Basic therapy drugs of the 1st stage are capable of maintaining the level of intragastric pH at a level of >3 during the day for only a relatively short time - up to 8-10 hours. Therefore, it is advisable to prescribe them when the course of a peptic ulcer is favorable: rare and short-lived exacerbations, small size of the ulcer, a moderate increase in acid production, and the absence of complications.

Basic therapy drugs of the 2nd stage maintain the level of intragastric pH for a much longer time - up to 12-18 hours. They are indicated, first of all, for frequent and prolonged exacerbations of the disease, large (over 2 cm in diameter) sizes of the ulcerative defect, pronounced hypersecretion of hydrochloric acid, the presence of complications (including anamnestic ones), and concomitant erosive esophagitis.

ANTACIDS

Classification

Traditionally, the group of antacid drugs is divided into absorbable(sodium bicarbonate, calcium carbonate, magnesium oxide) and non-absorbable antacids (aluminum hydroxide, aluminum phosphate, magnesium hydroxide, magnesium trisilicate).

Absorbed antacids are rarely used in clinical practice, due to the large number of adverse reactions. By entering into a direct neutralization reaction with hydrochloric acid, these drugs give a quick but very short-lived effect, after which the intragastric pH levels decrease again. The resulting carbon dioxide causes belching and bloating; a case of gastric rupture has been described after taking a large amount of sodium bicarbonate. Taking absorbable antacids (in particular calcium carbonate) can lead to a “rebound” phenomenon, that is, a secondary increase in the secretion of hydrochloric acid after the initial alkalizing effect. This phenomenon is associated both with the stimulation of gastrin-producing cells and with the direct effect of calcium cations on the parietal cells of the gastric mucosa.

Sodium bicarbonate and calcium carbonate are almost completely absorbed in the gastrointestinal tract and change acid-base balance organism, leading to the development of alkalosis (). If their intake is accompanied by the consumption of large amounts of milk, then “milk-alkali syndrome” may occur, manifested by nausea, vomiting, thirst, headache, polyuria, tooth decay, and the formation of kidney stones. However, this syndrome usually occurs only when taking very large doses of calcium carbonate (30-50 g per day), which is extremely rare in clinical practice.


Rice. 1.

Sodium bicarbonate can negatively affect water-salt metabolism. For example, at a dose of 2 g, it can retain fluid to the same extent as 1.5 g of sodium chloride. Therefore, in patients, especially the elderly, edema may appear, blood pressure may increase, and signs of heart failure may increase.

Numerous shortcomings of absorbed antacids have led to their almost complete loss of their importance in the treatment of ulcers. Currently, when using the term “antacids,” only non-absorbable antacid drugs are meant: Maalox, phosphalugel, almagel, gastal, etc.

Pharmacodynamics

Non-absorbable antacids differ from each other in chemical composition and activity. Carbonate, bicarbonate, citrate and phosphate anions can be used to neutralize hydrochloric acid, but hydroxides are most often used. Most modern antacids also contain magnesium and aluminum cations. Non-absorbable antacid drugs do not have many of the disadvantages of absorbable ones. Their action is not limited to a simple neutralization reaction with hydrochloric acid and therefore is not accompanied by the occurrence of the “ricochet” phenomenon, the development of alkalosis and milk-alkali syndrome. They realize their effect mainly by adsorbing hydrochloric acid.

The solubility of magnesium hydroxide is very low, so the content of OH - ions does not reach high concentrations. Despite this, magnesium hydroxide actively interacts with H + ions and is the fastest-acting antacid. Aluminum hydroxide is also poorly soluble in water; it acts more slowly than magnesium hydroxide, but lasts longer. Thus, the combination of magnesium hydroxide and aluminum hydroxide seems optimal from the point of view of achieving a quick (within a few minutes) and fairly long-lasting (up to 2-3 hours) alkalizing effect.

