Gastroesophageal reflux disease symptoms treatment. Gerb: causes and clinical manifestations. Extraesophageal manifestations of gerb
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RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2017
Gastroesophageal reflux (K21), Gastroesophageal reflux without esophagitis (K21.9), Gastroesophageal reflux with esophagitis (K21.0)
Gastroenterology
general information
Short description
Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated June 29, 2017
Protocol No. 24
Gastroesophageal reflux disease is a chronic recurrent disease caused by a violation of the motor-evacuation function of the organs of the gastroesophageal zone and characterized by spontaneous or regularly repeated reflux of gastric or duodenal contents into the esophagus, leading to the development of inflammatory changes in the distal esophagus and/or characteristic clinical symptoms.
INTRODUCTORY PART
ICD-10 code(s):
Date of protocol development/revision: 2013/
revision 2017
Abbreviations used in the protocol:
AlAT | alanine aminotransferase |
ASAT | aspartate aminotransferases |
VEM | bicycle ergometry |
GER | gastroesophageal reflux |
GERD | gastroesophageal reflux disease |
HH | hiatal hernia |
Gastrointestinal tract | gastrointestinal tract |
IPP | proton pump inhibitors |
NERB | endoscopically negative reflux disease |
NPC | lower esophageal sphincter |
OBP | abdominal organs |
RCT | randomized controlled trials |
CO | mucous membrane |
HS | cholesterol |
EGDS | esophagogastroduodenoscopy |
ECG | electrocardiography |
Protocol users: General practitioners, therapists, gastroenterologists.
Level of evidence scale:
A | A high-quality meta-analysis, systematic review of RCTs or RCTs with a very low probability (++) of bias, the results of which can be generalized to the relevant population. |
IN | High-quality (++) systematic review of cohort or case-control studies, or high-quality (++) cohort or case-control studies with very low risk of bias, or RCTs with low (+) risk of bias, the results of which can be generalized to the corresponding population. |
WITH | Cohort or case-control studies, or controlled studies without randomization with low risk of bias (+), the results of which can be generalized to relevant populations, or RCTs with very low or low risk of bias (++ or +), the results of which can be directly generalized to the relevant population. |
D | Case series or uncontrolled study or expert opinion. |
Classification
Classification of GERD:
according to clinical forms:
· non-erosive reflux disease (NERD) (60-65% of cases);
· erosive (reflux esophagitis) (30-35% of cases);
Barrett's esophagus (5%).
to assess severity:
clinical criteria:
mild - heartburn less than 2 times a week;
· moderate - heartburn 2 times a week or more, but not daily;
· severe - heartburn daily.
endoscopic criteria:
Currently, the modified Savary-Miller classification or Los Angeles classification of esophagitis, 1994 is used. (Table 1).
Table 1. Modified classification of esophagitis according to Savary-Miller
Severity | Endoscopic picture |
I | One or more isolated oval or linear erosions are located on only one longitudinal fold of the esophageal mucosa. |
II | Multiple erosions that can merge and be located on more than one longitudinal fold, but not circularly. |
III | Erosions are located circularly (on the inflamed mucosa). |
IV | Chronic damage to the mucous membrane: one or more ulcers, one or more strictures and/or a short esophagus. Additionally, there may or may not be changes characteristic of grades I-III of esophagitis. |
V | It is characterized by the presence of a specialized columnar epithelium (Barrett esophagus), extending from the Z-line, of various shapes and lengths. Possible combination with any changes in the mucous membrane of the esophagus, characteristic of grades I-IV of esophagitis. |
Table 2. Classification of reflux - esophagitis (Los Angeles, 1994)
Degree esophagitis |
Endoscopic picture |
A | One (or more) mucosal lesion (erosion or ulceration) less than 5 mm in length, limited to a mucosal fold |
IN | One (or more) mucosal lesion (erosion or ulceration) more than 5 mm in length, limited to a mucosal fold |
WITH | Damage to the mucous membrane extends to 2 or more folds of the mucous membrane, but occupies less than 75% of the circumference of the esophagus |
D | Mucosal involvement extends to 75% or more of the circumference of the esophagus |
by disease phases:
· exacerbation;
· remission.
complications of GERD:
· peptic erosive-ulcerative esophagitis;
· peptic ulcer of the esophagus;
· peptic stricture of the esophagus;
· esophageal bleeding;
· posthemorrhagic anemia;
Barrett's esophagus;
· adenocarcinoma of the esophagus.
Barrett's esophagus classification:
by type of metaplasia:
Barrett's esophagus with gastric metaplasia;
· Barrett's esophagus with intestinal metaplasia;
by length:
· short segment (length of the metaplasia area less than 3 cm);
long segment (the length of the metaplasia area is 3 cm or more).
The diagnosis of GERD includes:
· clinical form of the disease;
· degree of severity (in the case of esophagitis - an indication of its degree and the date of the last endoscopic detection of an erosive and ulcerative lesion);
· clinical phase of the disease (exacerbation, remission);
· complications (in Barrett's esophagus - type of metaplasia, degree of dysplasia).
Diagnostics
METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT
Diagnostic criteria: collection of complaints according to Table 3.
Table 3. Clinical manifestations of GERD
Esophageal symptoms |
Extraesophageal symptoms |
. heartburn - a burning sensation of varying intensity behind the breastbone in the lower third of the esophagus and/or in the epigastric region; . belching sour after eating; . regurgitation of food (regurgitation); . dysphagia and odynophagia (pain when swallowing) unstable (with swelling of the mucous membrane of the lower third of the esophagus) or persistent (with the development of stricture); . pain behind the sternum (typically associated with food intake, body position and relief by taking antacids). |
· bronchopulmonary - attacks of coughing and/or suffocation, mainly at night, after a heavy meal; · otolaryngological: constant coughing, food getting “stuck” in the throat or a feeling of a “lump” in the throat, soreness and hoarseness, pain in the ear; · dental: erosion of tooth enamel, development of caries; Cardiovascular: arrhythmias. |
Table 4. Basic laboratory and instrumental studies
Instrumental studies | |
esophagogastroduodenoscopy | Reduced distance from the anterior incisors to the cardia, gaping or incomplete closure of the cardia, transcardial migration of the mucous membrane, gastroesophageal reflux, reflux esophagitis, the presence of a contractile ring, the presence of foci of ectopic epithelium - Barrett's esophagus |
esophagogastroduodenoscopy with biopsy of the mucous membrane of the esophagus if Barrett's esophagus is suspected with biopsy of the mucous membrane of the distal esophagus | Histological specimen shows signs of epithelial metaplasia of the gastric type |
X-ray examination method using barium | Swelling of the cardia and vault of the stomach, increased mobility of the abdominal esophagus, flattened or absent angle of His, antiperistaltic movements of the esophagus (dance of the pharynx), prolapse of the esophageal mucosa into the stomach, the presence of folds of the mucous membrane in the area of the esophageal opening and above the diaphragm, characteristic of the gastric mucosa, which directly pass into the folds of the subphrenic part of the stomach, the hernial part of the stomach forms a round or irregularly shaped protrusion, with smooth or jagged contours, widely communicating with the stomach. |
pH - esophageal measurement | The change in intraesophageal pH from neutral to acidic; by changes in the pH of different parts of the esophagus, it is possible to determine to what level the contents of the stomach rise in the vertical and horizontal position of the patient; therefore, by the degree of change in pH to the acidic side in the abdominal, retropericardial and aortic parts of the esophagus, the size of the gastrointestinal tract is determined. esophageal reflux |
Additional diagnostic tests:
· radiography of the esophagus and stomach with contrast - for dysphagia, suspected hiatal hernia (HH);
· blood test for tumor markers - if an oncological process is suspected;
· daily pH-metry for endoscopically negative esophagitis (UDE) - according to indications;
· electrocardiogram - to exclude myocardial infarction.
Indications for consultation with specialists:
· consultation with an oncologist - if Barrett's esophagus or tumor, esophageal stricture is detected;
· consultation with other narrow specialists - according to indications.
Diagnostic algorithm for GERD
Differential diagnosis
Differential diagnosis of GERD | ||||
Signs | GERD | IHD |
Bronchial asthma |
Relaxation of the diaphragm (Petit's disease) |
Anamnesis |
Long-term dispensary. observation for GERD; constant use of anti- secretory drugs |
Substernal pain without connection with eating or changing body position; follow-up with a cardiologist; pain is relieved by taking nitroglycerin. | Long-term follow-up for bronchial asthma; attacks of suffocation; constant use of bronchodilator therapy | Congenital pathology of muscle elements; various injuries of the diaphragm, which are accompanied by disruption of the nerve innervation of the diaphragm. |
Labora- tor data |
Lipid metabolism indicators (cholesterol, LDL) may be elevated. | The CBC may show slight eosinophilia, an increase in the number of neutrophils and a shift in the leukocyte count to the left. | As a rule, no special changes | |
ECG |
No special changes |
In myocardial infarction, changes in the ST segment. For lower localization, an ECG should be recorded on the right half of the chest in leads V3R or V4R. |
No special changes |
No special Changes |
EGDS |
Reduced distance from the anterior incisors to the cardia, the presence of a hernial cavity, the presence of a “second entrance” to the stomach, gaping or incomplete closure of the cardia, GER, reflux esophagitis, contractile. ring, foci of ectopic epithelium of Barrett's esophagus. |
Without features | Without features | Without features |
X-ray research tion |
Swelling of the cardia and vault of the stomach, increased mobility of the abdominal esophagus, flattened or absent His angle, antiperistaltic movements of the esophagus, prolapse of the esophagus into the stomach. | Without features | During the interictal period at the onset of the disease, there are no X-ray signs. In stages 1 and 2, in severe cases, pulmonary emphysema and cor pulmonale are detected. |
A decrease in the resistance of the thoraco-abdominal obstruction, as a result of which the OBP moves into the chest cavity. Alshevsky-Winbeck's symptom, Wellman's symptom. The lower pulmonary field is darkened. The heart shadow may be shifted to the right. |
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Treatment
Drugs (active ingredients) used in treatment
Treatment (outpatient clinic)
OUTPATIENT TREATMENT TACTICS:
Treatment tactics include non-drug methods and pharmacotherapy.
Non-drug treatment:
Non-drug treatment consists of following recommendations for changes in lifestyle and diet (anti-reflux measures), the implementation of which should be given particular importance in the treatment of GERD (Table 5).
Recommendations | Comments |
1.Sleep with the head end of the bed raised by at least 15 cm. . |
Reduces the duration of acidification of the esophagus. |
2. Dietary restrictions: - reduce fat content (cream, butter, fatty fish, pork, goose, duck, lamb, cakes); - increase protein content: - reduce the amount of food; - do not consume irritating foods (alcohol, citrus juices, tomatoes, coffee, chocolate, strong tea, onions, garlic, etc.). |
. fats reduce LES pressure; . proteins increase LES pressure; . the volume of gastric contents and reflux decreases; . direct damaging effect. . coffee, chocolate, alcohol, and tomatoes also reduce LES pressure. |
3. Lose weight if you are obese . |
Excess weight increases reflux. |
4. Do not eat before bed, do not lie down immediately after eating. | Reduces the volume of gastric contents in a horizontal position |
5. Do not wear tight clothes or tight belts. | |
6. Avoid deep bending, prolonged stay in a bent position (gardener’s pose), lifting weights of more than 5-10 kg, and physical exercises with overstrain of the abdominal muscles. | Increase intra-abdominal pressure, increase reflux |
7. Avoid taking medications: sedatives, hypnotics, tranquilizers, calcium antagonists, anticholinergics. | Reduce LES pressure and/or slow down peristalsis. |
8. Stop smoking. | Smoking significantly reduces LES pressure and reduces esophageal clearance. |
Drug treatment is carried out depending on the severity of GERD and includes the use of antisecretory, prokinetic and antacid drugs. The main pathogenetic drugs are antisecretory drugs (H2histamine receptor blockers and proton pump inhibitors). There is evidence of the effectiveness of prokinetics in the treatment of mild to moderate GERD. Antacids can be used as symptomatic medications, used “on demand”.
Treatment goals:
relief of clinical symptoms
· healing of erosions
· preventing or eliminating complications
· improving quality of life
· prevention of relapse.
Purpose antisecretory therapy is to reduce the aggression of acidic gastric contents on the mucous membrane of the esophagus with GERD. The choice and dosage regimens of antisecretory drugs depend on the course and severity of GERD.
Non-erosive form of GERD and esophagitis of classes I-II:
1st line drugs:
H2histamine receptor blockers (famotidine, ranitidine)
2nd line drugs:
If therapy is ineffective/intolerant, proton pump inhibitors (PPIs) are used
Erosive forms of GERD:
1st line drugs:
PPI (omeprazole, pantoprazole, esomeprazole, rabeprazole, lansoprazole)
2nd line drugs:
· blockers of H2 histamine receptors (famotidine, ranitidine), if necessary, used with drugs that affect the cytochrome P450 system (see Table 5).
PPIs are potent antisecretory drugs and should only be used when the diagnosis of GERD is objectively documented. Adjunctive therapy with H2 blockers, along with PPI use, has been reported to be beneficial in patients with severe GERD (especially patients with Barrett's esophagus) who have nocturnal acid breakthrough. Forms and releases, average doses and dosage regimens of antisecretory drugs are presented in Table 6.
The duration of use of antisecretory drugs for GERD depends on the stage of the disease:
Non-erosive forms of GERD - duration 3-4 weeks
Erosive forms of GERD:
Stage 1 - single erosions, duration 4 weeks
Stages 2-3 - multiple erosions lasting 8 weeks.
Meanwhile, in some cases longer use is required, incl. maintenance therapy. Taking into account the fairly long-term use of these groups of drugs, it is necessary to assess the risk/benefit and constantly re-evaluate their prescription, including dosage regimens.
When using antisecretory drugs, it is necessary to take into account that when using H2histamine receptor blockers possible development:
- pharmacological tolerance
- caution is required when engaging in potentially hazardous activities that require increased concentration and speed of psychomotor reactions, because Dizziness may occur, especially after taking the initial dose.
With an overall good safety profile IPP can:
- disrupt calcium homeostasis
- aggravate heart rhythm disturbances
- cause hypomagnesemia.
There is an association between hip fractures in postmenopausal women and long-term use of PPIs. Therefore, these groups of drugs are not recommended for use in elderly patients for more than 8 weeks. In a study conducted by the Agency for Healthcare Research and Quality (AHRQ), based on Class A evidence, PPIs were superior to H2 blockers for resolution of GERD symptoms at 4 weeks and healing of esophagitis at 8 weeks. Additionally, AHRQ found no difference between individual PPIs for symptom relief at 8 weeks.
The basic PPI is omeprazole, due to its good study and low cost. There is evidence of a faster onset of effect when using esomeprazole; pantoprazole, in accordance with the official instructions for use, has a lesser effect on the cytochrome P450 system, therefore it is safer when used in combination with drugs metabolized by this system.
When assessing the interaction of antisecretory drugs with other drugs, it is necessary to take into account that all PPIs are metabolized by the cytochrome P450 (CYP) system and there is a risk of metabolic interaction between PPIs and other substances whose metabolism is associated with this system (see Table 6). More detailed information is provided in the instructions for use and international drug databases.
