Chronic subatrophic gastritis: measures taken during treatment

Alcoholic gastritis is an inflammation of the stomach lining due to exposure to alcohol. Treatment of alcoholic gastritis involves abstaining from alcoholic beverages as the main irritant and cause of the development of the disease. But since almost no one wants to completely give up alcohol, you need to figure out what drinks you can drink with gastritis, and what alcohol it is better to completely give up.

Important : The alcoholic form of the disease, which is a mucous membrane burned and inflamed due to alcohol, should not be confused with the bacterial form of ordinary gastritis. With chronic gastritis of the stomach, you can drink other alcoholic beverages and in other quantities.

Diagnostics

Diagnostic criteria

Complaints and anamnesis: pain in the navel and pyloroduodenal area, severe dyspeptic symptoms (nausea, belching, heartburn, less often - vomiting); combination of early and late pain; loss of appetite, weakness, fatigue, headache, sleep disturbance, local hyperhidrosis.

Physical examination: signs of polyhypovitaminosis, moderate symptoms of chronic intoxication, pain in the pyloroduodenal area in the navel area.

Laboratory tests: CBC, OAM - without features, coprogram - symptoms of impaired digestion (determination of neutral fat, undigested muscle fibers), feces may be positive for occult blood. Diagnosis of H. pylori (cytological examination, ELISA - detection).

Instrumental studies: fibrogastroduodenoscopy - endoscopic changes in the mucous membrane of the stomach and duodenum (swelling, hyperemia, hemorrhage, erosion, atrophy, hypertrophy of folds, etc.).

Indications for consultation with specialists:

3. Physiotherapist.

List of main diagnostic measures:

1. General blood test (Er, Hb, L, leukoformula, ESR).

2. General urine analysis.

4. Ultrasound of the abdominal organs.

6. Diagnosis of H. pylori (breath test, HpSA in stool, determination of IgG to HP, urease test, brush cytology).

7. Consultation: dentist.

9. Consultation: neurologist.

List of additional diagnostic measures:

2. Histological examination of the biopsy specimen.

3. Daily pH-metry of the upper gastrointestinal tract - (implementation required).

4. Determination of serum Fe.

5. Determination of diastase.

7. Study of gastric juice.

8. X-ray examination of the upper gastrointestinal tract with barium.

Types of chronic gastritis and ICD-10

Any branch of healthcare has its own statistical and methodological standards, as well as a system according to which gradation is carried out.
In the section that combines the diseases described to date, this is the International Classification of Diseases, 10th revision. In daily clinical practice, for convenience, this classification is usually called ICD-10. It is international in nature and designed to provide common starting points for diagnostic criteria for known diseases. The system is adopted for the work of practicing specialists in the field of medicine. This regulatory document is reassessed every 10 years. The complete edition of the classification consists of three volumes. This includes instructions for use, the classification itself and a short alphabetical index.

In the classification, the names of the disease are encrypted with a special code consisting of Latin letters and Arabic numbers. Acute or chronic gastritis according to ICD-10 reveals a number of varieties in morphology and severity of clinical manifestations. Acute gastritis according to ICD-10 is assigned code K 29.1

Differential diagnosis

Diseases

Clinical criteria

Laboratory indicators

Pain in the right hypochondrium, pain on palpation in the area of ​​​​the gallbladder projection, low-grade fever or periodic rises in temperature to febrile levels, intoxication

In the blood - leukocytosis, neutrophilia, accelerated ESR. Ultrasound reveals thickening of the gallbladder wall, mucus flakes in it, bile stagnation, perivascular reaction

Localization of pain on the left above the navel with irradiation to the left, there may be girdling pain

Medical terminology

Today, doctors do not use the entry “Chronic subatrophic gastritis”, since this is an outdated name, and there is also a hidden tautology.

How is this diagnosis interpreted:

  1. “Chronic”: old, sluggish, protracted course. That is, a long-standing, slowly developing pathological process.
  2. “Subatrophic”: the term consists of 2 parts. The prefix “ sub ” also indicates an ongoing pathological process of low intensity (chronic) course. The word “atrophic” (from atrophia ) suggests that the cells of the mucous membrane are reduced due to disruption of their nutrition and the tissue of the membrane loses weight, volume, and ceases to function properly.
  3. “Gastritis”: the term includes 2 parts “ gastro─ ” (stomach) and “─it (inflammation). This phrase means that the gastric mucosa is inflamed. In some cases, the pathological process spreads to all the membranes of the organ.

