of chest pain are traditionally considered as coronarogenic, that is, associated with pathology of the coronary arteries of the heart, most often angina pectoris. At the same time, a significant proportion of cases of chest pain have ex-

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tracardial origin (observed in diseases of the mediastinum, respiratory organs, ribs, sternum), a significant percentage of which is caused by pathology of the esophagus, in particular GERD. Thus, in 76% of 600 patients with complaints of chest pain, pathology of the heart and coronary arteries was excluded after examination. In the USA, out of over a thousand coronary angiographies, 180 thousand (30%) were found to have intact coronary arteries, and a significant number of patients are diagnosed with esophageal pathology. In GERD, the mechanism of pain is most often caused by irritation of the receptors of the mucous membrane of the esophagus by the aggressive contents of the stomach and duodenum during reflux. Reflux, entering the esophagus, can cause reflex spastic contractions of the esophagus, which entails pain in the sternum.

The nature of esophageal pain with GERD has its own characteristics. Most often, this is a burning substernal pain of an unattackable nature, which intensifies in a horizontal position or when bending the torso forward and is eliminated or weakened by changing the body position or taking antacids. Constant dull or burning pain behind the sternum can be caused by esophagitis, ulcers of the esophagus and its destruction during erosive forms GERD.

When talking with the patient, they find out the characteristics of the pain (nature, duration, cause, connection with food and other factors), as well as by what means this pain is relieved or eliminated. Examination of the patient will help identify symptoms of “alarm” to exclude neoplasms of the esophagus and neighboring organs.

Substernal pain with GERD can be of a dual nature, that is, pseudocoronary and truly coronary, so it is very important to be able to distinguish between them. The similarity of the nature, localization, irradiation of pseudocoronary and truly coronarogenic retrosternal pain can be explained by the same innervation of the esophagus and heart.

Thus, pain associated with spasm of the esophagus with GERD may have a substernal localization with irradiation to the neck, back, lower jaw, left hand. A similar pain mechanism is also characteristic of ischemic heart disease (angina). In both diseases, the pain can be burning and squeezing. With esophageal pain, the nature of the food, its volume, and the position of the body are of greatest importance. Yes, pain

can be caused by spicy, very hot or very cold food and/or large amounts of it. Provoked horizontal position body, or bending forward. However, as with angina, esophageal pain can sometimes occur during physical or emotional stress or anxiety. Unlike angina pectoris, esophageal pain, except for nitroglycerin, is usually eliminated by changing body position and disappears after a sip of water, taking baking soda or antacids.

During an attack of angina, due to viscero-visceral reflexes, belching and nausea can be observed, as with chest pain associated with GERD. Angina attacks are most often accompanied by a feeling of fear of death, shortness of breath, and weakness, which is by no means characteristic of esophageal pain with GERD.

Daily or multi-hour monitoring of the pH of the esophagus allows you to determine the presence and number of refluxes, their height and strength. The coincidence of reflux with the onset of pain may indicate its esophageal origin. Patients with pain along the esophagus need a thorough examination to determine the nature of the pathology. The examination should include a survey, examination, esophagogastroscopy, x-ray of the esophagus, daily (or multi-hour) esophageal pH monitoring, tests with antisecretory drugs and trial treatment. Pain caused by GERD can be clarified using a pharmacological test with proton pump inhibitors (PPIs). Thanks to PPI, the content of aggressive substances (hydrochloric acid and pepsin) in gastric secretions is reduced. Their irritating effect on the mucous membrane of the esophagus is reduced, which helps the pain subside or disappear. Such a test involves checking the alleged diagnosis by prescribing a drug from the PPI group. With short (from 1 to 14 days) courses of IPP, in most cases it is possible to establish the cause of pain. So, if a standard dose of PPI 2 times a day for 7 days eliminates pain, then, most likely, it is associated with GERD. The sensitivity and specificity of this test for detecting GERD are comparable to similar indicators for dynamic monitoring of esophageal pH (multi-hour pH measurements).

Diagnostic algorithms have been developed to confirm IHD. They

include identifying signs of damage to the cardiovascular system: by determining risk factors (age, heredity, arterial hypertension, hyperlipidemia, etc.), objective data (left ventricular hypertrophy, changes in heart sounds), data from instrumental examination methods (24-hour ECG monitoring, bicycle ergometry , Ultrasound of the heart and blood vessels, myocardial scintigraphy, coronary angiography), characteristic of IHD.

Bronchopulmonary manifestations of GERD include prolonged cough, especially at night, bronchial asthma, fibrosing alveolitis, aspiration pneumonia, paroxysmal sleep apnea, and hemoptysis. The entry of reflux into the lumen of the bronchi can provoke the occurrence of bronchospasm. Despite the availability of data on the mutual influence of BA and GERD, the clinical detection of this kind of concomitant pathology is difficult, since in 25-30% of patients with BA, pathological gastroesophageal refluxes are asymptomatic.

When examining patients with bronchopulmonary manifestations of GERD, one should use both standard methods for assessing morphological and motor-tonic changes in the esophagogastroduodenal zone, as well as additional studies of the respiratory system. Already at the stage of questioning the patient and collecting anamnesis, it is possible to identify factors indicating the likely role of GERD in the development or worsening of asthma symptoms: late onset of asthma; worsening asthma symptoms after eating, lying down, at night, after physical activity; temporary coincidence of cough, wheezing, dyspnea with symptoms of reflux.

Laryngophageal symptoms in many patients are caused by transient or chronically manifested dysphonia in the form of a rough barking cough, excessive mucus formation, a feeling of a lump in the throat and/or pain, the appearance of granuloma and/or ulcers of the vocal cords, laryngeal stenosis, as well as the development of sinusitis, laryngitis and tracheitis. In 50% of patients, these symptoms are associated with GERD (in particular, in 20-30% of cases with the manifestation of laryngotracheitis associated with GERD). Most often, inflammatory changes in the mucous membrane are observed on the posterior wall of the larynx, in the area of ​​the aryepiglottic fold, manifested by edema and hyperkeratosis, in some cases

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Dental symptoms. The entry of gastric contents into the esophagus and further into the oral cavity leads to an imbalance in the acid-base balance with the development of acidosis (normal saliva pH is 6.5-7.5). At a pH of 6.2-6.0, saliva acquires demineralizing properties: partial focal demineralization of tooth enamel occurs with the formation of cavities in them (caries), as well as with the formation of erosions of hard dental tissues - enamel and dentin. In 32.5% of cases, the upper and lower incisors are affected.