Table 6. Threatening interactions of antisecretory drugs
№ | Medicine | Type of interaction | Changes in drug levels in the blood | Tactics |
1 |
Nelfinavir Atazanavir Rilpivirine Dasatinib Erlotinib Pazopanib KetoconazoleItraconazole |
Increasing the pH of gastric juice reduces absorption in the gastrointestinal tract | Decreased blood levels and decreased pharmacological effectiveness | Concomitant use with antisecretory drugs is not recommended. Occasional use of antacids is possible. |
2 | Clopidogrel | inhibitory effect of PPI on CYP2C19 and bioactivation of Clopidogrel | Decrease in the level of Clopidogrel in the blood and decrease in pharmacological activity |
Empiric use of PPIs should be avoided in patients receiving clopidogrel. PPIs should only be considered in high-risk patients (dual antiplatelet therapy, concomitant anticoagulant therapy, risk of bleeding) after careful assessment of risks and benefits. If PPI use is required, pantoprazole may be a safer alternative. Otherwise, H2 receptor antagonists or antacids should be prescribed if possible. |
3 | Methotrexate | PPI inhibition of active tubular secretion of MTX and 7-hydroxymethotrexate by renal H+/K+ ATPase pumps. | An increase in the level of Methotrexate in the blood and an increase in its toxic effect | PPI therapy should preferably be discontinued several days before methotrexate administration. In addition, the use of PPIs with high-dose methotrexate is generally not recommended, especially in the presence of renal impairment. If concomitant use of a PPI is necessary, clinicians should consider the possibility of an interaction and closely monitor methotrexate levels and toxicity. The use of H2 receptor blockers may also be a suitable alternative. |
4 | Citalopram | Interaction with the CYP450 2C19 system | The concentration of Citalopram in the blood increases and the risk of prolongation of the QT interval increases | Given the risk of dose-dependent QT prolongation, the dose of citalopram should not exceed 20 mg/day when administered in combination with a PPI. If necessary, alternative drugs should be prescribed. Hypokalemia or hypomagnesemia should be corrected before treatment with citalopram and monitored periodically. Patients should be advised to seek medical attention if they experience dizziness, palpitations, irregular heartbeat, shortness of breath, or fainting. |
5 |
Tacrolimus |
Interaction at the level of CYP3A and P-gp substrate). | Increased blood concentrations of Tacrolimus | It is recommended to monitor tacrolimus plasma concentrations when starting or ending combination treatment with PPIs. |
6 |
Fluvoxamine other CYP2C19 inhibitors |
Inhibits the CYP2C19 isoenzyme | Increased concentration of PPI in the blood | PPI dose reduction should be considered |
7 |
Rifampicin preparations of St. John's wort (Hypericumperforatum) Other inducers of CYP2C19 and CYP3A4 |
Induce isoenzymes CYP2C19 and CYP3A4 | Reduced concentration of PPI in the blood | Regular assessment of antisecretory effectiveness is necessary and the dose of PPI may be increased |
H2histamine receptor blockers do not affect the cytochrome P450 system and can be safely used in combination therapy with drugs whose metabolism is associated with this system. In addition, all antisecretory drugs, causing an increase in gastric pH, can reduce the absorption of vitamin B12.
The duration of use of antisecretory drugs is from 4 to 8 weeks, but in some cases longer use is necessary. In this regard, it is necessary to monitor patients and reassess the effectiveness and safety of treatment. Maintenance therapy is carried out in a standard or half dose on demand when heartburn occurs (on average, once every 3 days).
Goal of therapy prokinetics - increasing the tone of the lower esophageal sphincter, stimulating gastric emptying. Prokinetics may be used symptomatically in patients with severe nausea and vomiting. Due to pronounced side effects and numerous drug interactions, it is recommended to conduct a risk/benefit assessment when using prokinetics, especially in combination therapy, and their long-term use is not recommended, especially in elderly patients (high risk of extrapyramidal disorders, prolongation of the QT interval, genicomastia, etc.).
Antacids and alginates can be used as a means to relieve infrequent heartburn (prescribed 40-60 minutes after meals, when heartburn and chest pain most often occur, as well as at night), however, preference should be given to taking PPIs on demand.
Treatment effectiveness criterion- permanent relief of symptoms. In the absence of effect from the therapy, as well as in stage 4-5 GERD (identification of Barrett's esophagus with epithelial dysplasia), patients should be sent to institutions where highly specialized care is provided to gastroenterological patients.
If the patient has responded to therapy, it is recommended to follow a stepdown&stop strategy: reduce the dose of PPI by half and gradually continue to reduce the dose until drug therapy is stopped (the duration of the course is not strictly fixed). If clinical manifestations of reflux recur after drug treatment is discontinued, the doctor may recommend that the patient continue taking the drugs at the lowest effective dose (the duration of maintenance therapy is also not regulated).
Table 7. List of essential medications used for GERD
№ | INN | Release form | Dosage regimen | UD |
H2histamine receptor blockers | ||||
1 | Famotidine | Film-coated tablets (including film) 20 mg and 40 mg | Orally 20 mg 2 times a day | |
2 | Ranitidine | Film-coated tablets (including film) 150 mg and 300 mg | Orally 150 mg 2 times a day | |
Proton pump inhibitors | ||||
3 | Omeprozole | Capsules (including enteric, extended-release, gastrocapsules) 10 mg, 20 mg and 40 mg | A | |
4 | Lansoprazole |
Capsules (including modified release) 15 mg and 30 mg |
Orally 15 mg 1 time per day in the morning on an empty stomach. | A |
5 | Pantoprazole | Film-coated tablets (including enteric-soluble); delayed release 20 mg and 40 mg | Orally 20 mg 1 time per day in the morning on an empty stomach. | A |
6 | Rabeprazole | Enteric-coated tablets/capsules 10 mg and 20 mg | Orally 10 mg 1 time per day in the morning on an empty stomach. | A |
7 | Esomeprazole |
Tablets/Capsules (including enteric, solid, etc.) 20 mg and 40 mg |
Orally 20 mg 1 time per day in the morning on an empty stomach. | A |
Table 8. List of additional medications used for GERD
№ | INN | Release form | Dosage regimen | UD |
Prokinetics | ||||
1 | Metoclopramide |
Tablets 10 mg Solution for injection 0.5% 2 ml Solution for injection 10 mg/2 ml |
IN | |
2 | Domperidone |
Tablets (including dispersible, film-coated) 10 mg Drops, syrup, oral suspension |
With severe nausea and vomiting. Prescribe a single dose every 40-60 minutes. After meals, at night |
IN |
Itopride | Film-coated tablets 50 mg | Dose for adults: 50 mg (1 tablet) 3 times a day before meals. | WITH | |
Antacids | ||||
4 | Magnesium hydroxide and aluminum hydroxide |
Chewable tablets Oral suspension 15 ml |
Single dose on demand | A |
5 | Calcium carbonate + sodium bicarbonate + sodium alginate |
Chewable tablets Oral suspension |
Single dose on demand | A |
Treatment (inpatient)
TREATMENT TACTICS AT THE INPATIENT LEVEL
Non-drug treatment: see Table 5 outpatient level.
Goals, treatment tactics, other treatment methods, criteria for treatment effectiveness: see outpatient level.
Surgical intervention:
Surgical treatment of GERD is an equally effective alternative to medical treatment and should be offered to patients with indications (Grade A).
Indications:
With a more precise diagnosis of GERD, the indications for surgical treatment are:
· ineffective drug treatment (inadequate control of symptoms, severe regurgitation, uncontrolled acid suppression and side effects from medications);
· choice of patients despite successful drug treatment (for reasons of quality of life, which is affected by the need to take medications throughout life, the high cost of medications, etc.) (Grade A);
· presence of complications of GERD (for example, Barrett's esophagus, peptic strictures, etc.);
· presence of extraesophageal manifestations (bronchial asthma, hoarseness, cough, chest pain, aspiration).
Preoperative examination:
The purpose of preoperative evaluation is to select suitable patients with reflux for surgical treatment.
Approaches regarding the volume and order of preoperative studies:
· Endoscopy with biopsy - confirms the diagnosis of GERD, and also identifies other causes of disorders of the esophagogastric mucosa and allows taking a biopsy;
· pH-metry;
· esophageal manometry - often performed before surgery and allows you to identify conditions that may be contraindications to fundoplication (such as achalasia of the esophagus), or change the type of fundoplication, according to an individual approach based on esophageal motility;
· barium suspension study - for patients with a large hiatal hernia who have a shortened esophagus.
Patients undergoing laparoscopic antireflux surgery should be informed preoperatively of the possible incidence of symptom recurrence and return to acid-reducing medications (Grade A).
Detection of Barrett's esophagus with adenocarcinoma involving the submucosal layer or deeper excludes the patient from those planned for antireflux surgery and requires full oncologic therapy (esophagectomy, chemotherapy, and/or radiation therapy) appropriate to the stage of the process.
Preventive actions:
· antireflux measures;
· antisecretory therapy;
· mandatory maintenance therapy;
· dynamic observation of the patient for monitoring (endoscopic with biopsy if indicated) complications (detection of Barrett's esophagus).
Further management:
Dynamic monitoring of patients to monitor complications, identify Barrett's esophagus and drug control of symptoms. Intestinal epithelial metaplasia is the morphological substrate of Barrett's esophagus. Its risk factors: heartburn more than 2 times a week, duration of symptoms more than 5 years.
If a diagnosis of Barrett's esophagus is established, control endoscopic and histological studies should be performed to identify dysplasia and adenocarcinoma of the esophagus after 3, 6 months and then annually during maintenance therapy with PPIs. When dysplasia progresses to a high degree, the issue of surgical treatment (endoscopic or surgical) is decided in a specialized institution at the republican level.
Indicators of treatment effectiveness and safety of diagnostic and treatment methods:
· relief of clinical symptoms;
· healing of erosions;
· preventing or eliminating complications;
· improving the quality of life.
Hospitalization
INDICATIONS FOR HOSPITALIZATION (UDA)
Indications for emergency hospitalization:
· bleeding from esophageal ulcers;
· strictures of the esophagus.
Indications for planned hospitalization:
· ineffectiveness of drug treatment (inadequate control of symptoms, severe regurgitation, uncontrolled acid suppression and/or side effects of drug treatment);
· complications of GERD (Barrett's esophagus, peptic strictures);
· if there are extraesophageal manifestations (asthma, hoarseness, cough, chest pain, aspiration).
Information
Sources and literature
- Minutes of meetings of the Joint Commission on the Quality of Medical Services of the Ministry of Health of the Republic of Kazakhstan, 2017
- 1) Gastroenterology. National leadership / edited by V.T. Ivashkina, T.L. Lapina - M.GEOTAR-Media, 2012, - 480 p. 2) Diagnosis and treatment of acid-dependent Helicobacter-associated diseases. Ed. R.R. Bektaeva, R. T. Agzamova, Astana, 2005 – 80 p. 3) S. P. L. Travis. Gastroenterology: trans. from English / Ed. S.P.L. Travis et al. - M.: Med lit., 2002 - 640 p. 4) Manual of gastroenterology: diagnosis and therapy. Fourth edition. / CananAvunduk–4th ed., 2008 - 515 p. 5) Practical Manual of Gastroesophgeal Reflux Disease /Ed.by Marcelo F. Vela, Joel E. Richter and Jonh E. Pandolfino, 2013 –RC 815.7.M368 6) Prevention and treatment of chronic diseases of the upper gastrointestinal tract / edited by B .T.Ivashkina.-3rd ed., revised. and additional - MEDpress-inform, 2014.-176 p. 7) Dyspepsia and gastrooesophageal reflux disease: investigation and management of dyspepsia, suggestive symptoms of gastro-oesophageal reflux disease, or both Clinical guideline (update) Methods, evidence and recommendations September 2014 https://www.nice.org.uk/guidance /cg184/chapter/1-recommendations 2.Evidence-Based Gastroenterology and Hepatology, Third Edition John W. D. McDonald, Andrew K Burroughs, Brian G Feagan and M Brian Fennerty © 2010 Blackwell Publishing Ltd. ISBN: 978-1-405-18193-8 8) 8. Diagnosis of extraesophageal manifestations of gastroesophageal reflux disease / N.A. Kovaleva [et al.] // Ros.med. magazine – 2004. – No. 3. – P. 15-19. 9) Diagnosis and treatment of gastroesophageal reflux disease: a manual for doctors / V.T. Ivashkin [et al.]. – M., 2005. – 30 p. 10) The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus / N. Vakil // Am. J. Gastroenterol. – 2006. – Vol. 101. – P. 1900-2120. 11) Peterson W.L. Improving the Management of GERD. Evidence-based therapeutic strategies / W.L. Peterson; American Gastroenterological Association. – 2002. – Access mode: http://www.gastro.org/user-assets/documents/GERDmonograph.pdf. 12) Gastroesophageal reflux disease: educational method. allowance / I.V. Maev [etc.]; edited by I.V. Maeva. – M. : VUNMC MH RF, 2000. – 52 p. 13) L I Aruin V A Isakov. Gastroesophageal reflux disease and Helicobacter pylori. Klin medicine 2000 No. 10 C 62 - 68. 14) V T Ivashkin A S Trukhmanov Diseases of the esophagus Pathological physiology clinic diagnostics treatment. M: “Triad - X” 2000 178 p. 15) Kononov A V Gastroesophageal reflux disease: a morphologist’s view of the problem. Ros Journal of Gastroenterology, Hepatology and Coloproctology 2004.- T 14 No. 1 P 71 - 77. 16) Maev I V, E S Vyuchnova E G Lebedeva Gastroesophageal reflux disease: educational manual. M: VUNMTsMZRF 2000 52 p. 17) C.A. Fallone, A.N. Barkun, G. Friedman. Is Helicobacter pylori eradication associated with gastroesophageal reflux disease? Am. J. Gastroenterol. 2000. Vol. 95. P. 914 – 920. 18) Bordin D.S. A new approach to increasing the effectiveness of proton pump inhibitors in a patient with gastroesophageal reflux disease. Attending doctor. 2015.- No. 2. pp. 17-22. 19) 19. Lazebnik L.B., Bordin D.S., Masharova A.A. and others. Factors influencing the effectiveness of treatment of GERD with proton pump inhibitors // Ter.arkhiv.- 2012.- 2: 16-21. 20) www.drugs.com Database on medicines, supported by the FDA (USA) 21) Instructions for the use of medicines from the database of the National Center for the Expertise of Medicines and Medical Medical Sciences of the Republic of Kazakhstan (www.dari.kz) 22) Gastroesophageal Reflux Disease Treatment & Management (www.http://emedicine.medscape.com/article/176595-treatment?src=refgatesrc1#d11) 23) Gastroesophageal reflux disease (GERD) / University of Michigan Health System (UMHS) and the National Guideline Clearinghouse (NGC) / Agency Healthcare Research and Qlity (AHRQ) / USA 24) O'Mahony D., O'Sullivan D., Byrne S. et. al. STOPP/START criteria for potentially inappropriate prescribing in older people: version 2 // Age and Ageing. 2014. DOI: 10.1093/ageing/afu145. 25) Körner T1, Schütze K, van Leendert RJ, Fumagalli I, Costa Neves B, Bohuschke M, Gatz G. / Comparable efficacy of pantoprazole and omeprazole in patients with moderate to severe reflux esophagitis. Results of a multinational study / Digestion. 2003;67(1-2):6-13.
Information
ORGANIZATIONAL ASPECTS OF THE PROTOCOL
List of protocol developers with qualification information:
1) Roza Rakhimovna Bektaeva - Doctor of Medical Sciences, Professor, Head of the Department of Gastroenterology and Infectious Diseases, Astana Medical University. Chairman of the National Association of Gastroenterologists of the Republic of Kazakhstan.
2) Iskakov Baurzhan Samikovich - Doctor of Medical Sciences, Professor, Head of the Department of Internal Medicine No. 2 with courses in related disciplines of the Kazakh National Medical University named after S.D. Asfendiyarov, chief freelance gastroenterologist of the Almaty Health Department, Deputy Chairman of the National Association of Gastroenterologists of the Republic of Kazakhstan.
3) Makalkina Larisa Gennadievna - Candidate of Medical Sciences, Associate Professor of the Department of Clinical Pharmacology, Internship of JSC "Astana Medical University", Astana.
Disclosure of no conflict of interest: No.
Reviewers:
1) Shipulin Vadim Petrovich - Doctor of Medical Sciences, Professor, Head of the Department of Internal Medicine No. 1 of the A.A. Bogomolets National Medical University. Ukraine. Kyiv.
2) Bekmurzaeva Elmira Kuanyshevna - Doctor of Medical Sciences, Professor, Head of the Department of Bachelor's Therapy of the South Kazakhstan Pharmaceutical Academy. The Republic of Kazakhstan. Shymkent.
Conditions for reviewing the protocol: revision of the protocol 5 years after its publication from the date of its entry into force or in the presence of new diagnostic and treatment methods with a level of evidence.
Annex 1
ALGORITHM FOR DIAGNOSIS AND TREATMENT AT THE STAGE OF EMERGENCY MEDICAL AID:
Diagnosis and treatment at the emergency stage:
· collection of complaints, medical history and life history;
· physical examination.