Now, after an examination, doctors write down a diagnosis of “chronic atrophic gastritis” or “subatrophic gastritis” in conclusion. They may also use other terms if during diagnosis they discover a different type or form of pathology.

Synonyms of the disease: chronic atrophic gastritis, Inveterata atrophic gastritis, chronic atrophic gastritis, subatrophic gastritis, subatrophic gastritis.

Treatment

Treatment tactics

Treatment goals:

- relieving the exacerbation of the disease;

— relief of pain and dyspeptic syndromes;

— eradication of Helicobacter pylori.

Therapy should be aimed at:

1. Reducing the excessive impact of aggressive factors by eliminating them (eradication of H. pylori) and neutralizing them directly in the lumen of the stomach and normalizing the secretory-motor activity of the stomach.

2. Improving the quality of the protective properties of the mucous membrane (M) of the stomach and duodenum by enhancing the formation of mucus, stimulating the secretion of bicarbonates in the antrum of the stomach, improving the trophism of the M, normalizing its reparative properties, etc.

3. Impact on the autonomic nervous system in order to correct the disturbed balance between its sympathetic and parasympathetic departments.

Non-drug treatment

Diet No. 1 (1a, 5) with the exclusion of dishes that cause or enhance the clinical manifestations of the disease (for example, hot seasonings, pickled and smoked foods). Small meals, 5-6 times a day.

Drug treatment

In accordance with the Maastricht consensus (2000) on methods of treating HP infection, priority is given to regimens based on proton pump inhibitors, as the most powerful of the antisecretory drugs. It is known that they are able to maintain a pH of more than 3 in the stomach for at least 18 hours a day, which ensures the reverse development of the inflammatory process of the mucous membranes of the stomach and duodenum. In addition, PPIs themselves have antibacterial activity. In terms of anti-Helicobacter activity, rabeprazole is superior to other PPIs /7/ and, unlike other PPIs, is metabolized non-enzymatically and is excreted primarily through the kidneys /8/. This metabolic pathway is less dangerous in terms of possible adverse reactions when combining PPIs with other drugs that are competitively metabolized by the cytochrome P450 system /8/.

First-line therapy is triple therapy.

Proton pump inhibitor (rabeprazole or omeprazole 20 mg, or lansoprazole 30 mg, or esomeprazole 20 mg) + clarithromycin 7.5 mg/kg (max-500 mg) + amoxicillin 20-30 mg/kg (max 1000 mg) or metronidazole 40 mg/kg(max 500 mg); All medications are taken 2 times a day for 7 days. The combination of clarithromycin with amoxicillin is preferable to clarithromycin with metronidazole, as it may help achieve a better outcome when prescribing second-line therapy.

In case of ineffectiveness of first-line drugs, unsuccessful eradication, a second course of combination therapy ( quadruple therapy ) is prescribed with the additional inclusion of colloidal bismuth subcitrate at 4 mg/kg (max 120 mg) 3 times a day for 30 minutes. before meals and the 4th time 2 hours after meals, before bed. The inclusion of this drug potentiates the anti-Helicobacter effect of other antibiotics.

Rules for the use of anti-Helicobacter therapy:

1. If the use of a treatment regimen does not lead to eradication, it should not be repeated.

2. If the regimen used did not lead to eradication, this means that the bacterium has acquired resistance to one of the components of the treatment regimen (nitroimidazole derivatives, macrolides).

3. If the use of one and then another treatment regimen does not lead to eradication, then the sensitivity of the H. pylori strain to the entire range of antibiotics used should be determined.

4. If bacteria appear in the patient’s body a year after the end of treatment, the situation should be regarded as a relapse of the infection, and not as a reinfection.

5. If the infection recurs, it is necessary to use a more effective treatment regimen.

After the end of combined eradication therapy, it is necessary to continue treatment for another 1 week using one of the antisecretory drugs. Preference is given to proton pump inhibitors (rabeprazole, pantoprazole, omeprazole, esomeprazole), because after discontinuation of the latter (unlike histamine H2 receptor blockers), the so-called secretory “rebound” syndrome is not observed.