Tooth erosion is a pathological change manifested by the destruction of enamel and exposure of dentin, in the occurrence of which (unlike caries) bacteria do not play a significant role. These erosions are irreversible and can lead to tooth loss. Such pathological changes can be observed in people working with acid vapors (for example, when installing car batteries), as well as in bulimia, with frequent consumption of citrus fruits and sour drinks. According to 24-hour pH measurements, dental erosions can indicate to the gastroenterologist the presence of GERD in these patients [2, 6-8].

Thus, the primary diagnosis of GERD may cause difficulties for doctors due to the variety of clinical manifestations. general practice. The situation is

It is also false because many patients are not able to adequately express their complaints to the doctor (for example, some of them understand heartburn as a completely different sensation). In order to improve primary diagnosis GERD abroad, a new scale for assessing symptoms in patients with suspected GERD - Reflux Questionnaire (ReQuest™) has recently been developed and introduced; the use of this scale has yielded good results in clinical studies.

During endoscopic examination, patients with GERD may show signs of reflux esophagitis varying degrees severity: hyperemia and looseness of the mucous membrane of the esophagus (catarrhal esophagitis, related to NERD), erosion and ulcers (erosive esophagitis, gradation of which is carried out depending on the area of ​​damage), the presence of exudate, contact bleeding, fibrin deposits or signs of bleeding. Prolapse of the gastric mucosa into the esophagus, true shortening of the esophagus, and reflux of gastric and/or duodenal contents into the esophagus also occur. In many cases, clinical symptoms do not correlate with endoscopic and morphological changes.

High-resolution endoscopy allows you to reliably identify and classify initial endoscopic changes in GERD and diagnose early stages reflux esophagitis - changes in the capillary network of the mucous membrane of the esophagus, jaggedness of the Z-line, triangular depressions of the mucous membrane. These data, along with the data of fluorescent endoscopy and chromoendoscopy, significantly increase the diagnostic capabilities of endoscopic diagnosis of GERD.

The most important method of instrumental verification of GERD is computer 24-hour pH-metry, recognized as the “gold standard” of diagnosis. With its help, you can not only determine the presence of pathological reflux, but also evaluate its nature (acidic, alkaline), duration, relationship with clinical symptoms, food intake, body position, smoking, and medication use. Computer 24-hour pH-metry makes it possible to individually select therapy and monitor the effectiveness of treatment.

Esophagomanometry is of particular importance in the diagnosis of GERD. The technique can provide valuable information

studies about a decrease in pressure in the area of ​​the lower esophageal sphincter, disturbances of peristalsis and tone of the esophagus. However, in clinical practice this method is rarely used.

To diagnose GERD, the use of a proton pump inhibitor (PPI) test is justified. A PPI (for example, pantoprazole) is prescribed 40 mg once a day for several days. The disappearance of GERD symptoms within 1-3 days indicates the presence of the disease, but the duration of this test has not been definitively established. In terms of diagnostic value, this test is not inferior to daily pH monitoring and endoscopic examination of the esophagus.

The goal of treatment for GERD is to eliminate complaints, improve the patient’s quality of life, prevent or treat complications, and influence symptomatic manifestations from other bodies. Conservative treatment involves adherence to a certain lifestyle and diet, and the use of pharmacological agents. Indications for surgical treatment: repeated bleeding, peptic strictures of the esophagus, Barrett's esophagus, ineffectiveness of drug therapy.

Sleep with the head of the bed raised at least 15 cm;

Loss of body weight when it is overweight;

Frequent split meals (at least 5-6 times a day);

For 1-1.5 hours after eating, do not lie down and do not eat before bed (last meal - 3 hours before bedtime);

Silence while eating (to reduce aerophagia);

Limiting fat intake, increasing the amount of protein in the diet;

Limiting (excluding) consumption of caffeine-containing (coffee, strong tea, cola) and carbonated drinks, citrus juices, ketchup, tomatoes;

Limiting intake of hot, spicy foods;

To give up smoking;

Avoiding tight clothing, tight belts;

Including foods rich in dietary fiber in your diet.

PPIs occupy a leading position in the treatment of GERD. The use of drugs that prevent reflux itself, as monotherapy

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effective in a limited number of patients with mild forms of GERD. In most cases, it is necessary to reduce the aggressiveness of the influence of the refluxate itself (gastric and/or duodenal) on the mucous membrane of the esophagus. This is achieved by using antisecretory drugs that affect the secretion mechanism itself (PPI) or its regulation (histamine H2 receptor blockers).

The widespread use of PPIs began after their clinical advantages over H2-blockers were demonstrated. Thus, according to a meta-analysis of 33 randomized trials, PPIs contributed to the achievement of clinical remission and improved quality of life in 83% of patients with GERD, H2-blockers and placebo - in 60 and 27%, respectively. The healing rate of erosions of the esophageal mucosa within 12 weeks of treatment is more than 80% when using PPIs, and less than 50% when using histamine H2 receptor blockers. These data fully confirm Bell's rule (1992), according to which esophageal erosions heal in 80-90% of cases, provided that pH>4 is maintained in the esophagus for at least 16-22 hours during the day, which is achieved only with the use of PPIs.