Diagnostic criteria (EL - D):
Complaints and anamnesis:
Complaints:
· heartburn (persistent, painful) both after eating and on an empty stomach;
· pain in the chest (burning) that intensifies with physical activity and bending over;
· feeling of discomfort in the chest area;
· weight loss;
· decreased appetite;
· cough and asthma attacks at night;
hoarseness in the morning;
· vomiting blood.
Anamnesis:
· constant use of acid-reducing drugs and antacids;
· the patient may have Barrett's esophagus.
Attached files
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Gastroesophageal reflux pathology (disease), or GERD for short, is not only one of the most common chronic diseases of the gastrointestinal tract, but is also accompanied by a large number of symptoms. Very often, the symptoms of GERD are mistaken for independent diseases, since they are diverse in nature and are practically indistinguishable from the symptoms of other diseases.
Common symptoms of gastroesophageal reflux disease
- The most common symptom of this disease is a burning sensation behind the breastbone, called heartburn. Heartburn with gerb usually occurs an hour and a half after eating or at night during sleep. This unpleasant sensation can migrate up to the epigastric region, and radiate to the cervical and interscapular region. The feeling of discomfort increases after physical activity, excessive eating, drinking carbonated drinks, coffee.
- An unpleasant phenomenon caused by the entry of food or liquid that has already entered the stomach back - directly into the esophagus through the lower esophageal sphincter, and then into the oral cavity. This is a burp. It causes an unpleasant taste of sour and stale food in the mouth. As a rule, belching occurs in a horizontal position of the torso, or in an inclined position.
- Chest pain, and/or a feeling of difficulty swallowing food and even liquids. The pain can be irradial in nature - painful sensations (disconnected from the center of the lesion) in various areas: in the interscapular region, in the lower jaw, in the cervical region, in the left half of the chest.
IMPORTANT! The listed manifestations and signs of GERD most often accompany the further development of complications of the disease: narrowing of the esophagus or tumor formation, which is explained by the constant inflammatory process in the area of damage to the mucous membrane of the esophagus. The longer the inflammation, the more serious the manifestations and the more often the symptoms occur.
- Vomiting of esophageal origin is also a symptom of gastroesophageal reflux disease caused by the development of further complications. Therefore, vomit is undigested food and liquids consumed immediately before the onset of vomiting.
- Hiccups are caused by a phenomenon called irritation of the phrenic nerve, which is caused by repeated and long-term contraction of the diaphragm. This is also considered a common symptom accompanying GERD.
- Non-esophageal signs of GERD with pulmonary symptoms (causeless cough, shortness of breath without mechanical and physical exertion), with otolaryngological signs (hoarseness, a feeling of dryness in the larynx, cough with gerb), as well as manifestations associated with gastric sensations (rapid satiety, bloating, nausea, vomiting).
Features of GERD symptoms
Doctors always warn patients with gastroesophageal reflux pathology that this disease is characterized by deterioration and intensification, an increase in all manifestations when taking a horizontal position, in an inclined state, with increased mechanical loads, heavy lifting, rapid movement, and physical exercise. All symptoms can be reduced by drinking alkaline liquids and milk.
Some patients experience non-esophageal symptoms of reflux disease - painful sensations in the chest, which they often mistake for symptoms of heart disease (the so-called acute coronary syndrome).
In cases where stomach contents return to the larynx, especially at night, during sleep, people experience symptoms of gastroesophageal reflux disease such as a dry cough, sore throat, and hoarseness when waking up. If the return of stomach contents occurs to the trachea and/or bronchi, then one must be wary of the occurrence of obstructive bronchitis and even aspiration pneumonia.
It is necessary to understand that signs of gastroesophageal reflux can occur under certain circumstances in absolutely healthy people. In such cases, reflux is not characterized by the development of pathological phenomena in the mucous membrane of the esophagus and other organs of the gastrointestinal tract. However, one should not be indifferent to the occurrence of these symptoms, especially if they appear more than 2 times a week for 1-2 months.
In these situations, it is mandatory to contact a specialist who will prescribe an appropriate examination and diagnosis of GERD.
Any extra-esophageal manifestations of this disease are directly dependent on the height of penetration of duodenal contents and/or food from the stomach into the esophagus and/or into the respiratory tract, as well as on the strength and frequency of spasms (contractions) of smooth muscles, which is created reflexively after reflux.
Given the similarity of symptoms between GERD and other diseases, it is necessary to clearly distinguish between them. And a detailed description of each frequent manifestation of gastroesophageal reflux disease by the patient himself significantly helps in establishing the correct diagnosis.
Heartburn as a symptom of GERD
Every person has experienced a burning sensation in the stomach and upper chest at least once. And the established diagnosis of “reflux disease” does not change the symptoms - the burning sensation spreads upward from the epigastric region. This very unpleasant phenomenon can last for seconds or 2-3 hours. May spontaneously disappear and reappear. The appearance of this sensation is explained by irritation of the mucous membrane and nerve endings on the inner walls of the esophagus by the contents of the stomach, which already contains enzymes, hydrochloric acid and components of the bile mass.
Signs associated with heartburn
Not only, in fact, heartburn with GERD causes unpleasant painful sensations, but also the accompanying phenomena, which are similar in their mechanism of action.
- When the diaphragm contracts, gases from the gastric sector and/or esophagus often enter the oral cavity. This causes an airy burp.
- Regurgitation is a type of belching, but food that has not yet been processed by gastric juices, with a bitter/sour aftertaste.
- Feeling of a “coma” in the throat with gerb.
- Nausea and/or vomiting.
- Profuse drooling.
- Burning pain radiating to the retrosternal region from the epigastric region, to the left side of the chest, to the cervical area and interscapular region.
- Swallowing dysfunction.
- Frequent coughing (trying to cough - cough with gerb).
- Hoarse voice, hoarseness.
There are many reasons for the occurrence of heartburn, but most often its appearance indicates the presence of gastroesophageal reflux disease (especially with frequently recurring attacks, with heartburn for a long time).
Heartburn is caused by several causes that accompany GERD:
- decreased tone of the esophageal sphincters: a muscular structure resembling a valve in its functioning mechanism, separating the lower esophageal section from the stomach (upper sphincter), as well as a valve located between the pharynx and the esophageal tract (lower sphincter).
- weakening of the esophageal function responsible for transporting food - the esophagus loses its ability to promptly eliminate contents abandoned from the stomach (sour or bitter).
- increased function of the stomach, responsible for the formation of acid (hyperacidity).
Heartburn is caused not only by GERD, but also by other diseases. For example, this phenomenon accompanies such pathological conditions as:
- complicated pathology of an oncological nature - Barrett's disease;
- esophagitis of various etiologies - infectious or allergic inflammation of the esophagus, inflammation of a medicinal and traumatic nature;
- spasm of the esophagus (esophagospasm);
- hiatal hernia in the diaphragm;
- dyspepsia (dysfunction of the motor mechanisms of the stomach);
- peptic ulcer.
In these cases, the symptoms of heartburn are only clinical signs of disease, and it is very important to promptly recognize the nature of the disease that caused this phenomenon. This is why correct diagnosis of GERD is so necessary.
Any type of heartburn, including that caused by GERD, can be provoked and aggravated by various factors that reduce the tone of the esophageal sphincters.
- bending over after eating;
- drinking alcohol;
- large meals;
- eating fatty, sour, salty and spicy foods;
- overexertion caused by physical activity, heavy lifting, fast walking (especially increased load on the abdominal muscles);
- lying down immediately after eating;
- taking certain types of medications (nitrates, etc.);
- wearing tight clothing (especially in the gastrointestinal tract);
- obesity;
- excessive smoking;
- pregnancy;
- sudden stress.
Substernal pain
Unpleasant pain behind the sternum is a common symptom of reflux disease. It is often confused with signs of pathologies of the cardiovascular system. Although, most often, this type of pain is associated with dysfunction of the esophagus and the upper (cardiac) gastric region.
If such sensations appear, you must immediately consult a doctor for examination and diagnosis - not only the gastrointestinal tract, but also the cardiovascular system, in order to determine GERD by symptoms and tests.
Esophagitis, caused by the process of gastroesophageal reflux, usually causes patients to experience a burning sensation deep in the chest area. The phenomenon intensifies when taking aspirin and aspirin-containing medications, when consuming alcohol and certain types of foods. To alleviate the condition, sometimes taking a small amount of food or a few sips of water is enough.
Associated manifestations are also typical: gastric reflux disease, the symptoms of which are described above, dysphagia, and sudden weight loss.
Extraesophageal (extraesophageal, non-esophageal) manifestations of GERD
Symptoms of an oropharyngeal nature among the signs of GERD consist of a series of manifestations:
- inflammation of the nasopharyngeal system and sublingual tonsil;
- formation of erosions on tooth enamel;
- stomatitis and/or caries;
- periodontitis and pharyngitis;
- a “lump”-type sensation in the throat (not only when swallowing, but also at rest).
In addition, signs of an otolaryngological nature manifest themselves in the form of hoarseness and hoarseness, dry cough with attempts to cough, laryngitis, laryngeal croup (rarely), the appearance of ulcers, the formation of granulomas and polyps on the vocal folds, stenosis of the larynx in the area located under the glottis, as well as otalgia of unknown etiology (ear pain) and rhinitis.
The listed symptoms of GERD appear with the development of gastroesophageal reflux, and are caused by direct damage to the trachea and larynx area by hydrochloric acid, contained in the stomach in already processed contents, thrown back into the area of the retrosternal sector and larynx. Damage to the mucous membrane, especially aggravated by smoking, can develop into a chronic stage and lead to cancer of the larynx.
Symptoms of a bronchopulmonary nature, caused by reflux (thrust) of gastric masses into the bronchial sector, are expressed by pathological conditions:
- chronic bronchitis, sometimes with the appearance of bronchiectasis;
- pneumonia, including aspiration;
- abscess;
- hemoptysis, with manifestations of atelectasis (collapse) of the lungs or one lung, its lobe;
- retention (gaps) of breathing at night during sleep (pathology - apnea);
- coughing attacks with the development of bronchial asthma;
- vomiting with gerb.
Respiratory pathologies, which are symptoms associated with the penetration of gastric masses into the bronchial tract, are especially dangerous for children. They are manifested by stridor breathing (a whistling sound when breathing, which is accompanied by noise), pneumonia, sudden suffocation, often sleep apnea, the appearance of asthma and cyanosis. In newborns, such manifestations are dangerous due to sudden death syndrome.
Reflux-induced bronchial asthma
Pain and tenderness in the chest area, which doctors associate with diseases of the cardiovascular system. However, reflux of gastric contents into the esophageal system provokes similar symptoms - reflex angina and initial myocardial ischemia. The painful sensations of GREB symptoms are often accompanied by arrhythmia and a sharp increase in blood pressure.
Painful sensations in the thoracic region, unrelated to heart pathology, are a fairly common complication of reflux disease. These symptoms of GERD are often mistaken for ischemic disease and pathology of the cardiovascular system, which, unlike the manifestations of uncomplicated types of GERD, is a direct threat to life.
IMPORTANT!!! If such symptoms appear, it is necessary to immediately perform a differential diagnosis - an ECG with stress tests, coronary angiography, which is a radiopaque, accurate and reliable method of research that allows you to determine not only the nature and site of narrowing of the artery, but also to distinguish the signs from the symptoms of GERD.
There are other extraesophageal signs, to which doctors include permanent bad breath - halitosis, gastroparesis, pain in the back area not identified by diagnostic methods, which imitates pathological diseases of the spine. Moreover, the symptoms of gerb in adults differ from the manifestations of this pathology in children.
Be sure to pay attention to the appearance of the symptoms described below.
Bloating
Such an unpleasant phenomenon as bloating is a feeling of fullness in the abdominal area, which patients often describe as a feeling similar to an artificial sensation of increasing the volume of the abdomen, or tightening it with tight clothing or a belt.
However, we must not forget that it is not only gastric reflux disease that causes such symptoms. In healthy people, the feeling of swelling and “stretching” of the abdomen occurs for various reasons:
- Swallowing excessive amounts of air when eating quickly;
- Excessive passion for carbonated waters;
- Frequently taking baking soda for heartburn symptoms;
- Excessive consumption of foods rich in fermentable carbohydrates, or starch and fiber.
Nausea
A very unpleasant pulling sensation in the epigastric region, in the chest, an uncomfortable feeling in the mouth, often causing vomiting, accompanying symptoms in the form of weakness, excessive sweating, increased salivation (hypersalivation), a feeling of cooling of the extremities, decreased blood pressure and expressed by abnormal pallor of the face - this is nausea.
VomitingA
Vomiting, as a sign of GERD, is a process that occurs reflexively, caused by the involuntary ejection of the contents of the esophagus into the pharynx or oral cavity, which occurs due to the increased function of peristalsis of the lower gastric sections, relaxation of the upper zones and mucous membrane of the esophagus with involuntary contraction of the muscles of the diaphragm and abdominal wall .
Despite the fact that gastroesophageal reflux pathology is distinguished by its traditional manifestations and signs, the most common of which is heartburn, we must not forget that in parallel there are numerous extra-esophageal symptoms of GERD. And doctors can mistakenly diagnose their patients with such diagnoses as bronchial asthma, heart pathologies, etc.
Gastroesophageal reflux (K21), Gastroesophageal reflux without esophagitis (K21.9), Gastroesophageal reflux with esophagitis (K21.0)
Gastroenterology
general information
Short description
Purpose of publication
To acquaint practicing physicians with the latest data on methods of adequate diagnosis, treatment tactics and features of rational pharmacotherapy for gastroesophageal reflux disease (GERD), based on the principles of evidence-based medicine.
Basic provisions
In terms of prevalence, GERD ranks first among gastroenterological diseases. The leading symptom of GERD - heartburn - is detected in 20-40% of the population of developed countries. In Russia, the prevalence of GERD is 18-46%. Diagnosis of GERD in the early stages is based on initial consultation and analysis of the clinical picture of the disease. Esophagogastroduodenoscopy (EGD) makes it possible to determine the presence of reflux esophagitis, assess the degree of its severity, and identify columnar cell metaplasia of the esophageal epithelium. In case of refractory course of the disease (lack of convincing clinical and endoscopic remission within 4-8 weeks of therapy with a proton pump inhibitor - PPI - at a standard dose), as well as the presence of complications of the disease (strictures, Barrett's esophagus), it is necessary to conduct an examination in a specialized hospital or gastroenterological clinics, including in the outpatient departments of these institutions. If necessary, patients should undergo endoscopy with a biopsy of the esophageal wall and histological examination of biopsy specimens to exclude Barrett's esophagus, adenocarcinoma and eosinophilic esophagitis; intraesophageal daily pH-metry or pH-impedansometry; high-resolution esophageal manometry; X-ray examination of the esophagus and stomach.
Treatment of patients with GERD should be individualized according to the clinical manifestations of the disease and the severity of symptoms. The goal of treatment is to eliminate symptoms, for erosive esophagitis - to heal erosions and prevent complications, for Barrett's esophagus - to prevent the progression and development of dysplasia and adenocarcinoma of the esophagus.
Today, PPIs are considered the most effective and safe drugs for the treatment of GERD. PPIs are used for long-term primary (at least 4-8 weeks) and maintenance (6-12 months) therapy. A pathogenetically substantiated therapeutic method for reducing the “acid pocket” and neutralizing acid in the area of the esophagogastric junction in patients with GERD is to take alginates, which form a mechanical raft barrier that prevents the reflux of stomach contents into the esophagus. Antacids are used both as monotherapy for rare heartburn, which is not accompanied by the development of esophagitis, and in complex treatment regimens for GERD to quickly eliminate symptoms. Adsorbents are used both as monotherapy for non-erosive reflux disease and as part of complex therapy for GERD, especially for mixed (acid + bile) reflux. Prokinetic drugs help restore the normal physiological state of the esophagus by affecting the pathogenetic mechanisms of GERD, reducing the number of transient relaxations of the lower esophageal sphincter and improving esophageal clearance due to stimulation of the motor function of the underlying parts of the digestive tract. Prokinetics can be used as part of complex therapy for GERD along with PPIs.
Antireflux surgical treatment is indicated for complicated course of the disease (repeated bleeding, peptic strictures of the esophagus, development of Barrett's esophagus with high-grade epithelial dysplasia, frequent aspiration pneumonia). Surgical treatment of GERD is more effective in patients with its typical manifestations and when PPI treatment is effective.