In order to reduce the tone and contractile activity of the smooth muscles of internal organs and reduce the secretion of exocrine glands, hyoscine butyl bromide (buscopan) is prescribed 10 mg 2-3 times a day. If necessary - antacids (maalox, almagel, phosphalugel), cytoprotectors (sucralfate, de-nol, ventrisol, bismofalk), synthetic prostaglandins E1 (misoprostol), mucous membrane protectors (solcoseryl, actovegin), vegetotropic drugs (Pavlov's mixture, valerian root infusion ). The duration of treatment is at least 4 weeks /5/.

Other classifications

In addition to the international classification of diseases, ICD 10, a number of different classifications have been developed that are widely used throughout the world. They are sometimes more convenient for clinical use than ICD-10, which is primarily aimed at statistical recording.

For example, in the 90s of the last century the “Sydney Classification” was developed. It includes two criteria by which diseases are classified. The histological section includes etiological factors, morphology and topographic criteria. According to the classification, all chronic inflammatory processes in the stomach are divided into Helicobacter, autoimmune, and reactive. Endoscopic classification considers the severity of mucosal edema and hyperemia of the stomach walls.

In recent years, a fundamentally new gradation of inflammatory processes in the stomach has been developed. The division of pathological conditions is carried out taking into account the severity of morphological changes. The advantages include the fact that it becomes possible to determine the extent of the spread of the pathological process and determine the severity of atrophy based on the results of the therapy.

Information

Sources and literature

  1. Protocols for diagnosis and treatment of diseases of the Ministry of Health of the Republic of Kazakhstan (Order No. 239 of 04/07/2010)
  1. Clinical recommendations based on evidence-based medicine: Trans. from English / Ed. I.N. Denisova, V.I. Kulakova, R.M. Khaitova. - M.: GEOTAR-MED, 2001. - 1248 p.: ill. Evidence-based medicine. Annual directory. - M - Media Sphere, 2003. Gastritis. Philadelfia: Intracorp, 2005. M.Yu.Denisov. Practical gastroenterology for pediatricians.-M, 1999. Children's gastroenterology / ed. A.A. Baranova - M. 2002, 592 p. Kawacami Y., Akahane T., Yamaguchi M. et al. In vitro activities of rabeprazole, a novel proton pump inhibitor, and its thiother derivative alone and in combination with other antimicrobials againts recent clinical isolates of H. pylori. Antimicrob Agents Chemother, 2000. vol.44, N2.-P.458-461. H. Holtmann, P. Bytzer, M. Metz, V. Loeffler. A randomized, double-blind, comparative study of standard-dose rabeprazole and high-dose omeprazole in gastro-oesophageal reflux disease/ Aliment Pharmacol Ther 2002; 16: 479-485 Diseases of older children, a guide for doctors, R.R. Shilyaev et al., M, 2002 Practical gastroenterology for pediatricians, V.N. Preobrazhensky, Almaty, 1999

Information

Head of the Department of Gastroenterology of the Aksai Children's Clinical Hospital, F.T. Kipshakbaeva.

Assistant at the Department of Childhood Diseases of KazNMU named after S.D. Asfendiyarova, Ph.D., S.V. Choi.

Doctor of the gastroenterology department of the Aksai Children's Clinical Hospital V.N. Sologub.

GASTRITIS - inflammation of the gastric mucosa. Gastritis can occur in acute or chronic (slowly developing over several months or years) form.

The cause of gastritis is most often the bacterium Helicobacter pylori, which affects the gastric mucosa. Also, chronic gastritis can occur against the background of an inflammatory disease - Crohn's disease, characterized by inflammation of the digestive tract. Long-term use of alcohol, aspirin or NSAIDs can also lead to chronic gastritis.

One form of gastritis , known as atrophic or autoimmune gastritis, is a consequence of a pathological reaction of the immune system (antibodies are produced that destroy the tissue of the gastric mucosa).