All PPIs have a common mechanism of action. Accumulating in the secretory tubules of the parietal cell, they are converted into sulfenamide derivatives, irreversibly blocking the enzyme, binding through a covalent bond at the 813th position with cysteine ​​molecules of K+/H+ ATPase (proton pump). Blockade of the pump leads to the suspension of hydrochloric acid synthesis, regardless of the nature and strength of the factors stimulating the parietal cell. Pantoprazole also binds to the deep cysteine ​​at position 822. As a result of a stronger connection with K+/H+ATPase, the duration of inhibition gastric secretion when using pantoprazole, it reaches 46 hours (lansoprazole - 15 hours, omeprazole - 30 hours), which makes it a very reliable PPI for the treatment of GERD. In a number of comparative studies, it is likely that these properties of pantoprazole determined the greater clinical effectiveness of the drug compared to other PPIs, assessed by the percentage of patients with relieved heartburn and the overall percentage of successful

treatment of GERD. Differences in PPI metabolism and therefore acidity levels may play a significant role in the treatment of GERD.

The first PPI was omeprazole. The IPPs synthesized after this differ in the structure of the radicals on the pyridine and imidazole rings. Omeprazole is completely metabolized and therefore almost never excreted from the body unchanged. Most of omeprazole is metabolized through the enzyme CYP2C19, and a smaller part (about 10%) through CYP3A4. In subsequent generations of PPI, this dependence also remains, but is less pronounced. For example, rabeprazole has a non-enzymatic pathway. Since all PPIs are metabolized to varying degrees in the liver via the cytochrome P450 enzyme system, their interactions with medicines, which are metabolized by the same system. Moreover, in clinical studies, pantoprazole (Nolpaza) has virtually no effect on the pharmacokinetics of other drugs metabolized in the liver by the cytochrome P450 system. So far, no significant interactions have been identified with digoxin, diazepam, diclofenac, ethanol, phenytoin, glibenclamide, carbamazepine, caffeine, metoprolol, naproxen, nifedipine, piroxicam, theophylline and oral contraceptives. However, in patients receiving coumarin anticoagulants concomitantly with pantoprazole, it is recommended that prothrombin time or international normalization ratio (INR) be regularly monitored. In addition, the dependence of the pH of the medium and the value of the dissociation constant (pK), which determines the permeability of cell membranes and the activation of PPI, is important for the rate of activation and efficiency of PPI. The pK value for the nitrogen of the pyridine ring of pantoprazole (Nolpaza) is minimal and equal to 3.0.

Pantoprazole (Nolpaza) dosage regimen

For erosive GERD stages A and B according to the Los Angeles classification or for NERD, the recommended dose is 20 mg/day; for GERD stage C or D, zero-gap is prescribed at 40-80 mg/day for 1 or 2 doses. Symptom relief usually occurs within the first two weeks. The course of therapy is 4-8 weeks.

As long-term maintenance therapy, 20 mg per day is prescribed, if necessary (for example, in

patients with Barrett's esophagus), the dose is increased to 40-80 mg per day. The drug can be taken “on demand” if symptoms occur.

It is considered proven that all patients with extraesophageal manifestations of GERD should be prescribed a high dose of PPI, and the duration of treatment should be at least three months. If such treatment is ineffective, it is indicated carrying out endoscopy and daily pH-metry with assessment of response to PPIs. If the diagnosis of GERD is confirmed, then drug therapy should be continued or even intensified; if it is ineffective, surgical treatment of the disease is indicated. If the examination results are negative, you need to return to the question of differential diagnosis, since another pathology is very likely. When symptoms are relieved, they switch to maintenance therapy, which is carried out according to the same regimens as for classic GERD.

In the absence of adequate therapy, in 7-23% of cases, GERD can be complicated by the formation of peptic strictures of the esophagus, which is facilitated by unreasonably shortened courses of treatment (less than 4 weeks), insufficient suppression of gastric secretion due to the use of inappropriate medicines and doses of drugs, patient non-compliance with medical recommendations.

L I T E R A T U R A

1. Babak, O.Ya. Gastroesophageal reflux disease / O.Ya.Babak, G.D.Fadeenko. - Kyiv, 2000. -175 p..

2. Vasiliev, Yu.V. Acid-dependent gastrointestinal diseases and coronary heart disease / Yu.V. Vasilyev // Lech. doctor. - No. 1. - 2006. - P.50-55.

3. Zhukova, T.V. Gastroesophageal reflux disease and its treatment / T.V. Zhukova // Med. news. - No. 4. - 2010. - P.45-48.

4. Ivashkin, V.T. Modern approach to the treatment of gastroesophageal reflux disease in medical practice/ V.T.Ivashkin, A.S.Trukhmanov // RMJ. - 2003. - No. 2. - P.43-48.

5. Isakov, V.A. Epidemiology of GERD: East and West / V.A. Isakov // Experiment. wedge. gastroenterol. - 2004. - No. 5 (Special issue). - P.2-6

6. Lazebnik, L.B. The effectiveness of pantoprazole in the treatment of gastroesophageal reflux disease / L.B. Lazebnik, Yu.V. Vasiliev // Experiment. and wedge. gastroenterol. - 2008. - No. 2. - P.102-104.

7. Maev, I.V. Comparative effectiveness of triple anti-helicobacter therapy of the first line using the drugs pantoprazole and omeprazole / I.V. Mayev, T.S. Oganesyan, Yu.A. Kucheryavy [and others] // Lech. doctor. - 2010. - No. 2. - P.2-7.

8. Bardhan, K.D. Evaluation of GERD Symptoms during therapy. Part I. Development of the new GERD

Lectures Im!

questionnaire ReQuest™ / K.D.Bardhan // Digestion. - 2004. - N69 (4). - P.229-237.

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10. Bhattacharjya, A. The impact of erosive esopbagitis on HRQL / A. Bhattacharjya // Gut. - 2000. -Vol.47 (suppl. 3). - P.53.

11. Blume H, Pharmacokinetic drug interaction profiles of proton pump inhibitors / H. Blume, F.A. Donath Warnke, B.S. Schug // Drug Safety. - 2006. -N29(9). - P.769-784.