The acid neutralizing activity (ANA) of antacids (expressed in milliequivalents of neutralized hydrochloric acid) varies widely and is not the same for different antacid drugs. According to studies of the antacid properties of Maalox and Almagel, conducted using intragastric pH-metry, after taking standard doses of these drugs (15.0 ml of suspension), the time for the onset of the pH response after taking Maalox was half as long as after taking Almagel, and the “alkaline time ", on the contrary, is twice as long. That is, Maalox acts twice as fast and longer than Almagel.

Non-absorbable antacids also have a number of other positive properties. They reduce the proteolytic activity of gastric juice (both through the adsorption of pepsin and by increasing the pH of the medium, as a result of which pepsin becomes inactive), have enveloping properties, bind lysolecithin and bile acids, which have an adverse effect on the gastric mucosa.

In recent years, data have been published on the cytoprotective effect of antacids containing aluminum hydroxide, in particular, their ability to prevent, under experimental and clinical conditions, the occurrence of damage to the gastric mucosa when taking ethanol and non-steroidal anti-inflammatory drugs. It was found that the cytoprotective effect of aluminum-containing antacids (in particular, Maalox) is due to an increase in the content of prostaglandins in the stomach wall, an increase in the secretion of bicarbonates and an increase in the production of gastric mucus glycoproteins. Cytoprotective properties of gel structure antacids may be associated with the formation of a protective film on the surface of the stomach.

It was also found that antacids are able to bind the epithelial growth factor and fix it in the area of ​​the ulcer, thereby stimulating cell proliferation, angiogenesis and tissue regeneration. This fact is an explanation of why, for example, the quality of the scar at the site of an ulcer is histologically better after the use of antacids than after the use of omeprazole.

Previously, antacids were recommended in the treatment of peptic ulcer mainly as ancillary drugs, for example, as an addition to antisecretory drugs, and mainly for symptomatic purposes: to relieve pain and dyspeptic disorders. As for the possibility of using antacids in the treatment of peptic ulcer as the main drugs, the attitude of many gastroenterologists until recently was skeptical: on the one hand, it was believed that these drugs were significantly inferior in their effectiveness to other antiulcer drugs, and on the other, It has been suggested that course treatment of exacerbations of peptic ulcer requires very high doses of antacids and their frequent use, which creates certain problems for patients.

However, work published in recent years has allowed us to reconsider this point of view. The results of controlled studies have convincingly proven that non-absorbable antacids are superior to placebo. When using Maalox and other combination drugs, scarring of duodenal ulcers was achieved within 4 weeks in 70-80% of cases, and when using placebo, only in 25-30%. In addition, it was found that the doses of antacids required for healing of ulcers were not as high as previously thought, and that during course therapy there is no need to increase the daily ANA of antacids above 200-400 mEq.

The results obtained provide the basis for the use of antacids in the treatment of exacerbations of duodenal ulcer and as monotherapy, but only for mild cases of the disease. An important advantage of antacids here is that these drugs, when taken once, relieve pain and dyspeptic disorders (for example, heartburn) much faster than antisecretory drugs (including H 2 blockers and omeprazole). However, most clinicians are of the opinion that for mild to moderate duodenal ulcers, antacids should be prescribed in combination with M1-anticholinergic blockers. For large duodenal ulcers, as well as for Zollinger-Ellison syndrome, accompanied by significant hypersecretion of hydrochloric acid, antacids must be combined with H 2 blockers.

The long-term maintenance use of antacids for the prevention of exacerbations of peptic ulcer justified itself. Maalox and cimetidine were shown to equally reduce the incidence of duodenal ulcer recurrence over a 10-month treatment period, with results significantly different from placebo. The use of antacids for prophylactic purposes avoids the year-round use of H2-blockers. Antacids are also indispensable means in the development of H2-blocker withdrawal syndrome.

With gastric ulcer, the secretion of hydrochloric acid is usually reduced. However, ulcers rarely occur in the setting of achlorhydria, so antacids are also warranted. The results of antacid treatment of gastric ulcers are not as clear as those of duodenal ulcers. Some authors note the advantage of antacids over placebo, while others do not. Nevertheless, most researchers recommend prescribing antacids in relatively small doses to patients with gastric ulcer.

