Treatment of erosive and ulcerative lesions of the stomach and duodenum. Erosion of the stomach what is it and how to treat

Numerous diseases of the gastrointestinal tract are now quite common. As a result of malnutrition, experienced stress and other factors, various disorders of the stomach appear. Erosive-ulcerative gastritis is one of such serious diseases that are difficult to treat. If possible, it is necessary to identify it as soon as possible in order to avoid even more trouble.

Features of the disease

This disease is a complex variety of gastritis, which is characterized by a severe course and can lead to much more serious consequences. Treatment of the disease, due to its specificity, can take a long period.

With any form of gastritis in humans, there is a violation of the activity of the mucous layer of the stomach. Erosive and ulcerative disease is characterized by the fact that hydrochloric acid contained in the digestive enzyme penetrates the mucous membrane of the walls of the stomach and corrodes them. This disease is characterized by increased secretion of gastric acid, with an increase in acidity.

A distinctive feature of erosive gastritis is that its acute form develops very quickly, within a few hours. On the epithelial, or surface layer of the walls, multiple lesions (erosion) are formed that can bleed. In the future, ulcers of various sizes appear in their place. If gastritis is not treated, the process progresses and becomes chronic, the treatment of which requires a more serious approach.

With timely and proper treatment, erosive formations pass without consequences. The epithelium is restored, mucosal defects heal without leaving scars.

Symptoms of the disease

Erosive gastritis, unlike other types, has pronounced symptoms that can be used to determine the presence of a serious indigestion. If you find yourself with several of the symptoms described, you should immediately contact a specialist.

This disease can occur in two forms: acute and chronic. If the disease occurs for the first time, it takes an acute form and has more pronounced symptoms. Pain in the abdomen is sharp and bright, while they can be of a different nature.

The pains are cramping when they fade and reappear, or there is a constant sharp pain that does not give rest. If the disease is advanced and has become chronic, the pain may not be so pronounced and appear from time to time.

In addition to painful manifestations in the abdomen, an erosive and ulcerative disease may have the following symptoms:

nausea, heartburn, sour eructation, vomiting with spotting;
lack of appetite, general weakness of the body, dizziness;
discomfort in the abdomen, pain on palpation;
pain in the stomach occurs at a time when a person is hungry. During the meal, the pain may subside, but after eating it appears again;
disruption of the intestinal tract: bloating, constipation, diarrhea;
elevated temperature.

Causes

There are many reasons that can provoke the appearance of erosive-ulcerative gastritis. This may be the wrong way of life, a careless attitude to one's own health, as well as factors beyond the control of a person. Irritation of the mucous layer of the stomach can also cause harmful effects of the environment.

This disease can occur due to long-term use of medications. In particular, this occurs after undergoing treatment for any infection. Violation of the stomach also occurs due to intoxication of the body, when working with industrial poisons and various chemicals.

Irritation of the mucosa can occur as a result of poor-quality food, spoiled food or chemicals added to the stomach. This can also lead to malnutrition, the constant use of fatty, spicy, too hot or cold food.

Often, the cause of erosive disease is alcoholism and constant smoking. In this case, regular poisoning of the body with toxic substances occurs. The development of the disease, in this case, is rather slow. First, the mucous layer of the stomach is irritated, then its microflora is destroyed and harmful elements corrode the inner surface of the digestive organ.

Strong experiences and stresses have a very negative effect on the body. Nervous disorders that last for a long time can provoke the appearance of erosive gastritis. Also, the disease can appear due to disturbances in the immune system of the body and against the background of hormonal changes.

The presence in the body of a bacterium called Helicobacter pylori causes inflammation of the gastric mucosa and the development of erosions. This is considered a common cause of many types of gastritis and peptic ulcers.

Types of erosive gastritis

Depending on the duration of the course, the method of occurrence and localization, erosive type gastritis can be divided into several types. They may have various symptoms and complications.

Acute ulcerative gastritis occurs as a result of abdominal trauma, chemical burns, the onset of pathology of the inner part of the stomach, which leads to bleeding. In this case, a person has symptoms such as fever, severe abdominal pain, dark-colored vomiting, with blood and mucus.

An erosive disease of a chronic type can occur against the background of an acute form of gastritis. If the erosions bleed, the gastritis is called hemorrhagic. In the chronic course of the disease, a cyclical change in the phases of the disease regularly occurs in the human body. Periodically, the symptoms disappear, after which an exacerbation occurs.

Ulcerative gastritis of the antrum is a common disease in which the lower part of the organ, passing into the duodenum, is affected. The cause of this type of gastritis, doctors believe the bacterium Helicobacter.

Erosive reflux gastritis is considered a rather severe form of such diseases. In this case, the duodenum and the mucous layer of the stomach are affected by erosive and ulcerative formations of various sizes.

Diagnosis and treatment

Modern diagnostic methods allow you to accurately determine the type of disease and the degree of damage to the gastric mucosa. In order to identify the presence of peptic ulcer at the initial stage, the patient is examined in several stages.

An analysis of the patient's feces, urine, as well as a general and chemical blood test is performed. According to the results, the acidity index and the presence of infection in the body are determined.

Gastroscopy allows you to conduct a visual inspection of the inner surface of the stomach through the use of a special probe. In this case, a flexible hose is inserted through the patient's oral cavity. Epithelial cells of the inner surface of the digestive organ can be taken to detect the presence of bacteria there.

A study using ultrasound radiation is prescribed for the diagnosis of internal organs (liver, kidneys, etc.) in order to exclude concomitant diseases.

Based on the results of the examination, the doctor prescribes medication and diet. Drug treatment is carried out by several types of drugs in order to comprehensively affect the inflammatory process:

To eliminate pain, the patient is prescribed analgesic drugs: Analgin, Paracetamol, No-shpa, etc.
In the event that Helicobacter pylori is present in the body, antibiotics are used. Antibiotics effectively destroy this bacterium and significantly reduce the possibility of new inflammation.
Enzymes are used to restore the normal functioning of the digestive organs. These can be drugs such as Mezim, Pancreatin, etc.
In case of peptic ulcers with high acidity, it is necessary to lower its level and bring the indicator back to normal. For this, Almagel, Maalox, Sanpraz, etc. are prescribed.
It is recommended to take vitamins and other means that improve the general condition of a person. If necessary, immunomodulators are prescribed.