12. Dean, B.B. Cost-effectiveness of proton-pump inhibitors for maintenance therapy of erosive reflux esophagitis / B.B. Dean // Amer. J. Health. Syst. Pharm. - 2001. - Vol.58, N14. - P.1338-1346.

13. DeVault, K.R. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease / K.R.DeVault, D.O.Castell // Am. J. Gastroenterol. -2005. - N100. - P.190-200.

14. French-Belgian Consensus Conference on Adult Gastro-esophageal Reflux Disease. Diagnosis and treatment report of a meeting held in Paris, France on 21-22 January 1999. The jury of the consensus

conference//Eur. J. Gastroenterol. Hepatol. - 2000. -Vol.12. - P.129-137.

15. Gardner, J.D. Integrated acidity and the pathophysiology of gastroesophageal reflux disease / J.D. Gardner // Am. J. Gastroenterol. - 2001. -N96. - P.1363-1370.

16. Horn, J. The proton pump inhibitors: similarities and differences / J. Horn // Clin. Ther. - 2000. - Vol.3. -P.266-280.

17. Inamori, M. Comparison of the effect on intragastric pH of a single dose of omeprazole or rabeprazole: which is suitable for on-demand therapy? / M. Inamori // J. Gastroenterol. Hepatol. - 2003. - Vol.18, N9. - P.1034-1038.

18. Juurlink, D.N. A population-based study of the drug interaction between proton pump inhibitors and clopidogrel / D.N.Juurlink, TGomes, DTKo et al. // CMAJ. - 2009. - N 180. - P.713-718.

19. Naumburger, A. Comparison of two treatment regimens in symptomatically homogenous GERD patient populations: pantoprazole relieves gastrointestinal symptoms significantly better than omeprazole / A.Naumburger, L.Schoffel, A.Gillessen // Gut. - 2004. - N53. (Suppl. VI). - P.A108.

20. Pantoflickova, D. Acid inhibition on the first day of dosing: comparison of four proton pump inhibitors / D. Pantoflickova // Aliment. Pharmacol. Ther. -2003. - N17. - R.1507-1514.

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Received 10/21/2013

The article is posted on the website www.mednovosti.by (MN Archive) and can be copied in Word format.

MINT WILL HELP GET RID OF

FOR IRRITABLE BOWEL SYNDROME

Researchers at the University of Adelaide explain that mint activates the “anti-pain” channel in the colon, soothing inflammatory pain in the gastrointestinal tract.

Dr Stuart Brearley notes that mint has long been widely used in naturopathy, but until now there has been no clinical evidence to understand why it is so effective in relieving pain.

“Our research shows,” he says, “that mint acts through a specific channel called TNPM8, reducing pain in sensory fibers, especially those activated by mustard and pepper. This is potentially the first step in defining a new type of overall clinical treatment for irritable bowel syndrome."

Irritable bowel syndrome (IBS) - gastrointestinal disorder, painful stomach, bloating, diarrhea or constipation. This disease affects approximately 15-20% of the adult population of the Earth (about 22 million), two thirds of patients are women. Currently, there is no specific cure for IBS. The syndrome may appear and disappear throughout a person's life.

Some people experience symptoms of IBS after consuming fatty and spicy foods, coffee and alcohol, but doctors say the causes of the disease may be more complex. There is an opinion that IBS is associated with gastroenteritis (inflammation of the stomach and intestines). In some cases the syndrome may be caused food poisoning, stress, a reaction to antibiotics, and sometimes due to heredity.

Based on materials from newsru.com

THIS IS USEFUL TO KNOW

mn COMPARISON OF TWO STRATEGIES FOR PROTECTING THE GASTROINTESTINAL TRACT DURING THERAPY WITH NON-STEROID ANTI-INFLAMMATORY DRUGS. RESULTS OF THE CONDOR STUDY Currently, to reduce the risk of adverse events (AEs) from gastrointestinal tract(Gastrointestinal tract) during long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs), it is recommended to use non-selective NSAIDs in combination with a proton pump inhibitor (PPI) or selective cyclooxygenase-2 inhibitors (COX-2 inhibitors). This situation is associated with the similar effectiveness of these approaches in the prevention of AEs from the upper gastrointestinal tract. However, NSAID therapy may also be associated with damage to the small and large intestines. Since lower gastrointestinal adverse events are not acid-related, theoretically, the tolerability of selective COX-2 inhibitors should be better than the combination of non-selective NSAIDs with PPIs. To test this hypothesis, F K. L. Chan et al. conducted a large randomized clinical trial, CONDOR.

This randomized, double-blind clinical trial showed for the first time that in patients with OA and RA without increased cardiovascular risk, who did not receive antiplatelet agents and anticoagulants, the frequency of clinically significant gastrointestinal AEs was 4 times higher during long-term therapy with the non-selective NSAID diclofenac in combination with PPI omeprazole than with COX-2 therapy with celecoxib. This fact should be reflected in recommendations for the management of patients with arthritis, the authors of the publication conclude.

Chan FK, Lanas A, Scheiman J et al. // Lancet. - 2010. - Vol. 376, N 9736. - P. 173-179.

GERD can also manifest itself with extraesophageal (atypical) symptoms, which include:

· respiratory symptoms: bronchial obstruction, chronic cough, especially at night, paroxysmal sleep apnea, recurrent pneumonia, idiopathic pulmonary fibrosis, clinical manifestations of chronic recurrent bronchitis, development of bronchiectasis, aspiration pneumonia, lung abscesses, clinical manifestations of bronchial asthma, sudden death of newborns);

· symptoms associated with heart and mediastinal diseases(cardialgia, palpitations, arrhythmias, development of hypertension, shortness of breath). Chest pain of non-coronary origin (angina-like chest pain) in most cases is associated with pathology of the esophagus. In this case, retrosternal pain can radiate to the interscapular region, neck, lower jaw and left half of the chest. When differentially diagnosing the genesis of pain, it should be taken into account that esophageal pain is characterized by a connection with intake and physical properties food, body position and their relief by taking alkaline mineral waters and antacids;

· symptoms from ENT organs(laryngitis, false croup, narrowing of the lumen of the larynx, pharyngitis, dysphonia, laryngeal tumors, recurrent otitis, chronic rhinitis, otalgia, ulcers, granulomas and polyps of the vocal folds);

· oropharyngeal symptoms(inflammation of the nasopharynx and sublingual tonsil, erosion of tooth enamel, caries, periodontitis, sensation of a lump in the throat).