Conclusion
Compliance with clinical recommendations can help improve the quality of medical care for patients with GERD and the prevention of complications, in particular, if the necessary treatment periods are observed and active outpatient monitoring of the relevant groups of patients is carried out.
Keywords: gastroesophageal reflux disease, gastroesophageal reflux, reflux esophagitis, non-erosive reflux disease, acid pocket, proton pump inhibitor, alginate, angtacid, prokinetic drug.
Introduction
Over the 3 years since the release of clinical guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD), new data have been obtained on effective methods for diagnosing and treating patients with this disease, and therefore it became necessary to publish this version of the guidelines.
The problem of GERD is still very relevant. In terms of prevalence, GERD ranks first among gastroenterological diseases. Heartburn, the leading symptom of GERD, is observed in 20-40% of the population of developed countries. In Russia, the prevalence of GERD is 18-46% [Ivashkin V.T., Maev I.V., Trukhmanov A.S., 2011]. The relevance of GERD is also due to the fact that it leads to a significant decrease in the patient’s quality of life, especially with nocturnal symptoms, the appearance of extraesophageal symptoms (chest pain, persistent cough) and the risk of complications such as bleeding from ulcers and erosions, the development of peptic strictures and, What causes the greatest concern is esophageal adenocarcinoma (AEC) against the background of Barrett's esophagus. Certain difficulties arise when treating patients with GERD. If the healing time for duodenal ulcers (DU) is on average 3-4 weeks, for gastric ulcers - 4-6 weeks, then the healing time for esophageal erosions in many patients can reach 8-12 weeks. At the same time, some patients are refractory to antisecretory drugs and have low adherence to treatment. After stopping medication, a relapse of the disease quickly occurs, which is the main risk factor for the development of Barrett's esophagus, a precancerous pathology of the esophagus.
Target These recommendations are a presentation of the latest reliable data on methods of adequate diagnosis, treatment tactics and features of rational pharmacotherapy for GERD, based on the principles of evidence-based medicine.
Definition
GERD- a chronic relapsing disease caused by a violation of the motor-evacuation function of the organs of the gastroesophageal zone and characterized by regularly repeated reflux of stomach contents into the esophagus, and sometimes duodenum, which leads to the appearance of clinical symptoms that worsen the quality of life of patients, damage to the mucous membrane (MS) of the distal esophagus with the development of dystrophic changes in non-keratinizing stratified squamous epithelium, catarrhal or erosive-ulcerative esophagitis (reflux esophagitis), and in some patients - columnar cell metaplasia.
Nonerosive reflux disease(NERD) and erosive esophagitis should be considered as two forms of GERD. NERD is a subcategory of GERD characterized by the presence of symptoms caused by reflux and reducing quality of life without erosions of the esophagus, detected during routine endoscopic examination, in the absence of antisecretory therapy at the moment. The diagnosis of NERD can be confirmed by the results of tests with proton pump inhibitors (PPIs), detection of pathological reflux by pH-metry or specific endoscopic signs of esophagitis when conducting studies using high-tech methods (high-resolution magnification, narrow-spectrum endoscopy).
NERD should be differentiated from functional heartburn, in which there is no pathological gastroesophageal reflux. In patients with functional heartburn, who form a small heterogeneous group, the mechanisms of symptom development are different. Drug tests using antisecretory drugs cannot be considered specific, but their negative result demonstrates a high probability of the absence of GERD.
Barrett's esophagus is the replacement of squamous epithelium with glandular columnar metaplasia in the mucosa of the distal esophagus, detected by endoscopic examination and confirmed by the presence of intestinal metaplasia during histological examination of the biopsy specimen, in some cases increasing the risk of developing ACP.
Coding according to ICD-10
K21 Gastroesophageal reflux
K21.0 Gastroesophageal reflux with esophagitis (reflux esophagitis)
K21.9 Gastroesophageal reflux without esophagitis
K22.1 Esophageal ulcer
Etiology and pathogenesis
Main factors of pathogenesis
GERD is an acid-dependent disease in which hydrochloric acid of gastric juice is the main damaging factor in the development of clinical symptoms and morphological manifestations of GERD. Pathological reflux occurs due to insufficiency of the lower esophageal sphincter (LES), i.e. GERD is a disease with an initial impairment of the motor function of the upper gastrointestinal tract.
A key factor in the pathogenesis of GERD is the pathologically high frequency and/or duration of episodes of reflux of stomach contents into the esophagus. The integrity of the mucous membrane of the esophagus is determined by the balance between aggressive factors and the ability of the mucous membrane to withstand the damaging effects of the stomach contents refluxed during gastroesophageal reflux (GER). Disruption of this balance in a large proportion of patients is accompanied by a significant slowdown in the recovery of pH in the distal esophagus after each episode of reflux. Clearance of the esophagus is impaired due to the influence of several factors: weakened peristalsis of the thoracic esophagus, decreased secretion of saliva and mucin.
The first barrier that provides a cytoprotective effect is the mucus layer covering the epithelium of the esophagus and containing mucin. The mucous layer is one of the key components of the chemical clearance of the esophagus and the restoration of the pH in it to normal levels, the violation of which contributes to the deterioration of the cleansing of the esophagus from acidic, slightly acidic or slightly alkaline stomach contents that have entered it. The secretion of mucins in mucus in GERD decreases depending on the severity of esophagitis, which is an additional factor predisposing to the development of erosive esophagitis in the context of ongoing GER, therefore, an additional increase in the protective properties of the mucous barrier, along with acid suppression, is an important component of the treatment of GERD (UDL 3, UUR B) .
With a significant increase in the secretion of hydrochloric acid in the stomach, the risk of GERD significantly increases.
In the vast majority of patients with GERD, episodes of reflux occur primarily during transient relaxations of the lower esophageal sphincter (LES), when the antireflux barrier between the stomach and esophagus usually disappears within 10-15 s, regardless of the act of swallowing. PRNPS, the principal mechanism of reflux, in patients with GERD occurs through the same pathways from the dorsal nucleus of the vagus (nucleus dorsalis and nucleus ambiguus) that mediate esophageal peristalsis and PRNPS in a healthy person. Mechanoreceptors located in the upper part of the stomach respond to increased pressure inside the organ and send signals to the hindbrain along the afferent fibers of the vagus nerve. In the centers of the hindbrain that perceive these signals, motor programs of the PRNPS are formed, reaching the LES along descending pathways. The efferent pathways are via the vagus nerve, where nitric oxide is a postganglionic neurotransmitter. Contraction of the crura of the diaphragm is controlled by the respiratory center located in the brain stem and the nucleus of the phrenic nerve. With an increase in intra-abdominal pressure, if it coincides with PRNPS, the likelihood of acid reflux significantly increases.
Currently, in understanding the mechanism of GER, one should be guided by the paradigm of the mutual influence of PRNPS and the consequences of destructuring of the esophagogastric junction zone. Weakness of the legs of the diaphragm leads to either a delay in the onset of action or to a significant degradation of the actual compressive effect of diaphragm contraction on the LES. A hiatal hernia (HHH), depending on its size and structure, has a mechanical effect on the LES: it worsens the anti-reflux function during PRNPS and/or reduces the actual tonic component of the sphincter. The most important consequence of the destructuring of the esophagogastric junction zone is the reflux of relatively large volumes of liquid gastric contents into the esophagus during the period of PRNPS.
In a significant number of patients, episodes of GER develop with normal LES pressure levels. The mechanism of GER is associated with a high pressure gradient between the stomach and esophagus, due to various reasons: in some patients - impaired evacuation of gastric contents, in others - high intra-abdominal pressure. In these cases, GER develops due to the inability of the obturator mechanisms to counteract the high pressure gradient between the stomach and esophagus.
In addition, after eating, a layer of acid (average pH 1.6) called an “acid pocket” is formed on the surface of the stomach contents in the area of the esophagogastric junction, which is formed in both healthy people and patients with GERD. This is an area in the stomach cavity and/or area of the esophagogastric junction, formed after eating, which is characterized by relatively high acidity and is a reservoir of acidic contents thrown into the esophagus during GER.
The risk of developing acidic GER is determined by the position of the “acid pocket” relative to the diaphragm. Moving it above the level of the diaphragm leads to the development of pathological acid reflux not only in the postprandial period. This suggests that the acid pocket may be a promising target for the treatment of GERD, especially when it comes to reducing the severity of postprandial heartburn. (UDD 1, UUR A).
Thus, from a pathophysiological point of view, GERD is an acid-dependent disease that develops against the background of a primary disorder of the motor function of the upper digestive tract. In the pathogenesis of NERD, features of the esophageal mucosa play a special role.
Epidemiology
The prevalence of GERD among adults is up to 40%. The results of extensive epidemiological studies indicate that 40% of people constantly (with varying frequency) experience heartburn, which is the main symptom of GERD. In Russia, the prevalence of GERD among the adult population is 18-46%, and esophagitis is found in 45-80% of patients with GERD. In the general population, the prevalence of esophagitis is estimated at 5-6%, while 65-90% of patients have mild and moderate esophagitis, and 10-35% have severe esophagitis. The incidence of severe esophagitis in the general population is 5 cases per 100,000 population per year. The prevalence of Barrett's esophagus among patients with esophagitis approaches 8%, ranging from 5 to 30%.
In recent decades, there has been an increase in the incidence of ACP, which develops against the background of the progression of dysplastic changes in the intestinal-type metaplastic epithelium of the mucosa of the distal esophagus. ACP and high-grade dysplasia develop annually in 0.4-0.6% of patients with Barrett's esophagus with intestinal metaplasia. ACP is formed annually in 0.5% of patients with a low degree of epithelial dysplasia, in 6% with a high degree and in less than 0.1% in the absence of dysplasia.
Clinical picture
Symptoms, course
Clinical picture
Esophageal manifestations
The most widely used in the world is the Montreal classification of clinical manifestations of GERD, in which they are divided into two large groups: esophageal and extraesophageal. Esophageal manifestations include such clinical syndromes as the typical symptom complex of reflux and non-cardiac chest pain, as well as syndromes in which, in addition to patient complaints, endoscopic signs of the disease are noted (esophagitis, Barrett's esophagus, strictures, etc.).
A typical symptom complex of reflux includes heartburn, belching, regurgitation, odynophagia, which are painful for patients, significantly worsen their quality of life, and have a negative impact on performance. The quality of life of patients with GERD, in whom its clinical symptoms occur at night, is especially significantly reduced.
Heartburn, the most characteristic symptom observed in 83% of patients, occurs due to prolonged contact of stomach contents with CO. This symptom is characterized by an increase in its severity with errors in diet, intake of alcohol and carbonated drinks, physical stress, bending over and in a horizontal position.
Belching, one of the leading symptoms of GERD, occurs in 52% of patients with GERD. As a rule, it intensifies after eating and drinking carbonated drinks. The regurgitation observed in some patients with GERD is exacerbated by physical exertion and body positioning that promotes regurgitation.
Dysphagia and odynophagia are observed in 19% of patients with GERD. Their occurrence is based on hypermotor dyskinesia of the esophagus, and the cause of odynophagia can also be erosive and ulcerative lesions of the esophagus. The appearance of more persistent dysphagia and a simultaneous decrease in the severity of heartburn may indicate the formation of esophageal stenosis, both benign and malignant.
Non-cardiac pain in the chest and along the esophagus can give the impression of coronary pain - the so-called symptom of “non-cardiac chest pain”. These pains are relieved by nitrates, but unlike angina pectoris, they are not associated with physical activity. They arise as a result of hypermotor dyskinesia of the esophagus (secondary esophagospasm), which may be caused by a defect in the inhibitory transmitter system - nitric oxide. The trigger point for the occurrence of esophagospasm and, accordingly, pain is pathological gastroesophageal reflux.
Extraesophageal manifestations
Extraesophageal manifestations of GERD include bronchopulmonary, otorhinolaryngological and dental syndromes.
The variety of symptoms and syndromes are divided into two groups: those whose connection with GERD is based on fairly convincing clinical evidence (chronic cough associated with reflux, chronic laryngitis, bronchial asthma and erosion of tooth enamel), and those whose connection with GERD is only assumed ( pharyngitis, sinusitis, pulmonary fibrosis, otitis media).
Numerous studies have shown an increased risk of developing bronchial asthma, as well as an increase in the severity of its course in patients with GERD. In 30-90% of patients with bronchial asthma, GER occurs, causing a predisposition to its more severe course. The reasons for the development of bronchial obstruction in GERD are the vago-vagal reflex and microaspiration. In such cases, when PPIs are included in complex therapy, the effectiveness of treatment of bronchial asthma increases.
A sore throat, hoarseness or even loss of voice, and a dry cough may be a consequence of the reflux of stomach contents into the larynx (otolaryngological syndrome). This possibility should be considered if the patient has heartburn. In the absence of heartburn, the only method to verify the connection of such symptoms with GER is 24-hour intraesophageal pH-metry/pH-impedancemetry (see below), which can be used to establish a correlation between the onset of a symptom and episodes of reflux (symptom index > 50 %).
Dental syndrome is manifested by dental damage due to damage to tooth enamel by aggressive stomach contents. Patients with GERD may develop caries and dental erosions. In rare cases, aphthous stomatitis develops.
Inflammatory changes in the mucous membrane of the esophagus (complications of GERD)
Reflux esophagitis, detected by endoscopic examination, includes simple (catarrhal) esophagitis, erosions and ulcers of the esophagus. The severity of erosive esophagitis can be different - from stage A to stage D according to the Los Angeles classification and from stages 1 to 3 according to the Savary-Miller classification - depending on the area of the lesion, while by the 4th stages according to the Savary-Miller classification include complications of GERD: esophageal strictures, ulcers (bleeding from ulcers), Barrett's esophagus.
To eliminate the stricture in the future, expensive surgical and endoscopic (often repeated) procedures (bougienage, surgery, etc.) are required. Each such case should be considered as a consequence of inadequate conservative therapy, which justifies the need for its improvement to prevent the development of strictures. Bleeding caused by erosive and ulcerative lesions of the esophagus can be observed both in the presence of esophageal varices and in their absence.
The most severe complication of GERD, Barrett's esophagus, is the development of columnar (intestinal) metaplastic epithelium in the esophageal mucosa, which subsequently increases the risk of developing PCA. When exposed to hydrochloric and bile acids in the esophagus, on the one hand, the activity of protein kinases that initiate the mitogenic activity of cells and, accordingly, their proliferation increases, on the other hand, apoptosis in the affected areas of the esophagus is inhibited.
In approximately 95% of cases, ACP is diagnosed in patients with Barrett's esophagus, so the diagnosis and effective treatment of Barrett's esophagus play a major role in the prevention and early diagnosis of esophageal cancer. After the use of PPIs in patients with Barrett's esophagus, there is a decrease in the level of proliferation markers, which is absent in those patients who have persistent pathological acid reflux (pH<4,0). Длительное применение ИПП может привести к частичной регрессии цилиндрической метаплазии на ограниченном участке.
Among the risk factors for the development of complications of GERD, the most important are the frequency of occurrence and duration of symptoms, in particular heartburn, the severity of erosive esophagitis, the frequency of its relapses, obesity, the presence of a hiatal hernia and nocturnal reflux.
Rapidly progressive dysphagia and weight loss may indicate the development of ACP, but these symptoms occur only in the later stages of the disease, so the clinical diagnosis of esophageal cancer is usually delayed. As a result, prevention and early diagnosis of esophageal cancer require timely detection and adequate treatment of Barrett's esophagus.
Diagnostics
STAGE DIAGNOSTICS
OUTPATIENT STAGE
Diagnosis of GERD in the early stages is based on initial consultation and analysis of the clinical picture of the disease. If necessary, additional research is carried out.
Endoscopic examination
In patients who complain of heartburn, endoscopic examination may show signs of reflux esophagitis of varying severity. These include hyperemia and looseness of the esophagus (catarrhal esophagitis), erosions and ulcers (erosive esophagitis of varying severity - from stage 1/A to stage 4/D - depending on the area of the lesion), the presence of exudate, fibrin or signs of bleeding.
To assess changes in esophageal mucosa during reflux esophagitis, many classifications have been proposed, but the most widely used are the classification created by M. Savary and G. Miller (1978) and the classification developed by the International Working Group of Experts, which was first proposed at the World Congress of Gastroenterology in Los Angeles in 1994.