Sometimes antacids are used in intensive care units and intensive care units for the prevention of so-called "stress" ulcers (in patients with severe burns, traumatic brain injuries, after abdominal operations, etc.), but controlled studies proving the effectiveness of antacids in such situations , was not carried out.

Adverse reactions

Undesirable reactions may be associated with changes in pH and CBS, as well as with the properties of individual components that make up the preparations. A change in CBS is usually observed with the systematic use of absorbable antacids. The most common adverse reaction with aluminum hydroxide is constipation, magnesium hydroxide has a laxative effect and may cause diarrhea. With the combined use of these substances (as part of Maalox, etc.), their undesirable effect on motor skills is mutually leveled.

The term “non-absorbable antacids” is somewhat arbitrary. The aluminum and magnesium included in their composition can be absorbed in the intestines in minimal quantities. However, a clinically significant increase in the level of aluminum and magnesium in the blood is observed only in patients with severe renal failure, which is the main and, apparently, the only serious contraindication for long-term antacid therapy, since in such cases aluminum accumulation can lead to encephalopathy and osteomalacia. In patients with normal or moderately reduced renal function, a noticeable increase in the level of aluminum in the blood does not occur during treatment with antacids. With long-term use of aluminum hydroxide, the absorption of phosphates in the intestine may decrease, which is sometimes accompanied by the occurrence of hypophosphatemia. This complication occurs more often in patients who abuse alcohol.

Drug interactions

Antacids reduce the absorption of many drugs from the gastrointestinal tract and thus reduce their bioavailability when taken orally. This is most clearly manifested in the example of benzodiazepines, NSAIDs (indomethacin, etc.), antibiotics (ciprofloxacin, tetracycline, metronidazole, nitrofurantoin), anti-tuberculosis drugs (isoniazid), H 2 blockers, theophylline, digoxin, quinidine, warfarin, phenytoin, iron sulfate (). To avoid unwanted interactions, antacids should be prescribed 2 hours before or 2 hours after taking other medications.


Table 2. Medicines whose absorption is reduced when combined with antacids

Forms of release and method of application

Antacids are used in the form of suspension, gel and tablets. Many doctors and patients prefer liquid forms of antacids, which are more palatable and easier to use. However, studies have shown that significant differences there is no difference between these forms and, moreover, tablet forms have an advantage in terms of duration of action, since they are evacuated from the stomach more slowly than liquid antacids.

Antacids are usually prescribed 4 times a day, 10-15 ml of suspension or gel, or 1-2 tablets. The tablets should be chewed or dissolved without swallowing whole. Some package inserts for antacids recommend taking them before meals. However, they are very quickly evacuated from the stomach, and their effect is neutralized by the buffering properties of the food itself. Most gastroenterologists consider it more reasonable to take antacids 1 hour after meals and at night. In special cases, for example, with significant intervals between meals, additional intake of antacids 3-4 hours after meals can be recommended.

Drugs

Maalox a combination of aluminum hydroxide and magnesium hydroxide in the following quantities: in 1 tablet 400 mg and 400 mg, respectively; in 100 ml of suspension in a bottle 3.49 and 3.99 g; in 15 ml of suspension in sachets 523.5 mg and 598.5 mg. Prescribe 1-2 tablets (chew or dissolve in the mouth) or 15 ml of suspension (1 sachet or 1 tablespoon) 4 times a day, 1 hour after meals and at night. Release forms: tablets, suspension in 250 ml bottles and 15 ml bags.

Phosphalugel contains in 1 sachet 8.8 g of colloidal aluminum phosphate, pectin gel and agar-agar. Prescribe 1-2 sachets 4 times a day 1 hour after meals and before bedtime. Release form: gel in sachets of 16 g.

Almagel contains in 5 ml of suspension 300 mg of aluminum hydroxide and 100 mg of magnesium hydroxide. Part Almagel A additionally includes anesthesin (100 mg per 5 ml of suspension) and sorbitol (800 mg). Prescribe 10-15 ml 4-6 times a day. Almagel A prescribed only for pain, the duration of its use should not exceed 3-4 days. Release form: suspension in bottles of 170 and 200 ml.