The consensus group (Montreal, 2006) proposes that extraesophageal symptoms of GERD be divided into:

Reliably associated with GERD (reflux cough, reflux laryngitis, reflux asthma and reflux caries);

Probably associated with GERD (pharyngitis, sinusitis, idiopathic pulmonary fibrosis, recurrent otitis media).

Complications.

Complications of GERD include esophageal strictures and bleeding from esophageal ulcers. The most significant complication of GERD is Barrett's esophagus, which involves the appearance of small intestinal metaplastic epithelium in the esophageal mucosa. Barrett's esophagus is a precancerous disease.

Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma, but these symptoms occur only late stages diseases, therefore clinical diagnosis of esophageal cancer is usually delayed. Therefore, the main way to prevent and early diagnose esophageal cancer is the diagnosis and treatment of Barrett's esophagus.

Esophageal complications of GERD include peptic ulcers, bleeding ulcers, strictures, Barrett's esophagus, and esophageal adenocarcinoma.

Erosive esophagitis is observed in 50% of patients, and esophageal strictures are observed in 10% of patients with GERD. Risk factors for the development of esophagitis are: the duration of GERD symptoms for more than 1 year, the presence of a hiatal hernia, male gender, age over 60 years, alcohol abuse.

Barrett's esophagus develops in 8–20% of patients with GERD. It is believed that an important role in its development also plays duodenogastric reflux bile and pancreatic proteases, mainly trypsin. Often, patients with GERD with Barrett's esophagus experience epithelial dysplasia (the appearance of small intestinal metaplastic epithelium in the mucous membrane of the esophagus), which allows Barrett's esophagus to be classified as a group of precancerous diseases of the esophagus. The incidence of esophageal adenocarcinoma in such patients can reach 16–23%. The development of adenocarcinoma may be indicated by rapidly progressing dysphagia and weight loss, but these symptoms occur only in the late stages of the disease, so the clinical diagnosis of esophageal cancer is usually delayed. Therefore, the main way to prevent and early diagnose esophageal cancer is the diagnosis and treatment of Barrett's esophagus. Risk factors for the formation of Barrett's esophagus are: age 50 years or more, male gender, white race, the onset of GERD symptoms at a young age and their long-term persistence.

Diagnostics.

Problems in diagnosing GERD are due to the following circumstances. Firstly, the presence of typical symptoms does not always coincide with endoscopic manifestations, which predetermined the identification of an endoscopically negative form of GERD, for confirmation of which it is necessary to determine the pH of the esophagus during the day. Secondly, the existing atypical clinical manifestations, hiding under the guise of cardiac, bronchopulmonary pathology, ENT diseases, are also often combined with an endoscopically positive or negative picture. According to the observations of some researchers, 17% of patients with erosive esophagitis have extraesophageal manifestations of GERD. Thirdly, GERD through the initiation of viscero-visceral interaction may already be a trigger existing diseases: bronchial asthma, chronic bronchitis, coronary heart disease, arterial hypertension.

Diagnosis of GERD is based primarily on the patient’s complaints, and instrumental methods diagnostics(esophagoscopy, X-ray examination of the esophagus with barium, 24-hour pH-metry of the esophagus) are additional or confirmatory of the diagnosis. In the diagnosis of atypical forms of GERD and confirmation of the diagnosis of NERD great importance has a trial of treatment with proton pump inhibitors (PPIs) or isomers of proton pump inhibitors (iPPIs).

Bernstein test consists of alternate infusion of first 60-80 ml of 0.1 N HCl solution at a rate of 6-8 ml/min into the distal esophagus, then the same volume of physiological solution. The test is considered positive if 1) the introduction of acid provokes the appearance of symptoms, 2) the symptoms disappear or do not recur when saline solution is introduced into the esophagus.

Endoscopic diagnostics reflux esophagitis with a violation of the integrity of the mucous membrane of the esophagus is carried out according to the Los Angeles classification of 1994, when used, depending on the volume of damage to the mucous membrane, 4 degrees of reflux esophagitis are distinguished (see Table 1).

Table 1

Basic criteria of the 1994 Los Angeles classification of reflux esophagitis.

An endoscopic examination may also reveal prolapse of the gastric mucosa into the esophagus, true shortening of the esophagus with the esophagogastric junction located significantly above the diaphragm, and reflux of gastric and/or duodenal contents into the esophagus.

Among other endoscopic classifications of reflux esophagitis, it is advisable to note the Savary–Miller classification (1987), in which an attempt was made to differentiate in detail the condition of the esophageal mucosa in GERD, highlighting diffuse pathological changes in the esophageal mucosa and erosive and ulcerative lesions of varying intensity and extent. . According to the Savary–Miller classification, there are 4 degrees of severity of reflux esophagitis (RE) (Fig. 2).

Norm	RE I Art.	RE II Art.	RE III Art.	RE IV Art.	Barrett's syndrome

Rice. 2. Savary–Miller classification.

RE I degree of severity. Endoscopically, a picture of predominantly catarrhal esophagitis is revealed, and single erosions cover less than 10% of the surface of the mucous membrane of the distal esophagus.

RE II degree of severity. Erosion becomes confluent and already covers up to 50% of the surface of the mucous membrane of the distal portion of the esophagus.

RE III degree of severity. There are circularly located drainage erosions, occupying almost the entire surface of the mucous membrane of the esophagus.

RE IV severity. EC is characterized by the formation of peptic ulcers and strictures of the esophagus, as well as the development of small intestinal metaplasia of the esophageal mucosa (Barrett's syndrome).