According to the Savary-Miller classification, there are 4 stages of reflux esophagitis:
Stage 1 - diffuse or focal hyperemia of the mucosa of the distal esophagus, individual non-confluent erosions with a yellowish base and red edges, linear aphthous erosions spreading upward from the cardia or esophageal opening of the diaphragm;
Stage 2 - erosions merge, but do not cover the entire CO surface;
Stage 3 - inflammatory and erosive changes merge and cover the entire circumference of the esophagus;
Stage 4 - similar to the previous stage, but there are complications: narrowing of the lumen of the esophagus, as a result of which it is difficult or impossible to pass the endoscope into the underlying sections, ulcers, Barrett's esophagus.
The Los Angeles classification provides a four-degree gradation of reflux esophagitis, it is also based on the prevalence of the process, but complications of GERD (strictures, ulcers, Barrett's esophagus), which can occur at any stage, are considered separately:
stage A - one (or more) area of damaged CO up to 5 mm in size, which does not capture CO between the folds (located at the top of the fold);
stage B - one (or more) area of damaged CO larger than 5 mm in size, which does not capture CO between the folds (located at the top of the fold);
stage C - one (or more) area of damaged esophagus, which extends to the esophagus between two (or more) folds, but covers less than 75% of the circumference of the esophagus;
stage D - one (or more) area of damaged esophagus, which covers more than 75% of the circumference of the esophagus.
In addition, there may be prolapse of the gastric mucosa into the esophagus, especially with gagging movements, true shortening of the esophagus with the location of the esophagogastric junction significantly above the diaphragm, reflux of the contents of the stomach or duodenum into the esophagus. It is difficult to assess the closure function of the cardia during esophagoscopy, since the cardia can be slightly opened reflexively in response to the insertion of an endoscope and air insufflation.
STATIONARY STAGE
In case of refractory course of the disease (absence of convincing signs of clinical and endoscopic remission within 4-8 weeks of PPI therapy at a standard dose), as well as in the presence of complications of the disease (strictures, Barrett's esophagus), it is necessary to conduct an examination in a specialized hospital or gastroenterology clinic, in including in the outpatient departments of these institutions. If necessary, patients should undergo:
Esophagogastroduodenoscopy (EGD) with esophageal biopsy and histological examination of biopsy samples to exclude Barrett's esophagus and ACP, as well as eosinophilic esophagitis;
Intraesophageal daily pH-metry or pH-impedansometry;
High resolution esophageal manometry;
X-ray examination of the esophagus and stomach;
Complex ultrasound examination (ultrasound) of internal organs;
Registration of an electrocardiogram and other special studies (see below).
Before performing probe studies (EGD, pH-metry), it is necessary to examine the blood for hepatitis, HIV infection, and syphilis. According to indications (differential diagnosis of extraesophageal manifestations of GERD), specialists should be consulted: otolaryngologist, pulmonologist, cardiologist.
Histological examination
Histological examination of biopsy samples of the esophagus is carried out to exclude Barrett's esophagus, ACP, eosinophilic esophagitis, and dystrophic, necrotic, acute and chronic inflammatory changes expressed to varying degrees are revealed. With simple (catarrhal) esophagitis, the layer of non-keratinizing stratified epithelium may have normal thickness. More often, its atrophy is detected, but occasionally areas of hyperplasia are also found, in particular the basal layer, which occupies up to 10-15% of the thickness of the epithelial layer. Characterized by varying degrees of intercellular edema, degeneration and foci of necrosis of epithelial cells (keratinocytes), especially in the superficial layers. The basement membrane of the epithelium is not changed in most cases, but in some patients it may be thickened and sclerotic. As a result of necrosis of different areas of the multilayered squamous epithelium, erosions are formed (erosive esophagitis), and with deeper lesions, up to the muscular layer and even deeper, ulcers (ulcerative esophagitis).
Along with dystrophic-necrotic changes in the epithelium in the mucus, microcirculation disorders with vascular hyperemia are noted. Characterized by an increase in the number and change in the length of vascular-stromal papillae. In the thickness of the epithelium and subepithelial layer, focal (usually perivascular) and in some places diffuse lymphoplasma cell infiltrates with an admixture of neutrophilic leukocytes and single eosinophils are detected. The appearance of intraepithelial neutrophilic leukocytes and their accumulation in the inflammatory infiltrate in the vascular-stromal papillae and in the lamina propria indicate the exacerbation and progression of the inflammatory process.
A significant increase in the number of eosinophilic leukocytes and, even more so, the presence of intraepithelial eosinophilic-cellular microabscesses in combination with subepithelial sclerosis of the lamina propria serve as criteria for the diagnosis of eosinophilic esophagitis. Smooth muscle cells of the lamina propria show signs of severe dystrophy or atrophy, and in rare cases, a state of coagulative necrosis.
Inflammatory, necrotic or hyperplastic changes can also extend to the esophageal glands. In a small number of patients, signs of active inflammation are not detected during histological examination. At the same time, in the esophagus there is a proliferation of loose, and in places dense fibrous connective tissue (sclerosis), as in the bottom of persistent erosions and ulcers.
Histological examination may reveal metaplasia of the stratified squamous non-keratinizing epithelium of the esophagus, which leads to the appearance in its place of columnar (glandular) epithelium with glands of the cardiac or fundic (gastric) type. Cardiac type OM usually has a villous surface, often characterized by small pitted depressions without properly formed glands (foveolar type), although the latter can be fully formed (glandular type), but are always represented only by mucous cells and do not contain parietal, chief or goblet cells. Fundal (gastric) type OM is distinguished by the presence of acid-producing parietal and chief cells in the glands, and typical ridges covered with integumentary pitted epithelium are sometimes formed from the integumentary epithelium. In this case, the glands are often few in number, “compressed” by proliferations of connective tissue and a diffuse lymphoplasma cell infiltrate with an admixture of neutrophilic leukocytes.
With metaplasia of the esophagus of the cardiac, cardiac acid-producing or fundic type, the risk of developing ACP does not increase. However, if metaplasia leads to the appearance of the so-called specialized epithelium, as in a number of sources the glandular epithelium of the intestinal type is called, the risk of malignancy increases. Specialized epithelium is intestinal metaplasia of the glandular epithelium, and its main criterion is
histological diagnosis - the appearance of goblet cells (at least one such cell within the biopsy, since the changes are mosaic in nature).
The morphological substrate of NERD can be considered expansion (edema) of intercellular spaces, especially in the basal layer of the epithelium, and dystrophic changes in keratinocytes.
High resolution manometry
The study of motor function of the esophagus is carried out using high-resolution manometry. In case of GERD, it is used to detect a decrease in the pressure of the LES, the presence of a hiatal hernia, an increase in the number of PRNS, quantitative indicators of the total peristaltic activity of the organ wall, esophagospasm, atypical cases of achalasia cardia, and diagnose rumination and supragastric belching syndromes. The study allows you to verify the position of the LES for pH measurement. It is a necessary attribute of the patient examination, which is carried out to decide on the surgical treatment of GERD. When analyzing the results of high-resolution manometry, the Chicago Classification of Esophageal Motility Disorders (UDD 1, UUR A) should be used.
pH-metry
The main method for diagnosing GER is pH-metry. The study can be carried out both on an outpatient basis and in an inpatient setting. When diagnosing GER, the results of pH-metry are assessed by the total time during which the pH is maintained<4,0, общему количеству рефлюксов за сутки, количеству рефлюксов продолжительностью более 5 мин, наибольшей длительности рефлюкса.
Main indications for pH testing:
Characteristic manifestations of GERD in the absence of endoscopic changes in the esophagus;
Extraesophageal manifestations of GERD: chest pain not associated with diseases of the cardiovascular system;
Planned surgical treatment of GERD and monitoring the effectiveness of treatment if symptoms of the disease persist;
Selection of medications and monitoring the effectiveness of conservative treatment.
Daily pH-metry has a very high sensitivity (88-95%) in the diagnosis of GERD and, in addition, helps in the individual selection of medications (UDL 1, UUR A).
pH-impedancemetry
Esophageal impedancemetry is a method for recording liquid and gas reflux, based on measuring the resistance (impedance) that the stomach contents provide to the electric current entering the lumen of the esophagus. This is a diagnostic technique for refractory GERD, which makes it possible to determine episodes of reflux into the esophagus, regardless of the pH value of the refluxate, as well as the physical state (gas, liquid) and clearance of the bolus that entered the esophagus during
reflux.
Main indications for pH impedance testing:
Atypical forms and extraesophageal manifestations of GERD: chronic cough, bronchial asthma, chronic pharyngitis, severe belching;
Evaluation of the effectiveness of antisecretory therapy for GERD without discontinuation of the drug in the presence of persistent symptoms of the disease;
Evaluation of the effectiveness of surgical treatment of GERD (UDL 1, UUR A).
X-ray examination
X-ray examination of the esophagus is not used to diagnose GERD, but it can detect hiatal hernia, diffuse esophagospasm, esophageal strictures and suspect a short esophagus in those patients for whom surgical treatment is planned.
Other diagnostic methods
In highly specialized institutions, methods such as measuring the impedance of the esophagus, determining the pepsin content in saliva, and impedance planimetry can be used in the diagnosis of GERD.
The introduction of high-resolution endoscopy, NBI endoscopy, ZOOM endoscopy (magnifying endoscopy) helps to detect metaplastic changes in the esophageal epithelium and perform a targeted biopsy to obtain material for histological examination.
Endoscopic ultrasound of the esophagus is the main method for identifying endophytically growing tumors.
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Treatment
Conservative treatment
Treatment of patients with GERD should be individualized and oriented in accordance with the clinical manifestations of the disease and their severity. The goal of treatment is to eliminate symptoms, and in case of erosive esophagitis, to heal erosions and prevent complications. In patients with Barrett's esophagus, the goal is to prevent the progression and development of dysplasia and PCA.
Treatment should be aimed at reducing the severity of reflux, reducing the aggressive properties of refluxate, improving esophageal clearance and protecting the esophageal mucus. Currently, the main principles of treatment for GERD are the prescription of PPIs and long-term primary (at least 4-8 weeks) and maintenance (6-12 months) therapy. If these conditions are not met, the likelihood of relapse of the disease is very high. Studies conducted in many countries around the world have shown that more than 80% of patients who do not receive adequate supportive treatment develop a relapse within the next 26 weeks, and the probability of relapse within a year is 90-98%. It follows from this that maintenance treatment is necessary.
Lifestyle changes should be considered a prerequisite for effective antireflux treatment in patients with GERD. First of all, it is necessary to reduce body weight, if it is excessive, and stop smoking. Patients should avoid overeating and stop eating 2 hours before bedtime. At the same time, you should not increase the number of meals: you must eat 3-4 meals a day and give up so-called snacks. Recommendations for frequent split meals are unfounded.
It is important to avoid as much as possible situations that contribute to an increase in intra-abdominal pressure (wearing tight belts, corsets and bandages, lifting weights of more than 8-10 kg on both arms, work involving bending the body forward, physical exercises associated with overstraining the abdominal muscles). Patients who experience heartburn or regurgitation when lying down should elevate the head of the bed.
Dietary recommendations should be strictly individualized, taking into account the results of a thorough analysis of the patient's medical history. You should avoid eating tomatoes in any form, sour fruit juices, products that increase gas formation, fatty foods, chocolate, coffee. It is necessary to limit the consumption of alcohol, very hot and cold foods, and carbonated drinks as much as possible.
Patients should be warned about the side effects of drugs that reduce the tone of the LES (nitrates, calcium ion antagonists of the nifedipine group, theophylline, progesterone, antidepressants), and those that themselves can cause inflammation (non-steroidal anti-inflammatory drugs, doxycycline, quinidine).
Drug treatment includes well-known groups of drugs.
Alginates
A pathogenetically substantiated therapeutic method for reducing the “acid pocket” and neutralizing acid in the area of the esophagogastric junction in patients with GERD is to take alginates, which form a mechanical raft barrier that prevents the reflux of stomach contents into the esophagus. By creating a protective barrier on the surface of the gastric contents, these drugs are able to significantly and long-term (more than 4.5 hours) reduce the amount of both pathological acidic GER and weakly alkaline duodenogastroesophageal reflux (DGER), thereby creating optimal physiological conditions for esophageal reflux. . In addition, alginates have a cytoprotective and sorption effect. The pharmacological compatibility of alginates with antisecretory drugs in the treatment of GERD has been proven. Alginates are taken 10 ml 3-4 times a day 30-40 minutes after meals and 1 time at night until the symptoms of the disease are persistently relieved, and then in the “on demand” mode (UDL 1, UUR A).
Antacids
Antacids (aluminum phosphate 2.08 g, combination preparations - aluminum hydroxide 3.5 g and magnesium hydroxide 4.0 g in the form of a suspension, aluminum hydroxide 400 mg and magnesium hydroxide 400 mg, as well as calcium carbonate 680 mg and magnesium hydroxycarbonate 80 mg in tablet form) is used to eliminate moderate and rarely occurring symptoms, especially those associated with non-compliance with the recommended lifestyle (LOD 1, LQR A).
Antacids can be used both as monotherapy for rare heartburn that is not accompanied by the development of esophagitis, and in complex treatment regimens for GERD, as they are effective in quickly eliminating symptoms. Antacids should be taken depending on the severity of symptoms, usually 1.5-2 hours after meals and at night. There is insufficient data to indicate the possibility of their continued use (UDD 2, UUR B).
Adsorbents(dioctahedral smectite) have a complex effect: firstly, they neutralize the hydrochloric acid of gastric juice, and secondly, they give a pronounced adsorbing effect, binding the components of the contents of the duodenum (bile acids, lysolecithin) and pepsin. Thus, dioctahedral smectite increases the resistance of esophageal mucus to the damaging effects of refluxate. Adsorbents can be used both as monotherapy for clinical manifestations of NERD, and as part of complex therapy for GERD, especially for mixed (acid + bile) reflux. Dioctahedral smectite is prescribed 1 sachet (3 g) 3 times a day (UDD 1, UUR A).
Prokinetics contribute to the restoration of the physiological state of the esophagus, affecting the pathogenetic mechanisms of GERD, reducing the number of PRNPS and improving esophageal clearance by stimulating the motor function of the underlying parts of the digestive tract. Prokinetics can be used as part of complex therapy for GERD together with PPIs. The prokinetic drug itopride hydrochloride (50 mg 3 times a day) is a means of pathogenetic treatment of GERD, since it normalizes the motor function of the upper digestive tract (UDL 1, UUR A).
In the presence of both esophageal and extraesophageal manifestations of GERD, they are effective PPI - drugs, suppressing the activity of the enzyme H+, K+-ATPase, located on the apical membrane of the parietal cell and carrying out the last stage of the synthesis of hydrochloric acid. PPIs are considered the most effective and safe drugs for the treatment of GERD. In clinical studies, PPIs have consistently demonstrated the greatest effectiveness in the treatment of erosive esophagitis and relief of GERD-associated symptoms (LOG 1, UUR A).
A decrease in acid production is considered the main factor promoting the healing of erosive and ulcerative lesions. In the presence of single erosions of the esophagus (A/1st stage of esophagitis), the likelihood of their healing within 4 weeks of treatment is high, so the duration of the main course in this case can be 4 weeks using a standard dose of PPI: rabeprazole 20 mg per day (LOD 1 , UUR A), or omeprazole 20 mg 2 times a day, or dexlansoprazole 60 mg per day (UDL 1, UUR A), or pantoprazole 40 mg per day, or esomeprazole 40 mg per day, preferably with a control endoscopic examination.
If multiple erosions of the esophagus (B-C/2-4 stages of esophagitis), as well as complications of GERD are detected, the duration of treatment with any drug from the PPI group should be at least 8 weeks, since in this case an effectiveness of 90-95% can be achieved .
If the course of treatment for multiple esophageal erosions is unreasonably shortened to 4 weeks, the rate of their healing is significantly lower. In addition, such an unjustified reduction in the duration of treatment for erosive forms of GERD may cause rapid subsequent recurrence, as well as the development of complications. For patients with typical reflux symptoms who do not respond adequately to PPI therapy at a standard once-daily dose, twice-daily PPI therapy may be recommended. It should be borne in mind that this dosage is not approved in the instructions for use of these drugs. The duration of maintenance therapy after healing of erosions should be at least 16-24 weeks. If complications of GERD occur, maintenance therapy should be carried out with PPI also in full dose (LOD 1, UUR A).