Diet for erosive gastritis

Diet for diseases of the gastrointestinal tract is an integral part of the treatment. If the patient does not follow a special diet, this can lead to exacerbations of erosive and peptic ulcer disease. It is necessary to eat regularly, every 5-6 hours, taking into account the recommendations of the doctor. Make sure that the food is at a normal temperature, not hot and not cold, this can adversely affect the healing process.

At the time of treatment, it is necessary to abandon junk food, which includes carbonated drinks, any canned food, fried, smoked and spicy foods. It is necessary to reduce salt intake to a minimum and exclude coffee, alcoholic beverages, strong tea from the diet.

It is recommended to eat dishes such as soups, cereals, vegetable and fruit purees. Raw vegetables and fruits are contraindicated, they must be steamed or boiled before use. You can drink green tea, purified non-carbonated water, fruit drinks, compotes.

Folk remedies

Gastrointestinal diseases such as ulcerative gastritis can also be treated with folk remedies, as an additional measure. Decoctions of medicinal injuries have an anti-inflammatory and restorative effect on the body.

The honey-olive mixture is an excellent restorative remedy. To prepare the medicine, you need to mix a glass of liquid honey and 0.5 liters of fresh olive oil. Add lemon juice from one fruit there. Mix the ingredients well until a homogeneous consistency is obtained. You need to take the composition half an hour before meals, one tablespoon.

Egg white has an enveloping effect and protects the lining of the stomach from damage. Take two fresh chicken eggs, break into a cup and carefully separate the whites from the yolks. Protein should be drunk two hours before meals, in the morning and in the evening.

Plantain tincture has antibacterial properties and accelerates the recovery of the mucosa. Take 200-250g of young leaves of the plant. Rinse well with water and grind. Fill the grass with 0.5 liters of alcohol. Then, let the composition brew for about a day. Take one teaspoon three times daily, before meals.

If there are signs of a serious violation of the gastrointestinal tract, consult a doctor to diagnose the disease. Remember that timely detection of an erosive disease and its treatment will help to avoid serious health problems.

For citation: Lapina T.L. Treatment of erosive and ulcerative lesions of the stomach and duodenum // RMJ. 2001. No. 13. S. 602

MMA named after I.M. Sechenov

E rozivno-ulcerative lesions of the stomach and duodenum are widespread and imply a certain range of differential diagnosis. Their significance is primarily due to the high frequency of occurrence: for example, when conducting an endoscopic examination for dyspeptic complaints, a stomach or duodenal ulcer is found in almost a quarter of patients, erosion of the gastroduodenal mucosa - in 2-15% of patients undergoing endoscopy. The significance of erosive and ulcerative lesions of the stomach and duodenum is also in the fact that they act as the main cause of bleeding from the upper gastrointestinal tract, and the mortality rates for this complication remain at the level of 10%. Ulcers underlie 46-56% of bleeding, erosion of the stomach and duodenum - at the heart of 16-20% of bleeding. The frequency of bleeding from varicose veins of the esophagus and stomach with portal hypertension is in third place, and erosive and ulcerative lesions of the esophagus, tumors of the esophagus and stomach and other diseases and conditions, as the cause of this complication, are hardly more than 15%. Therefore, it is so important to suspect erosive and ulcerative lesions of the gastroduodenal zone in time, and most importantly, to actively treat them and carry out adequate prevention.

Acute erosive and ulcerative lesions of the stomach and duodenum are caused by stress - trauma, burns, extensive surgery, sepsis. They are characteristic of severe renal, cardiac, hepatic, pulmonary insufficiency. As the cause of acute ulcers and erosions, alcohol and drugs (non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, digitalis, etc.), as well as pressure on the mucous membrane of formations located in the submucosal layer, are called. Chronic ulcer - a morphological substrate of peptic ulcer of the stomach and duodenum . Erosive and ulcerative lesions of the stomach caused by NSAIDs are currently considered in the framework of NSAID gastropathy. Ulcers and erosions are inherent in Zollinger-Ellison syndrome, some endocrine diseases, occur in Crohn's disease with stomach damage. Therapeutic tactics for erosive and ulcerative lesions of the gastroduodenal zone will almost always be based on the suppression of acid production, however, due to the variety of causes of mucosal damage and their manifestations, specific therapeutic approaches have been developed. This article will discuss the treatment of gastric and duodenal ulcers, erosive gastroduodenitis and gastropathy caused by NSAIDs, which are of crucial importance in clinical practice.

Medical treatment of ulcers venous disease of the stomach and duodenum currently based on two main approaches: 1) eradication therapy of infection Helicobacter pylori and 2) suppression of gastric acid production.

Rapid relief of peptic ulcer symptoms and successful ulcer healing, along with the use of antacids (Almagel) and alginates , achieved with the use of modern antisecretory drugs - blockers of H 2 receptors of histamine and inhibitors of the proton pump of parietal cells . Moreover, the latter, due to a more pronounced antisecretory effect, significantly replaced histamine receptor antagonists. Really, omeprazole - the most widely known and studied drug from the group of proton pump inhibitors can currently be considered the standard in the treatment of peptic ulcer. Omeprazole ( Losek® , AstraZeneca) has passed numerous clinical trials that meet the criteria of evidence-based medicine (for peptic ulcer, other acid-related diseases), and its effectiveness determines the standard of antisecretory response, the rate of relief of symptoms, the rate of scarring of the ulcer, safety.

Eradication therapy for infection H. pylori, which is of decisive importance in the pathogenesis of peptic ulcer, is primarily aimed at reducing the frequency of recurrence of the disease. Anti-helicobacter treatment due to the presence of proton pump inhibitors in the treatment regimens allows you to quickly cope with pain and dyspeptic syndrome during an exacerbation of the disease, and successful elimination H. pylori is the key to the rapid healing of the ulcer. Features of these two drug approaches - antisecretory therapy and infection eradication H. pylori- and determine the choice of one of them in each specific situation.

Data from an analysis of 21 clinical trials (N. Chiba, R.H. Hunt, 1999) that directly compared a proton pump inhibitor (omeprazole, lansoprazole, pantoprazole at a standard dose) with a histamine H 2 receptor blocker (cimetidine, ranitidine, famotidine at a standard dose) ) during exacerbation of duodenal ulcer, are very indicative. They once again confirm that proton pump inhibitors lead to faster ulcer healing in more patients than histamine receptor antagonists (Table 1). Processing of the study results allowed us to make some important conclusions, for example, to calculate the magnitude of the absolute risk reduction (the difference in the proportion of patients with a positive result of therapy in the group treated with proton pump inhibitors and in the group treated with histamine receptor antagonists). In gastric ulcer, the use of proton pump inhibitors is also more effective: according to a meta-analysis by C.V. Howden et al. (1993), who compared the percentage of patients with healed gastric ulcers during each week of use of various classes of antiulcer drugs, omeprazole, as a representative of proton pump inhibitors, was superior to all other drugs. The use of proton pump inhibitors is also characterized by a faster and more complete relief of symptoms of an exacerbation of the disease.