Many other combination antacid drugs are also available: alugastrin, gastralugel, gastal, gelusil, gelusil-lac, kompensan, pee-hoo, rennie, tisacid and etc.

SELECTIVE ANTIHOLINOLYTICS

The use of anticholinergic drugs as antiulcer drugs is explained by their influence on the main links in the pathogenesis of this disease. Anticholinergics reduce acid production, inhibit the release of gastrin, reduce the production of pepsin, prolong the effect of antacids, enhance the buffering properties of food, and reduce the motor activity of the stomach and duodenum.

At the same time, the use of drugs such as atropine, platyphylline and metacin in the treatment of peptic ulcer is limited due to the systemic nature of their anticholinergic action and, as a consequence, the high frequency of adverse reactions. The latter include dry mouth, impaired accommodation, tachycardia, constipation, urinary retention, dizziness, headache, insomnia.

Atropine and atropine-like drugs are contraindicated in glaucoma, prostate adenoma, and heart failure. Their use is undesirable in case of cardia insufficiency and gastroesophageal reflux, which often accompany peptic ulcer disease, since in such cases the backflow of acidic gastric contents from the stomach into the esophagus may increase. In addition, in recent years it has been found that the antiulcer activity of traditional (non-selective) anticholinergic drugs is insufficient. For example, the antisecretory effect of platyphylline turned out to be weak, and atropine was short-lived. Therefore, atropine, platiphylline and metacin have become less used in the treatment of peptic ulcers in recent years. At the same time, the drug has found widespread use in clinical practice pirenzepine (gastrocepin), also blocks cholinergic receptors, but its mechanisms of action differ significantly from atropine and other anticholinergics.

Pirenzepine is a selective anticholinergic drug that selectively blocks predominantly M1-cholinergic receptors of the fundic glands of the gastric mucosa and does not affect the cholinergic receptors of the salivary and bronchial glands, the cardiovascular system, eye tissue, and smooth muscles in therapeutic doses. Despite its structural similarity to tricyclic antidepressants, pirenzepine does not cause adverse reactions from the central nervous system, since, having predominantly hydrophilic properties, it does not penetrate the blood-brain barrier.

Pharmacodynamics

The leading mechanism of the antiulcer effect of pirenzepine is the suppression of hydrochloric acid secretion. When taken orally, the maximum antisecretory effect is observed after 2 hours and lasts depending on the dose taken from 5 to 12 hours. Night secretion of hydrochloric acid is inhibited by 30-50%, basal secretion by 40-60%, and secretion stimulated by pentagastrin by 30-40%. Pirenzepine suppresses basal and stimulated production of pepsin, but does not affect the secretion of gastrin and a number of other gastrointestinal peptides (somatostatin, neurotensin, secretin).

Pirenzepine somewhat slows down gastric emptying, but, unlike non-selective anticholinergic drugs, when taken orally in average therapeutic doses does not reduce the tone of the lower esophageal sphincter. At intravenous administration The drug reduces sphincter tone and esophageal peristalsis.

The effectiveness of pirenzepine in the treatment of peptic ulcers was initially explained by its antisecretory activity. However, subsequent work showed that the drug has a cytoprotective effect, that is, the ability to increase the protective properties of the gastric mucosa. This effect is to some extent associated with the ability to dilate the blood vessels of the stomach and increase the formation of mucus.

Pharmacokinetics

Bioavailability when taken orally on an empty stomach averages 25%. Food reduces it to 10-20%. The maximum concentration of the drug in the blood serum develops 2-3 hours after oral administration and 20-30 minutes after intramuscular injection. Only about 10% of the drug is metabolized in the liver. Excretion occurs primarily through the intestines and, to a lesser extent, through the kidneys. Half-life 11 hours.

Clinical efficacy and indications for use

Over the past years, many studies have been published indicating the fairly high effectiveness of pirenzepine in the treatment of exacerbations of gastric and duodenal ulcers. In particular, the drug’s ability to quickly relieve pain and dyspeptic disorders was noted. Pirenzepine did not have hepatotoxic or nephrotoxic effects and was effective in patients with so-called “hepatogenic” ulcers, usually resistant to treatment, in patients with chronic renal failure, and in the elderly. There are reports of successful use of the drug in the treatment of erosive and ulcerative lesions of the gastric mucosa caused by taking non-steroidal anti-inflammatory drugs.