PPIs effectively control the pH in the lower third of the esophagus, so symptoms quickly decrease and disappear in patients with both erosive esophagitis and NERD. In the absence of esophageal erosions, for the treatment of NERD, a PPI can be prescribed at half the dose, including rabeprazole at a dose of 10 mg once a day during a course of treatment and on-demand administration, which is pharmacoeconomically justified (UDL 1, UUR A), and also dexlansoprazole 30 mg once a day (UDL 1, UUR A).
When treating patients with GERD, it is recommended to use an individual approach to the prescription of antisecretory therapy and the choice of drug, based on a thorough analysis of the clinical picture and results of endoscopy. First of all, the patient’s complaints are analyzed, in particular about heartburn (in addition to heartburn, other proven symptoms of GERD can be taken into account). The criteria for assessing complaints are the frequency of their occurrence: rarely (1-2 times a week) and often (more than 2 times a week), as well as the duration of existence: short (less than 6 months) and significant (more than 6 months). When assessing the patient’s status and medical history, male gender and age over 50 years are taken into account as risk factors for relapse, indications of the presence of erosive esophagitis during endoscopy in the past, and the stage of previously existing erosive esophagitis is of significant importance. When assessing the patient's status, you should also pay attention to the presence of overweight (BMI>25), obesity (BMI>30) and hiatal hernia. It is necessary to exclude the presence of “anxiety symptoms” (dysphagia, weight loss, anemia).
It is necessary to take into account the characteristics of individual antisecretory drugs. Thus, H2-receptor blockers should not be used as first-line therapy due to their significantly lower effectiveness compared to PPIs.
Due to the high dissociation constant pKa, rabeprazole can quickly accumulate in a large number of parietal cells and lead to rapid and pronounced inhibition of acid secretion, binding the proton pump, which ensures a high speed of action and a persistent antisecretory effect after 1 day of taking the drug. The pharmacokinetic properties of rabeprazole determine the effective relief of daytime and control of nighttime heartburn from the 1st day of therapy, a high rate of healing of esophageal erosions and the maintenance of long-term remission of GERD, including when using the drug in an “on demand” mode (UDL 1, UUR A).
Dexlansoprazole is the only modified-release PPI. Its capsule contains two types of granules that release the active substance depending on the pH in different parts of the small intestine: release begins in its upper part 1-2 hours after taking the drug and continues in the distal part after 4-5 hours. Double delayed release of the active substance allows you to prolong its action and helps reduce the secretion of hydrochloric acid over a long period of time. Prolonging the effect of dexlansoprazole provides effective control of nocturnal symptoms of GERD (LOI 1, LUR A).
In general, PPIs have a low incidence of side effects (less than 2%), which may include diarrhea, headache, and nausea. Rabeprazole is characterized by a high level of safety in terms of the frequency of side effects and tolerability, and its metabolism is minimally dependent on the cytochrome P450 system (UDL 1, URL A). When prescribing PPIs in large doses for a long period, the possibility of developing side effects such as osteoporosis (although the use of PPIs should not be considered as an independent and independent risk factor for the development of osteoporosis), bacterial overgrowth, Clostridium dificile infection and pneumonia, in patients from risk groups, primarily over 65 years of age. For long-term treatment, PPIs can be used on an on-demand basis and in intermittent courses.
The decision on the duration of maintenance therapy for GERD must be made individually, taking into account the stage of esophagitis, existing complications, the patient's age, and the cost and safety of PPI treatment. In case of GERD, there is no need to determine the H. pylori infection, much less its eradication, however, the presence of H. pylori infection should be established and its eradication carried out when prescribing PPI therapy for a long period.
It has not been proven that treatment with PPIs can lead to a decrease in the effectiveness of clopidogrel when used together.
It must be especially emphasized that symptomatic improvement with PPI therapy can also be observed in other diseases, including gastric malignancies, so it is necessary to exclude such diseases.
The highest percentage of effective treatment of exacerbations of GERD and maintenance of remission is achieved with the combined use of PPIs, prokinetics, alginates/antacids/adsorbents. To quickly relieve heartburn in patients with GERD, as well as in patients who periodically experience reflux symptoms during PPI therapy, it may be recommended to take alginic acid preparations, while the pharmacokinetic properties of PPIs do not deteriorate and they do not affect the rate of formation and effectiveness protective alginate barrier (UDD 1, UUR A).
When treating GERD in pregnant women, individual selection of therapy is necessary, taking into account the potential harm. Recommendations for lifestyle changes and rules for taking alginate-containing drugs if clinically necessary and after consultation with a doctor can be considered universal. Due to proven high efficiency and safety in all trimesters of pregnancy, alginates are the drugs of choice for the treatment of heartburn in pregnant women (UDL 1, UUR A). Since these drugs have almost no side effects, they can be recommended not only to pregnant women, but also to nursing women and practically healthy individuals with occasional heartburn.
In complicated forms of GERD, it is possible to carry out short courses of therapy using forms of PPI for intravenous administration, the advantages of which are the rapid achievement of an antisecretory effect and a higher concentration of the drug in the blood.
As noted earlier, GERD is usually characterized by a chronic, relapsing course. Patients whose clinical symptoms of the disease are not accompanied by the development of esophagitis need to take drugs in the “pro re nata” mode - “on demand”. However, in patients with erosive-ulcerative esophagitis with this maintenance therapy regimen there is a high (80-90%) risk of developing a relapse of the disease within a year. The likelihood of relapses increases in cases of resistance of the initial stages of esophagitis to therapy with antisecretory drugs, as well as when low LES pressure is detected.
Patients with GERD should be under active clinical observation with control examinations, which are carried out at least once a year (Appendix No. 1). If complications occur, such patients must be examined 2 times a year, including endoscopic and morphological examination.
The term “refractory GERD” is used in the case of incomplete healing of the esophageal mucosa and/or persistence of typical symptoms of GERD after a full course (4-8 weeks) of PPI treatment at a standard (once daily) dose.
The most common reason for a decrease in the effectiveness of therapy is insufficient adherence of patients to treatment, i.e., their failure to comply with recommendations for lifestyle changes and rules for taking PPIs. For representatives of this group of drugs, an increase in activity is indicated when taken in the morning 30 minutes before meals. It should be borne in mind that, according to the instructions for use of rabeprazole, neither the time of day nor food intake affects its activity.
Compliance (or non-compliance) with the recommendations prescribed by the doctor is influenced primarily by the presence and severity of symptoms, knowledge of the basics of the pathogenesis of the disease, concomitant therapy, the taste and consistency of the drug taken, side effects, age, socio-economic status, and motivation of the patient. Of course, following the doctor’s recommendations, including those regarding diet and normalizing body weight, should be considered the basis for successful treatment. The reasons for the ineffectiveness of therapy are also often the incorrect prescription of PPIs, non-compliance with their dosage and timing of therapy.
A risk factor for the development of refractory GERD is the genetic polymorphism of CYP2C19. The risk of developing refractory to PPI therapy is higher in CYP2C19 extensive metabolizers than in poor metabolizers. Genetic polymorphism of CYP2C19 influences the pharmacokinetics and pharmacodynamics of PPIs, causing differences in the severity of their antisecretory action and clinical effectiveness in GERD, with pronounced interindividual and interethnic differences. In the European population, there is a high prevalence of genetic polymorphism CYP2C19 with a predominance of rapid metabolizers - more than 70%. At the same time, fast metabolizers have a lower rate of healing of esophageal mucus erosions and a higher rate of recurrence of GERD during therapy, due to faster clearance, low plasma concentrations and a possible insufficient antisecretory effect due to the peculiarities of PPI metabolism.
Currently, another type of metabolizer is identified for the CYP2C19 isoenzyme, called “ultrafast”, which can often occur in the European population. In metabolizers of this type, the metabolism of drugs broken down by the CYP2C19 isoenzyme occurs especially quickly, which must be taken into account when assessing their effectiveness.
A PPI dosing regimen based on CYP2C19 genotype may be a therapeutic strategy to overcome insufficient gastric acid inhibition in patients with refractory GERD. Rabeprazole has been proposed as a PPI that is least affected by the CYP2C19 genotype, since it is metabolized primarily as a result of a non-enzymatic process. (UDD 2, UUR B). When treating some of these patients, it is necessary to use antisecretory drugs in high doses, which should be verified using 24-hour pH-metry.
The timing of taking some PPIs is important because it has a significant impact on their effectiveness. Thus, after taking omeprazole and lansoprazole before breakfast, it is much easier to control the level of gastric pH than after taking them without subsequent food intake. Dexlansoprazole can be taken at any time of the day, regardless of meals (UDL 2, UUR B).
The reasons for the ineffectiveness of hydrochloric acid secretion inhibitors may be the presence of weakly acidic reflux, as well as the predominance of duodenal contents in the refluxate with a predominantly alkaline environment, when heartburn and other symptoms of GERD arise as a result of the action of bile components and pancreatic enzymes on the esophageal mucus. Reflux is predominantly acidic in nature in 50% of patients with GERD, acidic in nature with a bile component in 39.7%, and bile reflux occurs in 10.3% of patients. Components of the contents of the duodenum that cause damage to the esophageal mucus are bile acids, lysolecithin and trypsin. The effect of bile acids, which apparently play a major role in the pathogenesis of damage to the esophageal mucus in DGER, has been most well studied.
In case of mixed reflux (acid with bile component), the clinical effect of PPI is due not only to the suppression of acid production itself, but also to a decrease in the total volume of gastric secretion, which leads to a decrease in the volume of refluxate. However, increasing PPI doses to relieve symptoms in this case is not indicated.
If DGER occurs, the following drugs can be prescribed in various combinations (including with PPIs): adsorbents, alginates, antacids, prokinetics, ursodeoxycholic acid. For mixed/biliary reflux, adsorbents (dioctahedral smectite) are used not only to neutralize hydrochloric acid, but also to adsorb bile acids and lysolecithin, as well as increase the resistance of CO to the action of damaging aggressive factors.
The secretion of mucins in mucus in GERD decreases depending on the severity of esophagitis, which is an additional factor predisposing to the development of erosive esophagitis in the context of ongoing GER. The dual mechanism of action of rabeprazole - acid suppression along with cytoprotective properties: stimulation of the secretion of mucins and an increase in their concentration in the esophageal mucus - is its additional advantages in the treatment of GERD (LOG 4, URL C).
If treatment of patients with GERD within 4 weeks is ineffective, the presence of GER should be confirmed using an objective research method - 24-hour pH impedancemetry. In patients with persistent symptoms, in whom pathological reflux is not detected when performing pH impedance measurements and there is no correlation of reflux with the onset of symptoms, most likely, there is not GERD, but so-called “functional heartburn”.
Surgery
Antireflux surgical treatment is considered indicated for complicated course of the disease (repeated bleeding, peptic stricture of the esophagus, development of Barrett's esophagus with high-grade epithelial dysplasia, proven by two morphologists, frequent aspiration pneumonia). In some cases, if the patient, for one or another objective or subjective reason, cannot undergo conservative therapy for GERD, surgical treatment should be considered for its uncomplicated course. Surgery may be more effective in those patients with GERD who have typical disease manifestations and who are also effectively treated with PPIs. If PPI is ineffective, as well as in the presence of extraesophageal manifestations, surgical treatment will be less effective.
The issue of surgical treatment should be considered together with a surgeon experienced in this field if all measures to normalize lifestyle have been completed, the presence of pathological gastroesophageal reflux has been proven using pH impedance measurements, and the absence of pronounced disturbances in peristalsis of the thoracic esophagus has been proven using manometry.
Management of patients with Barrett's esophagus
The need for active clinical monitoring of patients with Barrett's esophagus is due to the fact that in the case of early diagnosis of epithelial dysplasia, the development of PCA can be prevented. Verification of the diagnosis of Barrett's esophagus and determination of the degree of dysplasia is carried out using histological examination. If low-grade dysplasia is detected, it is necessary to prescribe a PPI and repeat histological examination after 3 months. If low-grade dysplasia persists, patients are recommended to continue taking PPIs continuously at full dose and undergo histological examination after 3 and 6 months, then histological examination is performed annually. If high-grade dysplasia is detected, it is necessary to prescribe a PPI in a double dose with a parallel assessment of the results of histological examination and subsequent decision on the method of treating the patient - endoscopic or surgical. More detailed algorithms for the management of patients with Barrett's esophagus are presented in special clinical guidelines.
Conclusion
These clinical recommendations are intended for general practitioners, general practitioners (family doctors), gastroenterologists, surgeons, endoscopists, health care managers, and medical workers with secondary medical education.
Conservative treatment of patients with GERD can be carried out on an outpatient basis with the participation of a gastroenterologist. Inpatient treatment is carried out in a day or round-the-clock hospital setting in specialized gastroenterological and therapeutic departments in the presence of specialized gastroenterological beds and a specialist who has undergone professional retraining in the specialty “gastroenterology”.
Compliance with clinical recommendations can have a positive impact on the quality of medical care for patients with GERD and the prevention of complications, in particular, if the necessary treatment periods are observed and active outpatient monitoring of the relevant groups of patients is carried out. The authors hope that this manual will help practicing doctors and health care managers in realizing these goals.