Analysis of a large number of clinical trials allows us to identify the best regimens for the treatment of infection H. pylori. They were reflected in the final document of the Conciliation Conference on the Diagnosis and Treatment of Infection H. pylori, held in Maastricht in 2000 . This document formulates recommendations on this problem for the countries of the European Union. The schemes of eradication therapy indicated in the Maastricht Consensus-II are shown in Table 2. Peptic ulcer of the duodenum and stomach, both in the acute stage and in remission, is an unconditional indication for the appointment of anti-Helicobacter pylori therapy

Whereas for peptic ulcer disease therapeutic approaches have been developed at the level of standard recommendations, backed up by vast clinical experience in evidence-based medicine, for the so-called "erosive gastroduodenitis" such significant experience does not exist. The ratio of peptic ulcer and chronic erosions of the gastroduodenal mucosa has not been precisely established, perhaps this is an independent disease, sometimes combined with peptic ulcer. Exploring meaning H. pylori played an undeniable positive role in this matter. M.Stolte et al. (1992) based on the study of biopsy material of 250 patients with chronic erosions and 1196 patients with gastritis caused by infection H. pylori without erosions showed that the number of microorganisms, as well as the severity and activity of gastritis, are higher in patients with erosions. Thus, it should be concluded that chronic erosions are the result of Helicobacter pylori gastritis. The next logical conclusion is the conclusion about the need for eradication therapy for erosive gastroduodenitis. However, the consequences of eradication therapy for chronic erosions have not been studied in detail. In the final document of the Consensus Conference on Diagnosis and Treatment of Infection H. pylori(Maastricht, 2000), only one form of gastritis, atrophic gastritis, has been established as an indication for eradication therapy. It is important to note that the Standards (protocols) for the diagnosis and treatment of patients with diseases of the digestive system, approved by the Ministry of Health of the Russian Federation, call anti-Helicobacter pylori regimens as necessary therapeutic measures for gastritis with the identification H. pylori. Thus, in the domestic healthcare practice, the treatment of erosions against the background of Helicobacter pylori gastritis with the help of microorganism eradication is legitimate. At the same time, any doctor has his own experience in the treatment of gastroduodenal erosions with antisecretory drugs - proton pump inhibitors and histamine H 2 receptor blockers, which leads to a rapid improvement in well-being and normalization of the endoscopic picture. Thus, as with peptic ulcer, with erosive gastroduodenitis, modern tactics of drug therapy allows you to choose one of two main options - treatment with active antisecretory drugs or eradication of infection H. pylori.

NSAIDs are currently one of the most widely used groups of drugs, without which it is often impossible to manage patients with a number of inflammatory and arthrological diseases. Acitylsalicylic acid is widely prescribed for prophylactic purposes in coronary heart disease. Erosive and ulcerative lesions of the stomach and duodenum are detected during endoscopic examination in 40% of patients who are constantly taking NSAIDs. In some patients, they manifest themselves as dyspeptic complaints, in some patients they are asymptomatic. Especially dangerous is the development against the background of an almost asymptomatic course of bleeding or perforation of an ulcer. The relative risk of these complications associated with taking NSAIDs is estimated in case-control studies as 4.7, in cohort studies as 2.

Not all patients taking NSAIDs develop gastropathy phenomena. Risk factors for the development of erosive and ulcerative lesions of the gastroduodenal zone and complications have been established (Table 3). So, according to F.E. Silverstain et al. (1995), in patients taking NSAIDs and having three aggravating factors (age, history of peptic ulcer and concomitant diseases), gastrointestinal problems developed in 9% of cases over six months of observation, while in patients without risk factors - only 0, 4% of cases. In recent years, NSAIDs have been developed that selectively inhibit the activity of only cyclooxygenase-2 and do not affect cyclooxygenase-1, which is important for the synthesis of prostaglandins in the stomach. These selective drugs have less damaging effect on the gastroduodenal mucosa.

The treatment of NSAID-gastropathy and their prevention have been the focus of several dozen large clinical studies, and therefore have a strong base of clinical evidence.

Misoprostol - a synthetic analogue of prostaglandin E 1 significantly reduces the risk of ulceration when taking NSAIDs. The study was of particular importance MUCOSA (F.E. Silverstain et al., 1995), which showed that misoprostol prevents serious gastrointestinal problems associated with NSAIDs - ulcer perforation, bleeding, narrowing of the gastric outlet. Therefore, misoprostol is considered as a first-line drug for the primary prevention of complications of NSAID gastropathy, especially in the presence of risk factors. However, side effects (often diarrhea and epigastric discomfort) are associated with its intake, which force patients to refuse the drug. Tolerability issues may be related to the lower efficacy of misoprostol in preventing ulceration in public health practice compared to results from controlled trials.

In clinical studies blockers H 2 -histamine receptors successfully prevented duodenal ulcers caused by NSAIDs, but the standard dose was not enough to prevent gastric ulcers. Only double doses of histamine H2 receptor antagonists (eg, famotidine 80 mg) are effective in preventing both duodenal and gastric ulcers with NSAIDs.

proton pump inhibitors proved to be effective in NSAID-gastropathy. Let us dwell on two clinical studies of significant interest for the problem under consideration. Research OMNIUM (comparison of the effectiveness of omeprazole and misoprostol in the treatment of ulcers caused by NSAIDs) and ASTRONAUT (comparison of the effectiveness of omeprazole and ranitidine in the treatment of ulcers caused by NSAIDs) were planned in two phases: a treatment phase of 8 weeks and a secondary prevention phase of 6 months. The studies included patients who required continuous use of NSAIDs, with endoscopically confirmed presence of gastric ulcers, duodenal ulcers and/or erosions. A large number of patients were examined, which allows us to speak about the high statistical significance of the results (OMNIUM - 935 people, ASTRONAUT - 541).