During esophagoscopy, a sample can be taken for histological examination of the esophageal mucosa in order to assess microscopic signs of esophagitis and, above all, the presence of small intestinal metaplasia, epithelial dysplasia and adenocarcinoma of the esophagus.

Algorithm for diagnosing GERD in an outpatient setting

X-ray diagnostics for GERD is limited only to the visualization of hiatal hernia and gastroesophageal reflux when studied with a barium contrast agent under conditions as close as possible to physiological ones. Considering the fact that both hiatal hernia and gastroesophageal reflux exist in the absence of GERD, their detection cannot be a criterion for diagnosing the disease. However, if a certain picture is present, they can be taken as additional facts in confirming the diagnosis of GERD.

24-hour pH-metry of the esophagus used to identify pathological gastroesophageal reflux in non-erosive reflux disease (the gold standard for diagnosis) and in the atypical course of GERD, which can serve as a basis for making a diagnosis or prescribing a trial treatment.

Omeprazole the test can be performed on an outpatient basis. Its essence is that the clinical symptoms of gastroesophageal reflux disease are significantly reduced during the first 3 to 5 days of daily intake of 40 mg of omeprazole. It is believed that if this does not happen, the symptoms are likely due to another disease. The significance of this test is relatively high, but should not be overestimated.

In general, the process of diagnostic search for suspected GERD in an outpatient setting can be presented in the form of Scheme 1.

The consensus group (Montreal, 2006) believes that one of the key factors in diagnosing GERD is the degree of discomfort that GERD symptoms cause to the patient. Using a patient-centered approach, GERD can be diagnosed in an outpatient setting based on clinical presentation alone, without the need for additional testing.

Treatment

Treatment of patients with GERD schematically involves a certain set of basic measures: changing the diet and nature of nutrition; regulation of lifestyle; modern pharmacotherapy ( various schemes); surgery.

· in order to reduce body weight, food should not be too high in calories;

· it is necessary to exclude systematic overeating and “snacking” at night;

· It is advisable to eat in small portions;

· a 15-20 minute interval between dishes is justified;

· after eating you should not lie down, it is best to walk for 20–30 minutes;

· the last meal should be at least 3-4 hours before bedtime;

· after meals, it is advisable, if possible, to take a 30-minute walk;

· foods rich in fat (whole milk, cream, fatty fish, goose, duck, pork, fatty beef and lamb, cakes, pastries), drinks containing caffeine (coffee, strong tea, Coca-Cola), chocolate should be excluded from the diet , products containing peppermint and pepper (all of them reduce the tone of the lower esophageal sphincter), citrus fruits, tomatoes, onions, garlic, fried foods (these products have a direct irritant effect on the mucous membrane of the esophagus);

· do not drink beer, any carbonated drinks, champagne (they increase intragastric pressure and stimulate acid formation in the stomach);

· you should limit the consumption of butter and margarine;

Gastroesophageal reflux disease (GERD) is extremely common, affecting approximately 40% of adults in developed countries. In Eastern European countries, this figure reaches 40-60%, with 45-80% of patients with GERD having esophagitis.

G.D. Fadeenko, Doctor of Medical Sciences, Professor, Institute of Therapy named after. L.T. Small Academy of Medical Sciences of Ukraine, Kharkov

GERD and its manifestations are caused by the influence of hydrochloric acid and pepsin on the mucous membrane of the esophagus, where they enter from the stomach due to pathological gastroesophageal reflux. The effect of these damaging factors depends on the pH of the esophagus (more time of day when the pH of the esophagus is below 4.0).

The typical and most common symptom of GERD is heartburn. It can occur after eating or when eating certain foods, bending the body, physical stress, or lying down. Heartburn is often accompanied by sour belching and regurgitation. Symptoms characteristic of diseases of the esophagus, such as odynophagia (pain when swallowing and passing food through the esophagus), dysphagia (difficulty in passing food through the esophagus) occur much less frequently - in complicated forms of the disease (ulcers and strictures of the esophagus). The listed manifestations are regarded as “esophageal” symptoms, which makes it possible to suspect and confirm GERD with a high degree of probability. In accordance with the current situation (Genval Conference, 1998), if heartburn is the main or only symptom, then in 75% of individuals its cause is GERD. You may suspect you have GERD if you experience heartburn 2 or more days a week.

At the same time, in a fairly large proportion of patients, the manifestations of GERD are “extraesophageal” in nature and include a fairly wide spectrum. As a rule, they are underestimated, especially in the absence typical symptom- heartburn. This leads to diagnostic and therapeutic errors and inadequate management tactics for such patients.

Clinical extraesophageal manifestations of GERD are varied. They can be:

• abdominal;
• respiratory;
• cardiac (pseudocardial);
• otorhinolaryngological;
• dental.

Most studies examining the relationship of GERD with pathology of the upper gastrointestinal tract, respiratory, cardiovascular systems, ENT organs and oral cavity have been carried out only in recent years, due to the expansion of technical capabilities, in particular, monitoring of esophageal pH. This method allows you to reliably record and quantify refluxes (acid or alkaline, their height, frequency of episodes per day, refluxate exposure time and other parameters).

Abdominal manifestations of GERD

Abdominal manifestations of GERD can either be combined with typical “esophageal” symptoms or be independent. Abdominal symptoms in patients with GERD are essentially a dyspepsia syndrome, which includes pain and discomfort in the epigastric region.

Abdominal symptoms of GERD:

• nausea, vomiting;
• feeling of quick satiety, fullness;
• heaviness, epigastric pain associated with eating;
• flatulence.

The mechanism of abdominal manifestations of GERD is associated with concomitant dysfunction of the motor function of the stomach and intestines, as well as increased visceral sensitivity of these organs to stretching.

In order to exclude functional dyspepsia, such patients should monitor the pH of the stomach and esophagus, examine the motor function of the stomach (ultrasound, scintigraphy), and test for the presence of H. pylori infection.