Information
Sources and literature
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Short-term treatment with proton pump inhibitors, H2-receptor antagonists and prokinetics for gastrooesophageal reflux disease-like symptoms and endoscopy negative reflux disease. Cochrane Database Syst Rev 2013; 5:CD002095. 105. Robinson M., Horn J. et al. Clinical Pharmacology of Proton Pump Inhibitors. What the Practicing Physycian needs to know. Drug 2003; 63(24):2739-54. 106. Besancon M., Simon A., Sachs G. et al. Sites of reaction of the gastric H, K-ATPase with extracytoplasmic thiol reagents. J Biol Chem 1997; 272:22438-46. 107. Kromer W. Relative efficacies of gastric proton-pump inhibitors on a milligram basis: desired and undesired SH reactions. cokinetic profiles of PPIs can influence their safety Impact of chirality. Scand J Gastroenterol 2001; 234(Suppl):3-11. 108. Kromer W., Kruger U., Huber R. et al. Differences in pH dependent activation rates of substituted benzimidazoles and control over acid secretion and onset of symptom biological in vitro correlates. Pharmacology 1998; 56:57-70. 109. Pantoflickova D., Dorta G., Ravic M. et al. Acid inhibition on the first day of dosing: comparison of four proton pump inhibitors. Aliment Pharmacol Ther 2003; 17:1507-14. 110. Schrover R. et al. Indirect meta-analysis of rabeprazole versus esomeprazole via placebo in patients with healed erosive gastro-oesophageal reflux disease. Austral Gastroenterol Week 2004. 111. Dekkers C.P. et al. Double-blind placebo controlled comparison of rabeprazole 20 mg vs. omeprazole 20 mg in the treatment of erosive or ulcerative gastro-oesophageal reflux disease. The European Rabeprazole Study Group. Aliment Pharmacol Ther 1999; 13(1):49-57. 112. Kukulka M., Wu J., Perez M.C. Pharmacokinetics and safety of dexlansoprazole MR in adolescents with symptomatic GERD. J Pediatr Gastroenterol Nutr 2012; 54(1):41-7. 113. Vakily M., Zhang W., Wu J. et al. 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Pharmacokinetics and Pharmacodynamics of the Proton Pump Inhibitors. J Neurogastroenterol Motil 2013; 19:25-35. 118. Fass R. et al. The Effect of Dexlansoprazole MR on Nocturnal Heartburn and GERD-Related Sleep Disturbances in Patients With Symptomatic GERD. Am J Gastroenterol 2011; 106(3):421-31. 119. Freedberg D.E., Kim L.S., Yang Y.X. The Risks and Benefits of Long-term Use of Proton Pump Inhibitors: Expert Review and Best Practice Advice From the American Gastroenterological Association. Gastroenterology 2017; 152(4):706-15. 120. Moayyedi P., Delaney B., Forman D. Gastroesophageal reflux disease. Clin Evid 2005; (14):567-81. 121. Robinson M., Fitzgerald S., Hegedus R., Murthy A., Jokubaitis L. Onset of symptom relief with rabeprazole: a community-based, open-label assessment of patients with erosive oesophagitis. Aliment Pharmacol Ther 2002; 16(3):445-54. 122. Ogawa R., Echizen N. Drug-drug interaction profiles of proton pump inhibitors. Clin Pharmacokinet 2010; 49(8):509-33. 123. Targownik L.E., Lix L.M., Leung S. Proton-pump inhibitor use is not associated with osteoporosis or accelerated bone mineral density loss. Gastroenterology 2010; 138(3):896-904. 124. Ngamruengphong S., Leontiadis G.I., Radhi S. Proton pump inhibitors and risk of fracture: a systematic review and meta-analysis of observational studies. Am J Gastroenterol 2011; 106(7):1209-18. 125. Bavishi C., Dupont H.L. Systematic review: The use of proton pump inhibitors and increased susceptibility to enteric infection. Aliment Pharmacol Ther 2011; 34:1269-81. 126. Eom C.S., Jeon C.Y., Lim J.W. Use of acid-suppressive drugs and risk of pneumonia: A systematic review and meta-analysis. CMAJ 2011; 183:310-9. 127. Johnstone J., Nerenberg K., Loeb M. Meta-analysis: Proton pump inhibitor use and the risk of community-acquired pneumonia. Aliment Pharmacol Ther 2010; 31(11):1165-77. 128. Lind T., Havelund T., Lundell L. On demand therapy with omeprazole for the long-term management of patients with heartburn without oesophagitis - a placebo-controlled randomized trial. Aliment Pharmacol Ther 1999; 13(7):907-14. 129. Pace F., Tonini M., Pallotta S. Systematic review: Maintenance treatment of gastro-oesophageal reflux disease with proton pump inhibitors taken “on-demand”. Aliment Pharmacol Ther 2007; 26(2):195-204. 130. Juurlink D.N., Gomes T., Ko D.T., Szmitko P.E., Austin P.C., Tu J.V., Henry D.A., Kopp A., Mamdani M.M. A population-based study of the drug interaction between proton pump inhibitors and clopidogrel. CMAJ 2009; 180(7):713-8. 131. Gerson L.B., McMahon D., Olkin I. Lack of significant interactions between clopidogrel and proton pump inhibitor therapy: Meta-analysis of existing literature. Dig Dis Sci 2012; 57(5):1304-13. 132. Chen M., Wei J.F., Xu Y.N. A meta-analysis of impact of proton pump inhibitors on antiplatelet effect of clopidogrel. Cardiovasc Ther 2012; 30(5):227-33. 133. Reimer C., Lødrup A.B., Smith G., Wilkinson J., Bytzer P. Randomised clinical trial: alginate (Gaviscon Advance) vs. placebo as add-on therapy in reflux patients with inadequate response to a once daily proton pump inhibitor. Aliment Pharmacol Ther 2016; 43(8):899-909. 134. Dettmar P.W., Little S.L. Baxter T. The effect of omeprazole pre-treatment on rafts formed by reflux suppressant tablets containing alginate. J Int Med Res 2005; 33(3):301-8. 135. Washington N., Wilson C.G., Williams D.L., Robertson C. An investigation into the effect of cimetidine pre-treatment on raft formation of an anti-reflux agent. Aliment Pharmacol Ther 1993; 7(5):553-9. 136. Bordin D.S., Yanova O.B., Berezina O.I., Treiman E.V. Advantages of a combination of alginate and PPI in eliminating heartburn and regurgitation in the first days of GERD. Ros journal gastroenterol hepatol coloproctol 2016; 25(6):39-45. . 137. Strugala V. et al. Assessment of the Safety and Efficacy of a Raft-Forming Alginate Reflux Suppressant (Liquid Gaviscon) for the Treatment of Heartburn during Pregnancy. Int Scholarly Res Network Obstet Gynec 2012. 138. Lindow S.W., Regnéll P., Sykes J., Little S. An open label, multicentre study to assess the safety and efficacy of a novel reflux suppressant (Gaviscon Advance) in the treatment of heartburn during pregnanc. Int J Clin Pract 2003; 57(3):175-9. 139. Mandel K.G., Daggy B.P., Brodie D.A., Jacoby H.I. Review article: alginate-raft formulation in the treatment of heartburn and acid reflux. Aliment Pharmacol Ther 2000; 14(6):669-90. 140. Kaibysheva V.O., Trukhmanov A.S., Ivashkin V.T. Gastroesophageal reflux disease, resistant to proton pump inhibitor therapy. Ros journal gastroenterol hepatol coloproctol 2011; 20(4):4-13. . 141. Ichikawa H. et al Rapid metabolizer genotype of CYP2C19 is a risk factor of being refractory to proton pump inhibitor therapy for reflux esophagitis. 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A common novel CYP2C19 gene variant causes ultrarapid drug metabolism relevant for the drug response to proton pump inhibitors and antidepressants. Clin Pharmacol Ther 2006; 79(1):103-13. 148. Oestreich J.H. et al. Prevalence of CYP2C19 variant alleles and pharmacodynamic variability of aspirin and clopidogrel in Native Americans. Am Heart J 2014; 167(3):413-8. 149. Horn J. et al. Review article: relationship between the metabolism and efficacy if proton pump inhibitors - focus on rabeprazole. Aliment Pharmacol Ther 2004; 20(6):11-9. 150. Lee Y.C., Lin J.T., Wang H.P. et al. Influence of cytochrome P450 2C19 genetic polymorphism and dosage of rabeprazole on accuracy of proton-pump inhibitor testing in Chinese patients with gastroesophageal reflux disease. J Gastroenterol Hepatol 2007; 22(8):1286-92. 151. Sugimoto M., Shirai N., Nishino M. et al. Comparison of acid inhibition with standard dosages of proton pump inhibitors in relation to CYP2C19 genotype in Japanese. Eur J Clin Pharmacol 2014; 70(9):1073-8. 152. Pharmacogenetics Working Group of the Royal Dutch Pharmacists Association, https://www.pharmgkb.org/view/dosing-guidelines.do, accessed 05/23/2014. 153. Lee R.D., Mulford D., Wu J., Atkinson S.N. The effect of time-of-day dosing on the pharmacokinetics and pharmacodynamics of dexlansoprazole MR: evidence for dosing flexibility with a Dual Delayed Release proton pump inhibitor. Aliment Pharmacol Ther 2010; 31(9):1001-11. 154. Lee R.D., Vakily M., Mulford D. et al. Clinical trial: the effect and timing of food on the pharmacokinetics and pharmacodynamics of dexlansoprazole MR, a novel Dual Delayed Release formulation of a proton pump inhibitor - evidence for dosing flexibility. Aliment Pharmacol Ther 2009; 29(8):824-33. 155. Sarosiek I. et al. Significant Increase of Esophageal Mucin Secretion in Patients with Reflux Esophagitis After Healing with Rabeprazole: Its Esophagoprotective Potential. Dig Dis Sci 2009; 54(10):2137-42. 156. Takiuchi H., Asado S., Umegaki E., Tahashi Y., Ohshiba S. Effects of proton pump inhibitors: omeprazole, lansoprazole and E‑3810 on the gastric mucin. In: Proc. 10th World Congress of Gastroenterol. Los Angeles, CA; 1994. 1404 p. 157. Pandolfino J.E., Vela M.F. Esophageal-reflux monitoring. Gastrointest Endosc 2013; 15(4):316. 158. Galmiche J.P., Hatlebakk J., Attwood S. et al. Laparoscopic antireflux surgery vs esomeprazole treatment for chronic GERD: The LOTUS randomized clinical trial. JAMA 2011; 305(19):1969-77. 159. Wileman S.M., McCann S., Grant A.M. Medical versus surgical management for GERD in adults. Cochrane Database Syst Rev 2010, pp. CD003243. 160. Rouphael C., Gordon I.O., Thota P.N. Lymphocytic esophagitis: Still an enigma a decade later. World J Gastroenterol 2017; 23(6):949-56.
Information
List of authors:
V.T Ivashkin 1, I.V Maev 2, A.S. Trukhmanov 1, E.K. Baranskaya 1, O.B. Dronova 3, O.V. Zairatyants 2, R.G. Sayfutdinov 4, A.A. Sheptulin 1, T.L. Lapina 1, S.S. Pirogov 5, Yu.A. Kucheryavyi 2, O.A. Storonova 1, D.N. Andreev 2
1 Federal State Autonomous Educational Institution of Higher Education “First Moscow State Medical University named after. THEM. Sechenov" (Sechenov University) Ministry of Health of Russia, Moscow, Russian Federation
2 Federal State Budgetary Educational Institution of Higher Education “Moscow State Medical and Dental University named after. A.I. Evdokimov" of the Ministry of Health of Russia, Moscow, Russian Federation
3 Federal State Budgetary Educational Institution of Higher Education "Orenburg State Medical University" of the Ministry of Health of Russia, Orenburg, Russian Federation
4 Kazan State Medical Academy - branch of the Federal State Budgetary Educational Institution of Further Professional Education "Russian Medical Academy of Continuing Professional Education" of the Ministry of Health of Russia, Kazan, Russian Federation
Table 1
Levels of Evidence (Oxford Center for Evidence-Based Medicine)
Level | Diagnostic test | Therapeutic study |
1a | Systematic review of homogeneous level 1 diagnostic studies | Systematic review of homogeneous RCTs |
1b | Validation cohort study with gold standard quality | Single RCT (with narrow CI) |
1s | The specificity or sensitivity is so high that a positive or negative result allows one to exclude/establish the diagnosis | All or Nothing Study |
2a | Systematic review of homogeneous diagnostic studies >2 levels | Systematic review of (homogeneous) cohort studies |
2b | Exploratory cohort study with gold standard quality |
Separate cohort study (including low quality RCTs; i.e.<80% пациентов, прошедших контрольное наблюдение) |
2s | No | Outcomes research; environmental studies |
3a | Systematic review of homogeneous studies at level 3b and above | Systematic review of homogeneous case-control studies |
3b | A study with inconsistent recruitment or without conducting a gold standard study in all subjects | Single case-control study |
4 | Case-control study or study with poor quality or non-independent gold standard | Case series (and cohort studies or low-quality case-control studies) |
5 | Expert opinion without careful critical evaluation or based on physiology, laboratory animal studies or development of "first principles" |
Expert opinion without careful critical evaluation, laboratory animal studies or development of "first principles" |
table 2
These draft recommendations were reviewed by independent experts who were asked to comment primarily on the extent to which the interpretation of the evidence underlying the recommendations is understandable. Comments from outpatient doctors were received, which were carefully systematized and discussed at expert group meetings.
The latest changes to these recommendations were presented for discussion within the framework of the Twenty-second United Russian Gastroenterology Week (03.10.2016-05.10.2016). The draft guidelines were re-reviewed by independent experts and outpatient clinicians. For final revision and quality control, the recommendations were re-analyzed by members of the expert group, who concluded that all comments and comments were taken into account, and the risk of systematic errors in the development of recommendations was minimized.
Attached files
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Gastroesophageal reflux disease is a pathological process that results from deterioration of the motor function of the upper gastrointestinal tract. It occurs as a result of reflux - a regularly repeated reflux of stomach or duodenal contents into the esophagus, resulting in damage to the mucous membrane of the esophagus, and damage to overlying organs (larynx, pharynx, trachea, bronchi) can also occur. What kind of disease is this, what are the causes and symptoms, as well as the treatment of GERD - we will look at this in this article.
GERD - what is it?
GERD (gastroesophageal reflux disease) is the reflux of gastric (gastrointestinal) contents into the lumen of the esophagus. Reflux is called physiological if it appears immediately after eating and does not cause obvious discomfort to a person. This is a normal physiological phenomenon if it occurs occasionally after eating and is not accompanied by unpleasant subjective sensations.
But if there are many such reflux and they are accompanied by inflammation or damage to the mucous membrane of the esophagus, and extra-esophageal symptoms, then this is already a disease.
GERD occurs in all age groups, in both sexes, including children; the incidence increases with age.
Classification
There are two main forms of gastroesophageal reflux disease:
- non-erosive (endoscopically negative) reflux disease (NERD) - occurs in 70% of cases;
- (RE) - the incidence rate is about 30% of the total number of GERD diagnoses.
Experts distinguish four degrees of reflux damage to the esophagus:
- Linear defeat– individual areas of inflammation of the mucous membrane and foci of erosion on its surface are observed.
- Drain lesion– the negative process spreads over a large surface due to the merging of several foci into continuous inflamed areas, but not the entire area of the mucous membrane is yet covered by the lesion.
- Circular lesion– zones of inflammation and foci of erosion cover the entire inner surface of the esophagus.
- Stenosing lesion– against the background of complete damage to the inner surface of the esophagus, complications are already occurring.
Causes
The main pathogenetic substrate for the development of gastroesophageal reflux disease is gastroesophageal reflux itself, that is, retrograde reflux of stomach contents into the esophagus. Reflux most often develops due to incompetence of the sphincter located at the border of the esophagus and stomach.
The following factors contribute to the development of the disease:
- Decreased functional ability of the lower esophageal sphincter (for example, due to destructuring of the esophagus due to hiatal hernia);
- Damaging properties of gastrointestinal contents (due to the content of hydrochloric acid, as well as pepsin, bile acids);
- Gastric emptying disorders;
- Increased intra-abdominal pressure;
- Pregnancy;
- Smoking;
- Overweight;
- Decreased clearance of the esophagus (for example, due to a decrease in the neutralizing effect of saliva, as well as bicarbonates of esophageal mucus);
- Taking medications that reduce smooth muscle tone (calcium channel blockers, beta-agonists, antispasmodics, nitrates, M-anticholinergics, bile-containing enzyme preparations).
Factors contributing to the development of GERD are:
- disorders of motor functions of the upper digestive tract,
- hyperacidotic conditions,
- reduced protective function of the esophageal mucosa.
Symptoms of gastroesophageal reflux disease
Once in the esophagus, the contents of the stomach (food, hydrochloric acid, digestive enzymes) irritate the mucous membrane, leading to the development of inflammation.
The main symptoms of gastroesophageal reflux are as follows:
- heartburn;
- belching acid and gas;
- acute sore throat;
- discomfort in the pit of the stomach;
- pressure that occurs after eating, which increases after eating food that promotes the production of bile and acid.
In addition, acid from the stomach, entering the esophagus, has a negative effect on local tissue immunity, affecting not only the esophagus, but also the nasopharynx. A person suffering from GERD often complains of chronic pharyngitis.
GERD often occurs with atypical clinical manifestations:
- chest pain (usually after eating, worse when bending over),
- heaviness in the stomach after eating,
- hypersalivation (increased salivation) during sleep,
- bad breath,
- hoarseness.
Symptoms appear and intensify after eating, physical activity, in a horizontal position, and decrease in a vertical position, after drinking alkaline mineral waters.
Signs of GERD with esophagitis
Reflux disease in the esophagus can cause the following reactions:
- inflammatory process,
- damage to the walls in the form of ulcers,
- modification of the lining layer in contact with the refluxate into a form unusual for a healthy organ;
- narrowing of the lower esophagus.
If the above symptoms occur more than 2 times a week for 2 months, you should consult a doctor for examination.
GERD in children
The main reason for the development of reflux disease in children is the immaturity of the lower sphincter, which prevents the evacuation of food from the stomach back into the esophagus.
Other causes that contribute to the development of GERD in childhood include:
- functional insufficiency of the esophagus;
- narrowing of the gastric outflow tract;
- recovery period after surgery on the esophagus;
- operations for gastric resection;
- consequences of serious injuries;
- oncological processes;
- difficult childbirth;
- high intracranial pressure.
Common symptoms of GERD in a child are as follows:
- frequent burping or burping;
- poor appetite;
- pain in the stomach;
- the child is excessively capricious during feeding;
- frequent vomiting or retching;
- hiccups;
- labored breathing;
- frequent cough, especially at night.
Treatment for gastroesophageal reflux disease in children will depend on symptoms, age, and overall health. In order to prevent the development of this disease in a child, parents should closely monitor his diet.
Complications
Gastroesophageal reflux disease can cause the following complications in the body:
- esophageal stricture;
- ulcerative lesions of the esophageal mucosa;
- bleeding;
- the formation of Barrett's syndrome - complete replacement (metaplasia) of the stratified squamous epithelium of the esophagus with columnar gastric epithelium (the risk of esophageal cancer with epithelial metaplasia increases 30-40 times);
- malignant degeneration of esophagitis.