The results of the efficacy of omeprazole in healing NSAID-induced erosive and ulcerative lesions of the stomach and duodenum caused by NSAIDs, compared with misoprostol or ranitidine, are presented in Figures 1 and 2. Omeprazole (especially at a dose of 20 mg) is significantly more active than misoprostol for scarring of gastric ulcers. Omeprazole is particularly superior to misoprostol in scarring of duodenal ulcers. It is interesting to note that the healing of gastroduodenal erosions is more active when using a synthetic analogue of prostaglandin (the difference is significant). Omeprazole, both at a dose of 20 mg and at a dose of 40 mg, was more effective than ranitidine in the healing of gastric ulcers, duodenal ulcers or erosions caused by NSAIDs.

The second phase of these studies investigated the potential of omeprazole in the secondary prevention of erosive and ulcerative lesions caused by NSAIDs. Patients who managed to heal erosions or ulcers as a result of the first phase underwent repeated randomization and were selected into comparative groups, which were followed up for 6 months. In the OMNIUM trial, omeprazole 20 mg, misoprostol 400 mcg, or placebo were given maintenance therapy. The results presented in table 4 indicate the superiority of omeprazole as a drug for the secondary prevention of NSAID gastropathy. However, considering only the occurrence of erosions, misoprostol was more effective than either omeprazole or placebo. Omeprazole was more effective than ranitidine in preventing NSAID gastropathy in the ASTRONAUT study (Table 5).

Eradication therapy for infection H. pylori in NSAID-gastropathy is a controversial issue. In the Maastricht Consensus-II, NSAID gastropathy is named as one of the indications for anti-Helicobacter pylori treatment, but it is assigned to the second group of indications, when eradication can be considered appropriate. Indeed, if a patient with peptic ulcer takes NSAIDs, he needs to be treated H. pylori because NSAIDs and H. pylori are independent factors of ulcer formation. At the same time, the elimination of infection is unlikely to be a measure for the prevention of erosive and ulcerative lesions or to prevent bleeding in a situation where NSAIDs are required. As shown in the OMNIUM and ASTRONAUT studies, the absence H. pylori does not accelerate the healing of ulcers and erosions during antisecretory therapy.

Omeprazole, the gold standard drug for antisecretory therapy, has become available in a new dosage form. Classical omeprazole is a capsule, since the active substance is absorbed in the small intestine and it is necessary to protect it from the acidic environment in the stomach (this is true for all proton pump inhibitors). A new form of omeprazole - maps tablets ( Losek® maps® ), contain about 1000 acid-resistant microcapsules, the tablet quickly disperses in the stomach, enters the small intestine, and there comes the rapid absorption of omeprazole. This dosage form provides the best delivery of omeprazole to the targets - H +, K + -ATPase of the parietal cell, and as a result, a predictable and reproducible antisecretory effect. The bioequivalence of MAPs tablets and omeprazole capsules has been proven in clinical studies, its antisecretory effect has been well studied both in volunteers and in patients with various acid-dependent diseases. Thus, in case of erosive and ulcerative lesions of the gastroduodenal zone, discussed above, the MAPs tablets have the same effectiveness as the drug in the capsule. Not only is omeprazole tablet easier to swallow, it can be dissolved in water or juice, making it easy to use. The possibility of giving dissolved MAPs tablets through a nasogastric tube is especially relevant for seriously ill patients - a contingent of intensive care units, in whom the prevention of acute ulcers and erosions is an urgent task.

Dosage form of omeprazole for infusion expands the possibilities of using this proton pump inhibitor and has its own specific indications. Even a five-day course of intravenous drip infusions at a daily dose of 40 mg had a pronounced effect on the healing of erosive and ulcerative lesions of the stomach, duodenum and esophagus: with endoscopic control, erosion and ulcers healed during this time in 40% of patients diagnosed with duodenal ulcer, it was achieved a significant reduction in the size of the ulcer and the disappearance of erosion in other patients with duodenal ulcers and in all patients with gastric ulcers (V.T. Ivashkin, A.S. Trukhmanov, 1999). G. Brunner and C. Thieselmann (1992) reported on the rapid healing of gastric and duodenal ulcers in patients with the inability to take oral drugs for a short course - 14 days - of intravenous bolus administration of 80 mg of omeprazole in almost 90% of cases.

Of particular importance is the infusion form of omeprazole in the treatment of erosive and ulcerative lesions of the gastroduodenal zone, complicated by bleeding. Platelet aggregation does not occur at pH< 5,9; оптимальными для этого процесса являются значения рН в пределах 7-8. Повышение рН имеет принципиальное значение практически для всех этапов свертывания крови. При инфузионном введении омепразола (болюсно 80 мг, затем капельно из расчета 8 мг/час) средние значения рН 6,1 при суточной рН-метрии достигаются уже в первые сутки и стабильно поддерживаются в последующем (P. Netzer et al, 1999). Использование парентерального введения омепразола существенно уменьшает риск рецидива кровотечения из пептической язвы после эндоскопического гемостаза. Это было доказано в недавнем исследовании Y.W. James и соавторов (2000). Эндоскопический гемостаз осуществляли введением адреналина и термокоагуляцией, после чего больные рандомизированно получали или омепразол (80 мг внутривенно болюсно, затем капельно 8 мг/час в течение 72 часов), или плацебо. Затем в течение 8 недель всем больным назначали омепразол в дозе 20 мг per os. Критерием эффективности считалось предотвращение рецидива кровотечения в течение 30-дневного периода наблюдения: была показана необходимость назначения инфузионной терапии омепразолом после эндоскопического гемостаза для предотвращения повторного кровотечения (табл. 6). Инфузионная форма омепразола показана для профилактики возникновения стрессовых язв и аспирационной пневмонии у тяжелых пациентов. При подготовке к оперативному вмешательству у больных с осложненной стенозом привратника язвенной болезнью также может быть показано именно парентеральное введение омепразола, так как в связи с нарушением нормального пассажа может быть уменьшена эффективность пероральных препаратов.

Thus, erosive and ulcerative lesions of the stomach and duodenum are a common gastroenterological problem. Modern drug therapy allows using antisecretory drugs, among which proton pump inhibitors are in the lead, to achieve significant success in their treatment and prevention. Literature:

1. Diagnosis and treatment of Helicobacter pylori infection: current concepts (Report of the Second Consensus Conference in Maastricht, September 21-22, 2000). // Russian Journal of Gastroenterology, Hepatology, Coloproctology. - 2000. - No. 6. - S. 86-88.