In general, the use of pirenzepine at a dose of 100-150 mg per day allows achieving healing of duodenal ulcers within 4 weeks in 70-78% of patients. The drug can be used to prevent the occurrence of “stress” ulcers, as well as for preventive therapy.

Adverse reactions

Pirenzepine is generally well tolerated. Sometimes dry mouth, accommodation disorders are observed, and less commonly, constipation, tachycardia, and headaches. Moreover, the frequency of their occurrence clearly correlates with the dose. Thus, when prescribing average therapeutic doses (100 mg per day), dry mouth occurs in 7-13% of patients, and disturbance of accommodation occurs in 1-4% of patients. At higher doses (150 mg per day), the frequency of these adverse reactions increases to 13-16% and 5-6%, respectively. In most cases, adverse reactions are mild and do not require discontinuation of the drug.

Pirenzepine usually does not cause an increase intraocular pressure, urinary disorders and adverse reactions from the cardiovascular system. However, in case of glaucoma, prostate adenoma and a tendency to tachycardia, the drug should be prescribed with caution.

Drug interactions

Pirenzepine reduces the stimulating effect of alcohol and caffeine on gastric secretion. The simultaneous administration of pirenzepine and H 2 blockers leads to potentiation of the antisecretory effect, which can be used in patients with Zollinger-Ellison syndrome.

Dosage and methods of application

For exacerbation of peptic ulcer, 50 mg 2 times a day (morning and evening) half an hour before meals. The duration of the course is usually 4-6 weeks. For maintenance therapy 50 mg per day.

Intravenously or intramuscularly for very persistent pain syndrome (for example, in patients with Zollinger-Ellison syndrome) 10 mg 2-3 times a day. Intravenous administration is carried out slowly as a stream or (better) as a drip.

Release forms

Tablets of 25 and 50 mg; ampoules 10 mg/2 ml.

H2-HISTAMINE RECEPTOR BLOCKERS

H2-blockers, which have been used in clinical practice since the mid-70s, are currently among the most common antiulcer drugs. Several generations of these drugs are known. After cimetidine were sequentially synthesized ranitidine, famotidine, and a little later nizatidine And Roxatidine.

Pharmacodynamics

The main effect of H2 blockers is antisecretory: due to competitive blocking of H2 histamine receptors in the gastric mucosa, they suppress the production of hydrochloric acid. This is responsible for their high antiulcer activity. New generation drugs are superior to cimetidine in the degree of suppression of nighttime and total daily secretion of hydrochloric acid, as well as in the duration of the antisecretory effect ().


Table 3. Comparative pharmacodynamics of H 2 blockers

Treatment of uncomplicated gastric and duodenal ulcers. Peripheral M-anticholinergics in the treatment of peptic ulcer

Contents of the article:

Gastroenterologists always prescribe treatment for stomach and duodenal ulcers with medications, since such serious diseases can only be dealt with through diet and folk remedies it can be difficult. The treatment regimen is always selected individually for each patient, although there are standard regimens that can also be used by the doctor.

Drugs that reduce the aggressiveness of gastric juice

Drug treatment of stomach and duodenal ulcers is not possible without drugs that act on gastric juice, reducing his aggressiveness. There are several groups of such drugs.

Peripheral M-anticholinergics and calcium channel blockers

Peripheral M-anticholinergics block all subtypes of M-cholinergic receptors. Previously, these medications were often used to treat ulcers (Atropine sulfate, Pirenzepine), but in recent years they have been used less frequently. Although they have antisecretory properties, the effect is much lower, but there are many side effects.
Calcium channel blockers are also rarely used. These are drugs such as Verapamil, Nifedipine. But if the patient has not only an ulcer, but also heart disease, the doctor may prescribe these medications.