Respiratory manifestations of GERD

Respiratory manifestations of GERD include:

• bronchial asthma;
• recurrent pneumonia;
• chronic cough.

The connection between bronchial asthma and GERD is evidenced by the results of numerous studies. Thus, it has been shown that in patients with bronchial asthma, heartburn occurs in 70% of cases, including in the daytime - in 20%, during the day and at night - in 50%. In 60% of patients with bronchial asthma, a hiatal hernia is detected, which is the morphological substrate for the appearance of GERD. According to the data of many hours of pH-metry of the esophagus, it has been established that most attacks of suffocation in bronchial asthma coincide with gastroesophageal reflux. The presence of GERD is noted in 33-90% of patients with bronchial asthma, while in 25-30% pathological gastroesophageal refluxes do not have “esophageal” manifestations.

Currently, two main pathogenetic mechanisms for the development of bronchial asthma against the background of GERD are being considered. The first is reflex. Its essence is as follows. The aggressive components of refluxate, entering the esophagus during reflux, stimulate the chemoreceptors of the distal esophagus, in response to which the vago-vagal reflex develops, which causes bronchospasm. The second mechanism is associated with direct entry of refluxate into the respiratory tract (microaspiration), which causes chronic inflammation in the mucous membranes of the latter.

Pathological gastroesophageal reflux can aggravate the course of bronchial asthma, which arose under the influence of other endogenous and exogenous factors. All of the above gave rise to the term “reflux-induced bronchial asthma.”

In some cases, “unmotivated” chronic cough is caused by GERD. One study found that in patients with chronic cough, GERD was associated with GERD in 78% of cases. However, with chronic cough, a diagnosis of one or another respiratory disease is often incorrectly made and inadequate treatment is prescribed.

The mechanism of occurrence of chronic cough with GERD is irritation of the receptors of the laryngeal and tracheobronchial tracts, the esophagus along the afferent pathways (vagal, glossopharyngeal, phrenicus), which reach the cough center, where excitation connects with the center that controls breathing. Through the efferent pathways (phrenic, spinal nerves and nerves of the bronchial tree), excitation reaches the muscles: skeletal respiratory, diaphragm, bronchi, pharynx.

To diagnose bronchopulmonary manifestations of GERD, the following algorithm is required. After a thorough study of complaints and medical history (exclusion of smoking, taking ACE inhibitors) it is advisable to conduct an X-ray examination of the respiratory organs in order to exclude them possible pathology. Then a study of the function of external respiration is carried out. If there are changes, study bronchial patency (drug tests with b2-adrenergic agonists, etc.). The last stage is an examination of the esophagus: esophagogastroscopy and pH monitoring.

Cardiac manifestations of GERD

Cardiac symptoms with GERD are also quite common. According to coronary angiography, in almost a third of patients, pathology of the heart vessels is not detected, however, in a significant part of these patients, pathology of the esophagus is detected. Cardiac symptoms with GERD, as a rule, are as follows: chest pain and transient disturbances in heart rhythm and conduction.

Retrosternal pain always causes increased alertness and, in accordance with the established stereotype, is regarded as angina. As numerous studies show, in almost a third of patients, these pains are not of cardiac origin, but are associated with pathology of the esophagus, in the vast majority with GERD. In more than 50% of cases, patients with non-coronary pain exhibit characteristic signs of GERD (according to pH monitoring and esophageal endoscopy).

It is possible to differentiate between true cardiac and pseudocardial (caused by GERD) chest pain, first of all, according to clinical criteria (Table).

It is possible to definitively prove or disprove the assumption about the esophageal nature of chest pain by conducting an instrumental examination. Endoscopic examination can reveal inflammatory and destructive disorders in the mucous membrane of the esophagus, which may be the cause of chest pain. However, it should be remembered that in 60% of patients with GERD, changes in the esophagus are not detected. Therefore, it is possible to identify one of the causes of gastroesophageal reflux—hiatal hernia—by performing an X-ray examination of the chest organs with contrasting of the esophagus. When monitoring the pH of the esophagus, it is possible to record the coincidence of episodes of reflux with the occurrence of pain, which will indicate in favor of GERD. The most reliable method is considered to be simultaneous monitoring of esophageal pH and ECG monitoring. The coincidence of reflux episodes with episodes of ECG abnormalities also indicates GERD.

The following mechanisms for the occurrence of retrosternal pain associated with reflux are distinguished: irritation of the receptors of the mucous membrane of the esophagus by gastric contents when it enters the esophagus contributes to disruption of its motor function, leads to chaotic non-propulsive contractions of the lower third of the esophagus, spasm of its muscles, hypertension of the muscles of the lower esophageal sphincter, which can cause pain in the chest.

It should be remembered that with pain syndrome of reflux origin, visceral sensitivity is increased. In this regard, an increase in the excitability of the dorsal columns of neurons or a change in the central nervous processes of afferent stimulation can independently cause pain in the chest. Pseudocardial pain due to dysfunction of the esophagus can in some cases lead to a decrease in coronary blood flow and myocardial ischemia through the viscero-visceral reflex.

In addition to pseudocoronary pain, cardiac manifestations of GERD also include transient disturbances of heart rhythm and conduction. The most common rhythm disorder with GERD is extrasystolic arrhythmia. It should be noted that rhythm disturbances caused by GERD are always combined with signs of autonomic dysfunction: feelings of fear, anxiety, fever or chills, dizziness, sweating, shortness of breath, emotional lability.

The mechanism of occurrence of dysrhythmic manifestations of GERD is also mediated by the excitation of the reflexogenic zone of the distal part of the esophagus by acid refluxate with the development of viscero-visceral reflexes, modeled through n. vagus and leading to coronary spasm and arrhythmias.

Cardiac syndrome with GERD can occur not only in the so-called “pure” form, when there is no true coronary pathology, and chest pain with signs of abnormalities on the ECG are exclusively reflexive in nature. Quite often, a patient with GERD also has coronary artery disease, the course of which, due to the additional induction of coronary spasm and rhythm disturbances by reflux, can be significantly aggravated. In such cases, it is very difficult to isolate the leading mechanisms of the genesis of cardiac disorders, and only a special pharmacological test for the diagnosis of GERD can bring final clarity.