Omeprazole -

Losek (trade name)

Losek Maps(tradename)

(AstraZeneca)

Aluminum hydroxide + magnesium hydroxide-

Almagel (trade name)

(Balkanpharma)

Damage to the stomach mucosa that does not affect the submucosa and muscle layers is commonly referred to in gastroenterology as gastric erosion.

In terms of frequency of occurrence, pathology belongs to one of those encountered in gastroenterology. Every sixth or seventh patient studied by the endoscopic method detects erosive processes in the organs of the digestive system.

The disease was first described by the Italian founder of pathological anatomy Giovanni Morgagnier in the middle of the 17th century. The disease has since undergone a change of several generations of diagnostic methods and methods of treatment, but the nature of the pathology and the features of its symptoms have remained the same.

Causes of the disease

Understanding the cause of gastric erosion opens up the correct treatment regimen. It is especially important to clarify the etiology of primary and secondary causes to eliminate symptoms. All causative factors of the disease fit into systematic categories.

Excessive or incorrect oral use of drugs that can initiate erosion processes. These include cardiac glycosides, non-steroidal anti-inflammatory drugs.
The mucous membrane is irritated by both temperature and mechanical factors, so the use of spicy, too coarse and hot food is fraught with erosive processes in the mucosa.
Alcoholic drinks cause damage to the mucosa, and smoking triggers the mechanism of damaging factors that contribute to the rapid flow of erosion. A cigarette smoked on an empty stomach can not only affect the mucous membrane, but also endanger the life of the patient.
Liver pathologies (cirrhosis) cause spasms in the blood vessels of the stomach. Due to the anatomical proximity and unity of the functional system, circulatory disorders are the cause of erosive processes.
Production and domestic work associated with the use of harmful and toxic substances. Penetrating into the human body in various ways (through the skin, respiratory and digestive systems), toxins are a source of erosion of the stomach.
in the stomach they tend to become covered with erosion or the onset of oncology is accompanied by irritation of the mucous membrane, therefore it is difficult to determine the primacy of the process in this case.
Operational and traumatic processes with the stomach are the root cause of erosion of the gastric mucosa.
Erosion of the gastric mucosa is naturally a consequence of deviations in the content of carbohydrates in the blood, observed in diabetes mellitus.

Symptoms

The clinical picture of gastric erosion has many similarities with peptic ulcer. For this reason, an accurate diagnosis can be established after several diagnostic methods.

Usually, with endoscopy, erosion looks like small spots on the mucosa, similar to sores. Often the disease proceeds without symptoms or the nature of the manifestation of symptoms is not bright (except for heartburn, there are no other clinical signs).

The photo shows the endoscopic diagnosis of gastric erosions

The classic manifestation of gastric erosion is reduced to a complex of phenomena:

Pain in the stomach is the main symptom of pathology. The nature of the pain has no specificity: the intensity may increase, then temporarily fade away, a slight pain may appear (the patient takes a drug like No-shpa) or pain tolerance becomes impossible. Severe pain indicates acute erosion. Pain of medium and low intensity is more dangerous, when their relief with analgesics contributes to the rapid growth of the focus of the disease.
Bleeding is a warning sign m requiring immediate medical attention. Surgical intervention can be dispensed with if blood impurities are found in the patient's vomit or feces. In the event that the vomit becomes dark brown in color and there are obvious signs of internal bleeding, it is not always possible to maintain the integrity of the stomach; to save the patient, they sometimes resort to ectomy of the affected part of the stomach.
Nausea and vomiting, in the absence of other signs, are not specific signs of erosive processes. Nausea and vomiting should not be excluded from the signs of erosion if their frequency becomes regular or the symptom is accompanied by other manifestations of the disease.
For signs of brittle nails and hair, as well as dryness of the skin, erosion of the stomach is judged on the basis of the physiological justification for the pattern of anemia due to internal bleeding. Low hemoglobin causes blue skin, thinning and unhealthy color of nails and hair.

Classification

Kinds

Primary

In medicine, it is customary to consider primary erosion of the stomach as a pathology that occurs in the stomach itself. Sometimes a pathology with an unclear etiology is taken for primary erosion.

Secondary

Secondary erosion of the stomach is a pathological process that is the consequences of disruptions in the work of other organs and functional systems (liver, heart and circulatory system).

Malignant

Erosive processes occur in oncological diseases of the gastrointestinal tract, as well as lymphogranulomatous inflammatory processes with fragmentary erosive lesions of the gastric mucosa (Crohn's disease).

Forms

Acute

Regardless of the systematic variety of gastric erosion, 2 forms of this disease are distinguished, one of which is acute. Localization of the acute form of organ erosion - the body of the stomach or its bottom.

With proper treatment and a successful combination of circumstances, the disease can be eliminated in 6-7 days, in more severe cases, treatment has to be resorted to for several weeks.

Chronic

The chronic form of gastric erosion usually shifts the localization of the pathology to the pyloric (antral) part of the organ. The chronic form is characterized by a longer treatment, sometimes taking up to 5 years.

Types

Hemorrhagic

In the hemorrhagic form, erosion is accompanied by the release of blood into the vomit and feces.

Often, the disease does not manifest itself with pronounced symptoms, but signs of anemia, confirmed by laboratory diagnostics, become pronounced on the face.

In this case, the patient's hemoglobin is reduced. The hemorrhagic form of the disease is characteristic of an acute course. During the study, the pathological formation is surrounded by a ring of small cherry-colored dots. It is usually the edges of the hyperemic ring that bleed.

Surface flat

Erosion ulceration looks the same as in the hemorrhagic form, but the ring surrounding the affected area has a whitish color, without signs of hyperemia. Flat defects during erosion have slightly convex edges, distinguishable by color due to slight hyperemia of adjacent tissues.

Hyperplastic inflammatory or complete

On endoscopic examination, complete erosion of the stomach is observed in the pyloric region. Bulges are visible under the mucosa of the organ, resembling erupting large molars: a crater-shaped shape with a depression in the center with signs of ulceration.

In some cases, the formations are not sufficiently visible due to hyperemic areas of the mucosa covering convex pathologies.

What is dangerous erosion of the stomach?