H2-histamine receptor blockers

For stomach and duodenal ulcers, doctors often prescribe H2 receptor blockers, which have been used in medicine for more than 20 years. During this time, these drugs were well studied, doctors could not help but notice that it had become easier to treat ulcers. Thanks to the fact that these drugs began to be used, the percentage of scarring of ulcers became greater, the number of operations that had to be performed due to complications of the disease was reduced, and the treatment time was significantly reduced.

Another advantage of these drugs is that they increase the formation of mucus and improve microcirculation of the mucous membrane. However, these drugs cannot be abruptly discontinued, otherwise the patient may experience withdrawal syndrome, which will lead to increased acid secretion and relapse of the disease.

Generations of H2-histamine receptor blockers

There are several generations of H2 blockers -histamine receptors.

  1. First generation. Cimetidine. It only lasts 4-5 hours, so you need to take this medicine at least 4 times a day. It has many side effects, for example, it affects the liver and kidneys. Therefore, now these tablets are practically not used.
  2. Second generation. Ranitidine. They last longer, 8-10 hours, and have fewer side effects.
  3. Third generation. Famotidine. One of the best drugs, it is 20-60 times more effective than cimetidine and 3-20 times more active than rantidine. Must be taken every 12 hours.
  4. Fourth generation. Nizatidine. Not much different from Famotidine, there are no special advantages over other drugs.
  5. Fifth generation. Roxatidine. It is slightly inferior to Famotidine; it has less acid-suppressing activity.

Proton pump inhibitors

These medications block the production of hydrochloric acid. They are much more effective than H2 blockers, so these drugs are often prescribed for peptic ulcer.

  1. Omeprazole. This medicine helps the ulcer heal faster. After 2 weeks of treatment, duodenal ulcers are scarred in 60% of patients, and after 4 weeks – in 93%. If you treat a stomach ulcer with Omeprazole, then after 4 weeks it will scar in 73% of patients, and after 8 weeks – in 91%.
  2. Lanzoprazole. The patient should take 1 capsule for two or four weeks for duodenal ulcers and up to 8 weeks for gastric ulcers. This medicine should not be taken by pregnant women, nursing mothers or those with a cancerous tumor in the gastrointestinal tract.
  3. Pantoprazole. You should not take this drug if you have hepatitis or cirrhosis of the liver. The recommended dose is from 40 to 80 mg per day, the course of treatment lasts 2 weeks for exacerbation of duodenal ulcer and 4-8 weeks for exacerbation of gastric ulcer.
  4. Esomeprazole. It is used to treat duodenal ulcers (20 mg 1 week, taken with antibiotics to get rid of Helicobacter pylori) and as a prophylactic for stomach disease (also 20 mg 1 time per day for 1-2 months with long-term use NSAIDs).
  5. Paries. This is a modern medicine that rarely has side effects, moreover, it has a more persistent antisecretory effect, so already on the first day treatment will be lost heartburn and pain.

Antacids

Antacids neutralize hydrochloric acid, which is part of the gastric juice. They are often prescribed for ulcers as an additional remedy. They help relieve pain and also reduce the intensity of heartburn. These drugs act quickly, much faster than other drugs, but they have a shorter therapeutic effect.

  1. Almagel. Contains magnesium hydroxide and aluminum hydroxide. The medicine envelops the stomach and protects its walls; it is also an adsorbent. Cannot be used for Alzheimer's disease and liver diseases. If the patient has a duodenal ulcer or stomach ulcer, you need to drink this remedy between meals, 1 spoon up to 4 times a day. The course of treatment is from 2 to 3 months.
  2. Phosphalugel. Contains aluminum phosphate. Removes gases in the intestines and collects toxins, harmful microelements, envelops the mucous membrane. For ulcers, take this medicine a couple of hours after eating or when pain occurs, dissolving the contents of the sachet in half a glass of water.
  3. Maalox. When treating ulcers, drink 1 sachet dissolved in water half an hour before meals. It is an analogue of Almagel, but its effect is 2 times longer, and it does not provoke constipation, like Almagel.