Chronic gastritis often occurs without significant symptoms, but as a result of chronic gastritis, gradual damage to the gastric mucosa can occur, which will ultimately manifest itself in symptoms similar to those of acute gastritis. Symptoms of acute and chronic gastritis are:

  • pain or feeling of comfort in the stomach, often after eating;
  • nausea and vomiting;
  • loss of appetite;
  • stomach bleeding (may not appear until anemia develops); In case of severe bleeding due to gastritis , vomiting of blood or dark, tar-like stools may be observed.

Atrophic gastritis often occurs without pain, and the only symptom of atrophic gastritis may be pernicious anemia, leading to a deficiency of vitamin B12 in the body. In atrophic gastritis, the stomach is unable to produce enough intrinsic factor, a protein necessary for the absorption of vitamin B12. Patients suffering from atrophic gastritis have an increased risk of developing stomach cancer.

What alcoholic drinks can you drink if you have gastritis?

Alcohol is generally contraindicated for gastritis and you should not drink it. However, such serious celebrations as birthdays are rarely complete without a wide range of alcoholic drinks. Among them there should be those that you can drink for gastritis during remission, without fear of too serious consequences.

  1. Unfiltered beer. We are talking about fresh beer that does not contain preservatives. Even in various beverage stores it is almost impossible to find such beer. But in beer bars and restaurants you can order fatty, unfiltered beer. One mug of such a drink should pass without any noticeable harm to health. Increasing the dosage is at the patient's own risk.
  2. High quality spirits. High-quality strong alcohol like cognac and vodka will not cause much damage during remission of gastritis. Again, the amount of alcohol more than one or two shots leads to intoxication and all other consequences of alcohol poisoning, and here there is no need to talk about the absence of harm to health.
  3. Dry red wine. In addition to alcohol, it contains antioxidants and other beneficial substances. Therefore, 150-200 grams of wine will most likely only benefit the body. If you start drinking wine in bottles, the harm will naturally be greater than the benefit.

It should be remembered that alcohol should not be consumed on an empty stomach. You will also have to re-read the instructions for the medications you are using to determine their compatibility with alcohol. If you experience discomfort after drinking alcohol, you should not take the usual analgesics to prevent double load on the liver.

Symptomatic manifestations

Damage to the stomach in the final section is characterized by clinical manifestations associated with food intake. After eating, the following symptoms occur:

  • belching;
  • feeling of fullness in the stomach;
  • heartburn;
  • severe nausea;
  • vomiting with a bitter taste, often - vomit contains bile;
  • pain occurs in the epigastric region some time after eating;
  • decreased appetite;
  • unpleasant, bitter taste in the mouth;
  • bowel disorders with a tendency to constipation or diarrhea;
  • dry and vulnerable skin;
  • signs of asthenia.

The listed subjective and objective signs cannot be used to make a diagnosis. Next you need to go through the diagnostic stage.

Reasons for the development of pathology

In addition to the above-mentioned cause and effect relationships, there are a number of factors that can lead to gastritis of the pyloric stomach. Among them it is worth mentioning the following:

  • chronic diseases of the duodenum;
  • increased pressure in the lower intestines;
  • prolonged irritation of the mucous membrane by taking certain medications;
  • impaired motor function with backflow of duodenal contents;
  • smoking;
  • alcohol abuse;
  • diet with a predominance of fatty, spicy, smoked foods;
  • low physical activity;
  • a combination of external factors and internal causes.

All these reasons and factors lead to the reverse movement of the food bolus, which is not physiological.

Useful video

The causes of the disease and other important issues are discussed in this video.

Treatment prognosis

Unfortunately, pathologically affected and degenerated mucosal cells cannot be restored. This significantly worsens the prognosis of treatment.

If you do not seek medical help in a timely manner, even the deep layers of the membrane atrophy. In thinned areas, the ability of cells to participate in the secretion of secretions, enzymes, and hydrochloric acid is completely lost, and the higher the degree of damage, the more the functioning of the entire digestive system and other internal organs is disrupted.

Conclusion

If you suspect the development of gastritis, it is recommended to undergo examination as soon as possible and begin treatment. Any delay increases the risk that simple inflammation of the membrane will develop into more complex forms of the disease.

In the case of the development of subatrophic gastritis, the treatment prognosis will be favorable only if a person starts taking the medicine in the initial stages of the pathology, while the glandular tissue has the ability to recover. A belated start of therapy can only stop the progression of the disease, but not save the functionality of the organ.

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