Untimely or illiterate treatment of gastric erosion increases the severity of the pathology and can develop according to one of the options:

Ulcerative condition. With an ulcer, damage to the stomach is localized not only in the internal membrane (mucosa), but also affects deeper layers (submucosa, muscular membrane). For the course of an ulcer, exacerbations and relapses of the disease are characteristic. An ulcer is a more dangerous form of stomach pathology, as it reveals the patient's weight loss, nausea and vomiting after any meal. Healing of erosion of the stomach is not accompanied by the formation of scars, with an ulcer, a section of the mucous membrane and a deeper layer is replaced by a connective scar tissue with a loss of functionality.
In the hemorrhagic form, internal bleeding causes a state of anemia. Kidney failure can be one of the options for the development of anemia. With vomiting, internal bleeding is recognized by the color and consistency of the coffee grounds.
Ulcerative-erosive conditions of the stomach have unpleasant possible consequences that worsen the quality of life for a long time: resection of a part of the stomach, a strict diet prior to surgery and during a long recovery period. Operations often take place in the state of an ulcer, although in rare cases erosive phenomena require surgical intervention.
Polyps in the stomach- one of the more severe reactions in response to mucosal irritation. occurs infrequently due to infrequent occurrence. The prognosis after resection of polyps is favorable.
The most dangerous development of erosion is a malignant neoplasm. The relationship between the two pathologies is bilateral: after the onset of gastric cancer, the pathologies are covered with erosive spots, and cancer can form at the site of erosion.

Diagnostics

Endoscopic examination is one of the few methods for detecting erosion. The procedure is unpleasantly painful for the patient, vomiting, however, a more informative method about the state of the gastric mucosa does not exist in modern times.

An endoscope is a telescopic tube that is inserted into the mouth and then through the esophagus into the stomach. necessary to study the histological section of the gastric mucosa.

The scheme of treatment of erosion of the stomach

Medicines

If the pathogenic bacterium Helicobacter pylori is detected, antibiotics are required.

In other cases, treatment does without antibacterial agents according to the scheme of using drugs - cytoprotectors (gastroprotector in the form of colloidal bismuth on a substrate or De-Nol tablets), proton pump inhibitors, synthetic prostaglandins and H2-blockers (Kvamatel). In secondary etiology, preference is given to prostaglandins and cytoprotectors.

Diet: menu for the week

Successful treatment of gastric erosion requires adherence to dietary nutrition by the patient as part of the treatment regimen. The nature of nutrition during treatment should have the direction of the absence of irritation and stimulation of the mucosa.

In this regard, rough foods rich in fiber, an excess of spices, spicy, salty and smoked dishes are excluded. Fatty foods, coffee, vegetables with bitterness (radishes), fruits with a high content of organic acids are excluded.

When choosing products, you should choose those that create an enveloping of the mucosa with a large amount of mucus (milk, low-fat sour cream, eggs, butter, milk porridge from oatmeal and semolina, low-fat hard cheeses, jelly).

The number of meals should be at least 6. At each meal, you should not eat a lot. You need to take only warm food, waiting for it to cool, but do not eat cold food.

Folk remedies at home

Healing is faster if the patient takes sea buckthorn oil 20-30 minutes before breakfast. To achieve a therapeutic effect, sea buckthorn oil is consumed three times a day before meals.

You can enhance the effect of the oil with linseed oil, for which both oils are mixed in half a spoon. Honey also has healing properties in relation to gastric erosion, but it is better to take it dissolved in warm water or milk.

Of herbal teas, infusions and decoctions, used both in mixtures and as a separate healing agent, have healing properties in relation to the gastric mucosa. The main plant used in the treatment of erosion is the great celandine. In the mixture, it can be used with common cudweed, highlander bird, St. John's wort, chemist's chamomile.

A glass of boiled hot water is poured over a mixture of herbs and after half an hour the product is ready for use. Three times a day, use 100 grams of this drink.

When pain occurs, bee propolis is used.

Epidemiology . Over the past decade in Ukraine, the number of patients with erosive and ulcerative lesions (EJI) of the gastrointestinal tract has increased. So, for example, only the number of patients with peptic ulcer (PU) of the stomach (F) and 12 duodenal ulcer (DU) increased by 38%, and the prevalence of these diseases reached 150 cases per 100 thousand of the population. There is also an increase in the complications of PU - the number of ulcer bleeding has increased over the same time by 2 times, which is associated with an increase in the prevalence of not only PU, but also symptomatic ulcers, especially those caused by the use of non-steroidal anti-inflammatory drugs (NSAIDs).

Damage to the gastric mucosa and duodenum, leading to the development of erosions and ulcers, may be associated with both the action of endogenous (hypersecretion, bile reflux) and exogenous ( Helicobacter pylori, NSAIDs, alcohol) aggressive factors, and a decrease in protective factors (decreased secretion of bicarbonates and synthesis of prostaglandins, impaired microcirculation).

Classification . EFP are usually classified by etiology into infectious (primarily HP-associated, as well as tuberculosis, syphilis); medication (most often NSAID-associated, as well as those associated with the use of glucocorticosteroids, reserpine, cytostatics); hemodynamic (with shock, vasculitis); endocrine (gastrinoma, hyperparathyroidism, pheochromocytoma, diabetes mellitus); neoplastic (cancer and lymphoma of the stomach); granulomatous (Crohn's disease, sarcoidosis). According to the depth of the lesion, EJP are divided into erosions (superficial, complete) and ulcers; by the nature of the process - into acute (symptomatic) and chronic; by prevalence - into single and multiple; by localization - on gastric (cardiac, body, pyloric, antral), duodenal (bulbous, post-bulbous) and erosion and ulcers of gastroenteroanastomosis (postoperative). Traditionally, PU is divided into active and inactive; to uncomplicated and complicated by perforation, penetration, bleeding, stenosis, malignancy.

Clinical manifestations The syndrome of dyspepsia in EJP is not very specific. Its main manifestation may be pain in the upper abdomen. It is localized in the epigastrium or pyloroduodenal zone, much less often in the left or right hypochondrium. The nature of the pain can be varied: burning, aching; sometimes the patient is only concerned about the feeling of hunger. Pain is most often periodic, usually lasting several weeks, disappearing on its own or when taking antacids or antisecretory drugs. Relapses are associated with stress or the change of seasons (spring, autumn). With the localization of the pathology in the stomach, pain occurs immediately after eating, and with a duodenal ulcer, “hungry” and night pains are characteristic.

Ulcers of the pyloric canal are very often accompanied by symptoms of a transient violation of evacuation from the stomach - heaviness in the epigastrium, rapid satiety, belching, vomiting. When the ulcer is located in the cardial part of the stomach, the patient may be disturbed by retrosternal pain, which is aggravated in a horizontal position, which often requires differential diagnosis with heart disease.