Diagnostics
In addition to the diagnostic methods described, it is important to visit the following specialists:
- cardiologist;
- pulmonologist;
- otorhinolaryngologist;
- surgeon, his consultation is necessary in case of ineffectiveness of the ongoing drug treatment, the presence of large diaphragmatic hernias, or in the event of complications.
To diagnose gastroesophageal reflux, the following methods are used:
- endoscopic examination of the esophagus, which allows to identify inflammatory changes, erosions, ulcers and other pathologies;
- daily monitoring of acidity (pH) in the lower part of the esophagus. Normal level pH should be between 4 and 7, changes in evidence may indicate the cause of the disease;
- radiography - allows you to detect ulcers, erosions, etc.;
- manometric examination of the esophageal sphincters - performed to assess their tone;
- scintigraphy using radioactive substances - performed to assess esophageal clearance;
- biopsy - performed if Barrett's esophagus is suspected;
- ECG and daily ECG monitoring; Ultrasound examination of the abdominal organs.
Of course, not all methods are used for accurate diagnosis. Most often, the doctor only needs the data obtained during the examination and interview of the patient, as well as the conclusion of the FEGDS.
Treatment of reflux disease
Treatment of gastroesophageal reflux disease can be medication or surgery. Regardless of the stage and severity of GERD, during therapy it is necessary to constantly adhere to certain rules:
- Do not lie down or lean forward after eating.
- Do not wear tight clothes, corsets, tight belts, bandages - this leads to an increase in intra-abdominal pressure.
- Sleep on a bed in which the part where the head is located is raised.
- Do not eat at night, avoid large meals, do not eat too hot food.
- Quit alcohol and smoking.
- Limit consumption of fats, chocolate, coffee and citrus fruits, as they are irritating and reduce LES pressure.
- Lose weight if you are obese.
- Stop taking medications that cause reflux. These include antispasmodics, β-blockers, prostaglandins, anticholinergic drugs, tranquilizers, nitrates, sedatives, calcium channel inhibitors.
Medications for GERD
Drug treatment of gastroesophageal reflux disease is carried out by a gastroenterologist. Therapy takes from 5 to 8 weeks (sometimes the course of treatment lasts up to 26 weeks) and is carried out using the following groups of drugs:
- Antisecretory agents (antacids) have the function of reducing the negative effect of hydrochloric acid on the surface of the esophagus. The most common are: Maalox, Gaviscon, Almagel.
- As a prokinetic Motilium is used. The course of treatment for catarrhal or endoscopically negative esophagitis lasts about 4 weeks, for erosive esophagitis 6-8 weeks, if there is no effect, treatment can be continued up to 12 weeks or more.
- Taking vitamin supplements, including vitamin B5 and U in order to restore the mucous membrane of the esophagus and generally strengthen the body.
GERD can also be caused by an unbalanced diet. Therefore, drug treatment must be supported by proper nutrition.
With timely identification and compliance with lifestyle recommendations (non-drug treatment measures for GERD), the prognosis is favorable. In the case of a prolonged, often relapsing course with regular refluxes, the development of complications, and the formation of Barrett's esophagus, the prognosis noticeably worsens.
The criterion for recovery is the disappearance of clinical symptoms and endoscopic findings. To prevent complications and relapses of the disease, monitor the effectiveness of treatment, it is necessary to regularly visit a doctor, therapist or gastroenterologist, at least once every 6 months, especially in the fall and spring, and undergo examinations.
Surgical treatment (operation)
There are various methods of surgical treatment of the disease, but in general their essence comes down to restoring the natural barrier between the esophagus and the stomach.
Indications for surgical treatment are as follows:
- complications of GERD (repeated bleeding, strictures);
- ineffectiveness of conservative therapy; frequent aspiration pneumonia;
- diagnosing Barrett's syndrome with high-grade dysplasia;
- the need of young patients with GERD for long-term antireflux therapy.
Diet for GERD
Diet for gastroesophageal reflux disease is one of the main areas of effective treatment. Patients suffering from esophagitis should adhere to the following dietary recommendations:
- Eliminate fatty foods from your diet.
- To stay healthy, avoid fried and spicy foods.
- If you are ill, it is not recommended to drink coffee or strong tea on an empty stomach.
- People prone to esophageal diseases are not recommended to consume chocolate, tomatoes, onions, garlic, mint: these products reduce the tone of the lower sphincter.
Thus, the approximate daily diet of a patient with GERD is as follows (see daily menu):
Some doctors believe that for patients diagnosed with gastroesophageal reflux disease, these dietary rules and a healthy lifestyle are more important than the foods from which the menu is composed. You should also remember that you need to approach your diet taking into account your own feelings.
Folk remedies
Alternative medicine involves a large number of recipes; the choice of a specific one depends on the individual characteristics of the human body. But folk remedies cannot act as a separate therapy; they are included in the general complex of therapeutic measures.
- Sea buckthorn or rosehip oil: take one teaspoon up to three times a day;
- The home medicine cabinet of a patient with reflux disease should contain the following dried herbs: birch bark, lemon balm, flax seeds, oregano, St. John's wort. You can prepare a decoction by pouring a couple of tablespoons of the herb with boiling water in a thermos and letting it sit for at least an hour, or by adding a handful of the medicinal plant to boiling water, remove the pan from the stove, cover with a lid and let it brew.
- Crushed plantain leaves(2 tbsp.), St. John's wort (1 tbsp.) Place in an enamel container, pour boiling water (500 ml). After half an hour, the tea is ready to drink. You can take the drink for a long time, half a glass in the morning.
- Treatment of GERD with folk remedies involves not only herbal medicine, but also the use of mineral waters. They should be used at the final stage of the fight against the disease or during remissions in order to consolidate the results.
Prevention
In order to never encounter an unpleasant disease, it is important to always pay attention to your diet: do not overeat, limit the consumption of unhealthy foods, and monitor your body weight.
If these requirements are met, the risk of GERD will be minimized. Timely diagnosis and systematic treatment can prevent the progression of the disease and the development of life-threatening complications.
Diseases of the digestive system are common pathologies that, according to statistics, affect every third person on earth. Among the list of numerous functional and organic pathologies, gastroesophageal reflux disease (GERD) is far from the last in terms of frequency of cases, and its symptoms are sufficiently pronounced to diagnose the disease in time and begin treatment.
Gastroesophageal reflux disease - what is it?
The function of the stomach is to digest food, and for this purpose a secretion is released that digests all substances that enter the stomach. This secretion is called gastric juice - and its acidity is quite high, so other digestive organs associated with the stomach are protected from acid by the sphincters.
The sphincter, which connects the stomach and esophagus, opens to allow food to enter the stomach, and then closes tightly.
If this process is disrupted, the contents of the stomach, including gastric juice, enter the esophagus. This pathology is called gastroesophageal reflux disease.
Stomach acids, getting on the walls of the esophageal mucosa, cause damage to it, and with chronic, regular reflux of gastric juice into the esophagus, ulcers and erosions form, and sometimes internal bleeding that is life-threatening.
How dangerous is the disease?
Erosions and ulcers on the mucous membrane of the esophagus often go unnoticed by humans, since the disease may not have clinical signs of manifestation for a long time, or the symptomatic picture will be distorted, making it impossible to understand in which organ the problem is localized.
It is important to know! If treatment is not started promptly, erosions can turn into perforations of the esophagus, which can be fatal if surgery is not performed in a timely manner.
In addition, acid from the stomach, entering the esophagus, has a negative effect on local tissue immunity, affecting not only the esophagus, but also the nasopharynx. A person suffering from GERD often complains of chronic pharyngitis, tonsillitis, and sinusitis.
Development of sinusitis with GERD |
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Forms and types of pathology
GERD is roughly divided into two categories:
- with signs of inflammation of the esophagus;
- without inflammation of the esophagus.
If there are no signs of inflammation, there is reason to talk about it not as a separate subtype of this pathology, but as an initial, asymptomatic stage of the disease. If treatment is not carried out, inflammation of the esophagus will certainly occur.
If the inflammatory process on the mucous membrane is already diagnosed, doctors divide GERD into 4 types, depending on the degree of tissue damage.
- Stage 1 - endoscopic examination reveals erosions, the length of which is no more than five millimeters, and tissue damage extends to no more than two folds of the mucosa;
- Stage 2 – damage affects more than two folds of the inner lining of the esophagus, the length of each erosion is more than 5 mm;
- Stage 3 – erosions cover a large amount of tissue, but not more than 75 percent of the total tissue of the esophagus;
- Stage 4 – pathology has covered more than 75% of the tissues of the esophagus.
At any stage and for any subtype of GERD, mandatory treatment is required after a thorough diagnosis.
Symptoms
Recognizing GERD is very difficult. The main symptom of the disease is pain, but it is of a “wandering nature,” that is, it can occur in different parts of the sternum. In some people, the pain is localized in the heart area, then the person seriously believes that he has heart disease and goes to a cardiologist. For some, the pain “wanders” along the lateral parts of the sternum, hinting at pathologies of the liver or gallbladder. For others, all pain is concentrated in the spine, and the person experiences all the symptoms of osteochondrosis of the thoracic region.
Important! It is easy to distinguish the pain that occurs due to GERD from diseases of the heart or spine if you remember that discomfort due to GERD always appears after eating.
In addition to pain, the symptomatic picture can be supplemented by the following signs:
- constantly appearing heartburn;
- hoarseness of voice;
- shortness of breath, feeling of lack of air;
- cough;
- recurrent bacterial infections of the nasopharynx;
- increased salivation;
- unpleasant sour odor from the mouth.
The described symptoms are not always present simultaneously; most often they are grouped, causing a false clinical picture. That is, a person experiencing chest pain due to a feeling of lack of air will certainly attack the cardiologist’s office, being sure that he is at risk of a heart attack. Some patients, before diagnosing GERD with chest pain and cough, suspect serious lung pathologies.
Thus, until a good physician refers the patient to a gastroenterologist, the diagnostic process may not begin.
Picture of GERD |
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Diagnostics
The first stage of diagnosis is a survey and examination of the patient: the doctor finds out how long ago the symptoms of the disease appeared, what precedes the onset of symptoms, and whether there are close blood relatives suffering from this disease. The gastroenterologist also finds out the patient’s lifestyle, his diet, alcohol consumption, smoking, and constant or long-term use of medications.
After this, a diagnostic plan is prescribed.
Laboratory examination includes:
- general blood test: the level of hemoglobin and leukocytes is assessed to determine the presence of internal bleeding and inflammation;
- biochemical blood test: the function of all organs of the digestive system is assessed as complications of GERD;
- stool occult blood test.
The list of functional examinations is wider and provides more accurate data for the diagnosis of gastroesophageal reflux disease:
- FEGDS is an endoscopic examination, when the esophagus and stomach are examined using a special probe that visualizes an image in real time on a monitor - thus, signs of damage to the esophagus, the degree of tissue damage, and the fact of narrowing of the lumen of the esophagus can be detected;
- Ultrasound of the abdominal organs to identify complications - lesions of other organs of the digestive system;
- MRI, CT or X-ray of the esophagus to assess the condition of the organ tissues;
- daily pH-metry - the acidity of gastric juice is checked over 24 hours, the dynamics of changes in indicators under the influence of various factors;
- esophageal scintigraphy is a method by which the condition of the tissues of the esophagus is assessed, the speed of passage of the food bolus from the pharynx to the stomach;
- biopsy of esophageal tissue is a rarely used method, which is prescribed if there is a suspicion of a tumor of the organ;
- alkaline test - the patient is given an antacid drug, after which an alkaline test is performed, if the result is positive, GERD is diagnosed.
Of course, not all methods are used for accurate diagnosis. Most often, the doctor only needs the data obtained during the examination and interview of the patient, as well as the conclusion of the FEGDS. A biochemical study of blood composition is required to create a more complete picture of the disease: it allows you to understand whether there are complications associated with the pathology.
Traditional treatment for GERD
For GERD, drug therapy is the most effective. A complex effect of three types of drugs is used.
Antacids are drugs that neutralize the hydrochloric acid of gastric juice, thereby reducing its acidity. This drug is intended for symptomatic treatment, that is, after the drug stops working, the acidity of the stomach returns to its previous levels.
Antacids can be found in pharmacies under the names:
- “Phosphalugel gel” (300-500 rubles);
- “Renny” (80-160 rubles);
- “Almagel Neo” (150-200 rubles);
- “Rutacid” (100-200 rubles);
- "Gaviscon")150-300 rub.);
- “Relzer” (100-200 rubles);
- "Gastal" (250-350 rubles).
H2-histamine blockers are drugs that help reduce the production of hydrochloric acid in the stomach. Unlike antacids, these drugs have a longer lasting effect, but in order to prevent relapse of the pathology, the course of taking the medication must be repeated regularly.
The names of H2-histamine blockers in the form of pharmaceutical products are as follows:
- "Cimetidine" (2500-3600 rub.);
- "Famotidine" (50-80 rub.);
- "Ranitidine" (30-70 rub.);
- “Acylok” (220-280 rub.);
- "Lansoprazole" (20-30 rubles).
Proton pump inhibitors - reducing the secretion of hydrochloric acid by blocking the proton pump of the cells of the mucous membrane of the stomach and esophagus.
You can find drugs in this group by name:
- “Pantoprazole” (200-330 rubles);
- “Pantap” (4 – 20 rubles);
- “Nolpaza” (150-700 rub.);
- “Ezokar” (12-25 rubles);
- "Rabeprazole" (240-320 rubles).
But treatment is not limited to taking pharmaceutical drugs. It is also necessary to change your lifestyle, adhering to a list of special rules.
- Stop drinking alcohol and smoking.
- Eat small portions with breaks of 3-4 hours - “fractional meals”.
- Do not lift heavy objects, limit physical activity.
- Choose a wardrobe that is not tight around the waist.
- Don't eat before bed.
Important! If no positive dynamics are observed after the therapeutic courses, the doctor may recommend surgical treatment.
Diet for GERD
Patients should exclude the following foods and dishes from their diet:
- sweet and fresh baked goods;
- rich broths and sour soups (cabbage soup, borscht, okroshka);
- fatty types of meat, poultry and fish prepared by frying or smoking;
- cheeses and sour kefir;
- cereals: millet, barley, pearl barley, corn;
- beans;
- all sour vegetables and fruits;
- chocolate and ice cream;
- carbonated drinks;
- dressings: mustard, horseradish, sauces, lecho.
Thus, the approximate daily diet of a patient with gastroesophageal reflux disease is as follows:
- Breakfast:
- buckwheat porridge;
- omelette;
- tea with milk.
- Snack:
- sweet curd cheese.
- Dinner:
- vegetarian puree soup;
- a piece of boiled meat;
- salad of boiled vegetables;
- sweet dried fruit compote.
- Afternoon snack:
- crackers or bread.
- Dinner:
- boiled fish or chicken;
- a piece of apple pie;
- tea with milk.
Important! The diet should be made taking into account the normalization of body weight: if the patient is overweight, you need to calculate the approximate number of calories for the daily diet and reduce it by no more than 15%.
Traditional methods
Traditional medicine for GERD suggests including decoctions of medicinal herbs in the diet. They can be taken instead of tea, or as a snack. It is noteworthy that the pleasant taste of the drink will help eliminate the unpleasant taste in the mouth, which is often found in patients.
The home medicine cabinet of a patient with GERD should contain the following dried herbs:
- birch bark;
- lemon balm;
- flax seeds;
- oregano;
- St. John's wort.
You can prepare a decoction by pouring a couple of tablespoons of the herb with boiling water in a thermos and letting it sit for at least an hour, or by adding a handful of the medicinal plant to boiling water, remove the pan from the stove, cover with a lid and let it brew.
But the most popular method of unconventional treatment is the use of potatoes. For therapy, the juice of fresh raw potatoes is used, which is not easy to squeeze out: you either need to grate the vegetable or grind it in a blender. After grinding the pulp, place it in cheesecloth and squeeze it out. The resulting juice is drunk before meals for a month.
Prevention
In order to never encounter an unpleasant disease, it is important to always pay attention to your diet: do not overeat, limit the consumption of unhealthy foods, and monitor your body weight.
It is important not to take drugs that can provoke the development of the disease without strict indications:
- tranquilizers;
- sedatives;
- antispasmodics.
It is also important to visit a doctor at least once a year for medical examination.