Otorhinolaryngological manifestations of GERD

An important extraesophageal manifestation of GERD is reflux-induced pathology of the ENT organs - the nasal cavity, larynx, and pharynx. According to various authors, their frequency is quite high.

Otorhinolaryngological manifestations of GERD include the following:

• dysphonia;
• otalgia;
• pain when swallowing;
• hoarseness of voice (in 71% of cases);
• globus pharyngeus (in 47-78% of cases);
• chronic cough (in 51% of cases);
• sore throat;
• increased mucus formation (in 42% of cases);
• lateral neck pain;
• laryngospasm;
• aphonia.

Damage to the larynx and pharynx due to GERD includes:

• chronic laryngitis;
• contact ulcers and granulomas of the vocal folds;
• chronic pharyngitis;
• laryngeal stenosis;
• "cervical symptoms" - discomfort in the neck and pharynx area of ​​unclear localization;
• laryngeal papillomatosis (Fig. 1);
• laryngeal cancer (Fig. 2);
• stridor, subglottic laryngitis, or recurrent pneumonia in newborns (due to gastric contents entering the nose, trachea, and lungs).

With high duodenogastroesophageal reflux, a direct connection has been traced between the degree of tissue damage to the ENT organs and the duration of exposure to refluxate (pepsin, gastric acid, bile, trypsin), which can lead to erosive and ulcerative lesions of the mucous membranes and swelling.

The prevalence and severity of damage to the ENT organs in GERD does not raise doubts about the need to include consultation with an otolaryngologist in the diagnostic algorithm for managing patients with GERD. And if the above pathology of the ENT organs is difficult to correct with medication, otolaryngologists should not neglect consultation and examination of such patients with gastroenterologists.

Dental manifestations of GERD are very common. The most common oral lesions associated with GERD include:

• damage to soft tissues (aphthae of the oral mucosa, changes in the papillae of the tongue, burning of the tongue) (Fig. 3);
• inflammatory diseases periodontal tissues (gingivitis, periodontitis);
• non-carious lesions of hard dental tissues (enamel erosion);
• halitosis

The mechanism of dental damage in GERD is determined by the degree of acidification of the salivary fluid (pH below 7.0) and changes in the physicochemical properties of saliva (mineral composition, viscosity).

These changes are closely related to the duration of the course and the degree of compensation in the treatment of GERD. Effective treatment of GERD helps reduce these disorders.

The mechanisms discussed above for various extraesophageal manifestations of GERD have similar ways of implementation. They include: the direct damaging chemical effect of refluxate on tissue, a reflex mechanism mediated by vagal influences, and impaired esophageal clearance due to motility disorders. Considering the serious pathogenetic changes outside the esophagus that occur with various extra-esophageal manifestations of GERD, correct and timely diagnosis of the latter is of particular importance. In this regard, special attention should be paid to the developed algorithm for diagnosing this pathology.

So, methods for diagnosing extraesophageal manifestations of GERD include:

• clinical examination (complaints, anamnesis, objective examination data);
• pH monitoring;
• esophagogastroduodenoscopy;
• X-ray of the esophagus and stomach;
• Ultrasound of the abdominal organs;
• study of external respiration function;
• lung scintigraphy;
• ECG, coronary angiography;
• laryngoscopy;
• consultation with an otorhinolaryngologist;
• dentist consultation.

As practice shows, correct and quick diagnosis of extraesophageal manifestations of GERD turns out to be difficult due to both purely technical and clinical reasons, in particular, the presence of combined pathology, which in some cases does not allow us to isolate the contribution of each to the development of extraesophageal manifestations. It is for this purpose that a readily available and simple pharmacological test with a proton pump inhibitor (PPI) has been developed and is used. The essence of the test is that PPIs are powerful inhibitors of gastric acid, the main aggressive component of refluxate, which has an irritating effect on receptors located in the mucous membranes of the esophagus, respiratory tract, and oral cavity. Inhibition of the production of hydrochloric acid helps to increase intragastric pH, reducing irritation of receptors and eliminating any manifestations of gastroduodenal reflux, including extraesophageal ones. This test is based on the possibility of achieving correction of the patient’s symptoms when prescribing a PPI in the form of short therapy ex juvantibus.

Initially, omeprazole was proposed as a test drug, and the test was called the “omeprazole test.” The test method consists of prescribing a standard dose of omeprazole (40 mg) once a day for 2 weeks. The test is considered positive (confirms the presence of GERD) if, as a result of taking it, the manifestations of reflux decrease or disappear. The first assessment of the omeprazole test can be carried out on the 4th-5th day of administration.

In recent years, another drug from the PPI group, rabeprazole (Pariet) at a dose of 20 mg per day, is more often used instead of omeprazole. The use of the rabeprazole test makes it possible to reduce the testing time from 2 weeks to 7 days, and the first assessment to 1-3 days due to the faster onset of the maximum antisecretory effect of the drug. The specificity and sensitivity of the rabeprazole test are 86% and 78%, respectively. It has been proven that this PPI test is not inferior in diagnostic value to daily monitoring pH and endoscopic examination of the esophagus. This test is of particular value in patients with extraesophageal manifestations of GERD with concomitant pathology. A positive test is the basis for treatment of all manifestations of GERD, using PPIs as basic drugs. In case of combined pathology, PPIs are included in complex therapy (for example, for bronchial asthma, coronary heart disease, obesity), which significantly alleviates the course of the disease.

Thus, GERD is a widespread disease that leads to a significant decrease in the quality of life of such patients. Due to the high incidence, as well as the presence of extraesophageal manifestations caused by pathological reflux, GERD has become relevant not only for gastroenterologists, but also for doctors of other specialties. GERD can be considered not as a “gastroenterological”, but as an “internal” pathology.

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