In many patients, pain may be mild or absent, while other manifestations of dyspepsia syndrome may come to the fore - heaviness in the epigastrium, nausea, vomiting, heartburn. Unfortunately, in some patients, especially those with symptomatic ulcers, the disease can manifest itself only by its complications - perforation or bleeding. At the same time, the uncomplicated course of EJP is often clinically completely asymptomatic.

Diagnostics . If EJP is suspected, endoscopic examination is indicated to confirm the diagnosis. Previously widely used X-ray diagnostic methods turned out to be of little information, especially in the presence of erosions and acute ulcers. Currently, an x-ray examination is performed when endoscopy is impossible, if a malignant nature of ulceration is suspected (modern methods are more informative - NMR and X-ray tomography and / or intragastric sonography) and, if necessary, an assessment of the evacuation function of the stomach. However, the identification of erosions and ulcers in the stomach or duodenum requires further clarification of the etiological causes of the disease listed above.

Etiology . The most common cause of EEP is Helicobacter pylori infection. As shown by large-scale studies conducted in many countries of the world, 70-80% of duodenal ulcers and up to 50-60% of gastric ulcers are associated with this infection. HP is a unique microorganism that has adapted to life in the highly aggressive environment of the stomach, using the ability to break down urea to form ammonia, a substance that has an alkaline environment, to protect against hydrochloric acid. This microorganism can cause various types of gastric lesions: acute and chronic gastritis, peptic ulcer, MALToma (Mucosa-associated lymphoid tissue lymphoma) and carcinoma. Helicobacter pylori infection is transmitted by the fecal-oral and oro-oral route, so children living in large families are most easily infected, especially under poor living conditions. This is more typical for developing countries, to which our country can be attributed to some extent. In Ukraine, many people are infected with HP in childhood, and in adults it reaches 70-90%. In industrialized countries, the incidence of HP infection is much lower - 0.5-1% per year.

The mechanisms of damage to the gastric mucosa and duodenum in H. pylori infection include both a decrease in resistance and an increase in aggressiveness. HP after adhesion to epitheliocytes immediately causes an increase in the synthesis of pro-inflammatory interleukins and the attraction of leukocytes from the bloodstream. A typical inflammatory reaction occurs, leading to varying degrees of damage to the CO. Toxins produced by HP also damage the mucosa, activate inflammation and impair microcirculation, which exacerbates the changes that have occurred. In patients with helicobacteriosis, gastric secretion first increases, i.e., the aggressiveness of gastric juice increases. This is due to the predominant damage to D-cells that produce somatostatin (histamine antagonist), which stimulates histamine-mediated gastric secretion. It should be noted that only 10% of people infected with HP develop EFP, while the rest have chronic non-erosive gastritis. The strains that produce a vacuolating toxin and a cytotoxic protein are most often led to ENP. Of great importance are the features of the human immune response and the hereditarily determined mass of the glands of the body of the stomach and the presence of receptors for HP adhesins on epitheliocytes.

Diagnosis of HP infection carried out using a variety of tests. Biopsy specimens of CO, blood, feces, saliva, dental plaque can serve as material for the study. Depending on the method of obtaining biological materials, non-invasive tests are distinguished (urease respiratory, serological determination of antibodies to HP in saliva and feces, polymerase chain reaction [PCR] in saliva, feces and plaque) and invasive (determination of urease activity, fragments of Microorganism DNA by PCR, direct HP microscopy, detection of antibodies to HP in blood serum).

Usually, the first diagnostic test for HP in our country is the determination of the urease activity of the gastric mucosa during endoscopic examination and microscopic identification of the pathogen in biopsy specimens of the mucosa. Non-invasive diagnostic methods are most often used to assess the completeness of HP eradication not earlier than 4 weeks after completion of anti-Helicobacter therapy.

In the case of negative tests for HP, other causes of EJP must be excluded. Most often this turns out to be gastroduodenopathy associated with NSAIDs. The mechanism of damage to the gastric mucosa and duodenum when taking these drugs is both inhibition of cyclooxygenase-1 (COX-1) with a subsequent decrease in the synthesis of prostaglandins, and direct damage to the mucosa by the drugs themselves. As you know, COX-1 is present in all tissues of the body, including the gastrointestinal mucosa. Here it stimulates the production of prostaglandins E 2 , I 2 , F 2 , which increase the resistance of the mucosa to damage. The protective effect of prostaglandins is to stimulate the secretion of mucus bicarbonates, increase blood flow and cell proliferation, and stabilize cell lysosomes and membranes. Depending on the chemical structure of NSAIDs, the risk of developing gastropathy ranges from 4% for diclofenac to 74% for ketoprofen. Ultrastructural changes in the mucosa can develop within a few minutes after taking NSAIDs, macroscopic - after a few days.

More selective COX-2 inhibitors - nimesulide, meloxicam ( movalis), celicoxib, roficoxib.

Factors that increase the risk of EEP when taking NSAIDs include:

age over 65 years;

history of peptic ulcer;

large doses and / or simultaneous intake of several NSAIDs;

treatment with glucocorticosteroids;

long duration of therapy;

· female;

smoking;

alcohol intake;

presence of HP.

For the diagnosis of NSAID gastropathy, esophagogastroduodenoscopy is indicated, which should be performed in all patients taking these drugs and having an increased risk of complications, regardless of the presence of any complaints. Repeated endoscopic examinations are performed every 6 months. In contrast to peptic ulcer, in patients with NSAID-gastropathy, ulcerations are often multiple, they are localized in the body of the stomach, periulcerous inflammation is not very pronounced.

In patients with long-term non-scarring ulcers, it is necessary to exclude primary ulcerative form of stomach tumors- carcinoma, much less often lymphoma. Risk factors for the development of gastric cancer include pronounced dysplasia and metaplasia of the epithelium, which develop against the background of a long-term atrophic gastritis, which in most cases is associated with HP. Polyposis of the stomach is also of great importance. The opinion that existed earlier (in the "pre-endoscopic era") about the high frequency (up to 50%) of malignancy of primary benign PU was not confirmed by subsequent studies; in reality it does not exceed 2%. Quite often, against the background of active antiulcer therapy with modern antisecretory drugs, epithelialization of even malignant ulcers occurs. In this regard, all patients with localization of the ulcer in the stomach before the start of treatment need morphological verification of its benign nature, which requires gastrobiopsy both from the periulcerous zone and from the scar zone. If the diagnosis of a stomach tumor is confirmed, the patient should be treated by surgeons and oncologists.

The detection of multiple erosive and ulcerative lesions of the gastric mucosa is very often a manifestation symptomatic non-helicobacter lesions. In this situation, it is necessary to think about the so-called rare diseases: Zollinger-Ellison syndrome (gastrinoma), hyperparathyroidism, systemic vasculitis. Somewhat more often, such changes in the mucous membrane are associated with systemic or local circulatory disorders (stress ulcers). Classical examples of such ulcers are Cushing's and Curling's ulcers associated with burns, acute cerebrovascular accident, shock in myocardial infarction, or acute blood loss. Shock ulcers are usually difficult to diagnose, as there are practically no symptoms of dyspepsia, and signs of shock come to the fore. Very often, the first and only manifestation of such ulcers are symptoms of complications - bleeding or perforation.

Over the past two decades, approaches to peptic ulcer treatment , since the principle “no ulcer without acid” proposed more than 90 years ago was replaced by the principle “no ulcer without Helicobacter and acid”. Therefore, the development of effective methods for eliminating HP infection and the emergence of new antisecretory drugs have led to what was previously considered chronic, i.e. incurable, PU can currently be completely cured.

Much less importance is now given to diet therapy. Numerous studies have shown that with adequate drug therapy there is no significant difference in the timing of ulcer scarring, depending on whether or not patients comply with a strict diet. Elimination of alcohol, caffeinated beverages and individually intolerable foods, as well as smoking cessation, are considered appropriate. Most patients with uncomplicated ulcers can be treated on an outpatient basis and do not require mandatory hospitalization.

It is well known that for successful scarring of the ulcer, it is necessary to increase the intragastric pH to 3 or more and maintain it for at least 18 hours a day. In this regard, antacids have almost completely lost their significance, since it turned out that in order to adequately reduce gastric secretion, their very frequent use in large doses is necessary. The M-cholinergic blockers that replaced them also turned out to be insufficiently effective. Remain important in antisecretory therapy blockers of the second type of histamine receptors - ranitidine, famotidine ( kvamatel), nizatidine. However, due to insufficient antisecretory activity, they are not recommended for the treatment of ulcers as first-line drugs; they are used with great effect in patients with ulcer-like form of FD.

The main group of antisecretory drugs at present are PPIs - drugs that act on the final link of gastric secretion and suppress the release of hydrochloric acid by 90% or more. There are several generations of these drugs, but the most common in our country are omeprazole (1st generation) and lansoprazole (2nd generation). As our studies confirm, they allow achieving a high frequency of scarring of ulcers (over 80%) within 10 days of taking even without anti-Helicobacter pylori drugs. Due to the higher cost, rabeprazole, pantoprazole, esomeprazole, which belong to subsequent generations, are used much less frequently in Ukraine, although esomeprazole today ranks first in the world in terms of sales among all PPIs.

Based on data from multicenter clinical trials (GU-MACH, 1997 and DU-MACH, 1999), numerous recommendations have been developed for the treatment of diseases associated with HP. In September 2000, the second Maastricht agreement was adopted, providing for mandatory anti-Helicobacter therapy for gastric ulcer and duodenal ulcer (both active and inactive), MALToma, atrophic gastritis; treatment of HP-positive patients after gastric resection for cancer and their relatives of the 1st degree of kinship is also recommended. Treatment regimens have also been developed. Schemes are considered effective that provide elimination (eradication) of HP in at least 80-85% of patients, preferably with minimal side effects.

To first line therapy (triple therapy) includes a combination of PPI or ranitidine-bismuth-citrate (not registered in Ukraine) with two antibacterial drugs: clarithromycin and amoxicillin or clarithromycin and metronidazole for at least 7 days. Second line therapy (quadrotherapy) involves the appointment of a PPI in combination with a bismuth drug, metronidazole and tetracycline also for a minimum of 7 days.

Unfortunately, the irrational use of antibacterial drugs has led to the emergence of HP strains resistant to metronidazole or clarithromycin. The true prevalence of such strains in Ukraine is unknown, however, in some regions, 70% of microorganisms were resistant to metronidazole. Clarithromycin-resistant strains are much less common, because due to the high cost and the recent appearance of this antibiotic in our country, they simply did not have time to appear. Nitrofurans have been proposed as an alternative to metronidazole, and azithromycin may be a cheaper substitute for clarithromycin. There are reports of studies demonstrating the effectiveness of rifampicin and fluoroquinolones.

In the stomach, for some reason, various damages can occur. In some cases they are minor, in others they are very dangerous. Consider two types of serious defects, or rather, find out how erosion differs from an ulcer.

Definition

Erosion of the stomach- a pathology that affects the mucous membrane of the corresponding organ.

Ulcer- a defect that is characterized by deep penetration into the tissues of the stomach.

Comparison

Two phenomena in some cases represent steps of a single destructive process. At the same time, the difference between erosion and ulcers is that the first of them is formed at an early stage, and the second - after some more time.

Initially, there is a negative impact of one or more factors. Disturbances in the stomach can occur, for example, with irregular meals, the constant use of hot liquids or the intake of irritating medications. All this, and much more, can lead to the destruction of mucosal cells and the occurrence of erosion.

It is a milder form of the disease, since it affects only the surface layer. In this case, the damaged area has a rounded or jagged shape and differs in color from the surrounding healthy tissues. The integrity of the mucosa during erosion can be violated simultaneously in several places, which aggravates the situation.

The development of erosion is evidenced by spasms, discomfort when food is ingested, as well as bloody inclusions in feces or vomiting. Fortunately, such a defect does not always degenerate into an ulcer. The disease process may stop at this stage, especially if the necessary treatment has been carried out. With a favorable outcome, the tissues are completely restored, not even a scar remains.

But if the provoking factors continue to act and the person is in no hurry to see a doctor, there is a risk of earning a more dangerous defect - an ulcer. With it, in addition to the mucous membrane, the deeper layers of the organ are also corroded. Unlike erosion, this damage is detected not only during endoscopic, but also during X-ray examination.

What is the difference between erosion and ulcer in terms of symptoms? The fact that the latter, for obvious reasons, is felt stronger. Pain here occurs during and after eating. The stomach may not accept food consumed, vomiting occurs. An ulcer is often accompanied by severe heartburn, periodic stool disorders.

The disease is treated for a long time and tends to periodically worsen. The diet is prescribed in both cases, but with an ulcer it is more strict. In place of such a deep defect, with successful healing, a scar remains.