Antibacterial drugs

Peptic ulcers are often caused by the bacteria Helicobacter pylori. To cure this disease, it is necessary to carry out antibacterial therapy. The doctor may prescribe 1 or 2 courses of antibiotics, as well as bismuth-based drugs.

Antibiotics

The following antibiotics may be prescribed:

  1. Amoxicillin. This is a bactericidal drug that is used for gastritis, if it is necessary to treat duodenal ulcers or stomach ulcers caused by Helicobacter pylori bacteria. 250-500 mg of medication is prescribed every 8 hours.
  2. Clarithromycin. This medicine is also used in the treatment of peptic ulcers, but only in combination with other drugs. Contraindicated in the first trimester of pregnancy and while breastfeeding.
  3. Tetracycline. There are several types of this medicine, but tablets are used to treat ulcers. They are not prescribed to children under 8 years of age, pregnant women and nursing mothers, and people with kidney or liver dysfunction. Do not drink at the same time as antacids.

Preparations based on bismuth

These bismuth-based medications also help destroy bacteria:

  1. De-nol. This drug is taken for stomach or duodenal ulcers, as it has bactericidal activity. It is also an anti-inflammatory agent. It protects the mucous membrane by increasing mucus production and also by creating a protective film on the surface of the ulcer or erosion. The course of treatment lasts from 4 to 8 weeks; for the next 8 weeks you should not take medications with bismuth.
  2. Tribimol. These are tablets that take 120 mg up to 4 times a day, half an hour before meals or 2 hours after meals, with water. The course of treatment is 28-56 days, after which a break of 8 weeks is necessary.
  3. Vikalin. A combined preparation that contains not only bismuth subnitrate, but also buckthorn bark, calamus root and other components. It also has an antacid effect, relieves pain, helps to get rid of constipation. The course of treatment is 1-3 months, the treatment can be repeated in a month.

Treatment with this group of medicines not only helps to cope with Helicobacter pylori, but also contributes to the speedy healing of the ulcer.

Medicines that increase the protective properties of the mucosa

There are drugs that increase the protective properties of the mucosa. All of them can be divided into two groups.

Drugs that improve the protective properties of mucus

The first is drugs that increase the production of mucus, its protective properties. The attending physician may prescribe them for stomach ulcers, since these drugs are less effective for duodenal ulcers. These include the well-known De-nol, as well as the following medicines:

  1. Sodium carbenoxolone, which is synthesized from the acid found in licorice root. Among the side effects are increased blood pressure, the appearance of edema. This medicine is not prescribed to pregnant women and children, people with arterial hypertension, heart failure, and with caution to the elderly.
  2. Sucralfate. This drug also applies to absorbents and antacids. Used for stomach and duodenal ulcers. Not prescribed for kidney disease, bleeding in the gastrointestinal tract, or for young children (under 4 years old).
  3. Enprostil. It also has antisecretory properties, increases the stability of the mucous membrane, and promotes the healing of ulcers.

Drugs that restore mucous membranes

For duodenal ulcers, treatment includes medications that accelerate the healing of the mucosa. They also help with stomach ulcers and other diseases. gastrointestinal tract.

  1. Liquiriton. The active ingredient is an extract of the root of naked licorice and Ural licorice, this is a drug plant origin. It has an anti-inflammatory effect, relieves pain, and is also an antacid.
  2. Solcoseryl. Activates metabolic processes in tissues, promotes their regeneration, rapid recovery and healing. Made from the blood fraction of calves. It is available in the form of gels, ointments, and so on, but dragees are used to treat ulcers.
  3. Methyluracil. This is an anti-inflammatory drug that stimulates the human immune system and accelerates tissue growth. For diseases of the digestive system, tablets are used, which the patient can take for about 30-40 days, 4 times a day.

We talked about the main medications that are often prescribed for ulcers. But the choice of drugs is the prerogative of the doctor; it is the gastroenterologist who must decide which pills the patient should take, and which in this case it is better to refuse. Therefore, self-medication is not allowed; all medications must be prescribed after a thorough examination. The doctor not only prescribes treatment, but also monitors its effectiveness and may change the treatment regimen if the previous one did not help the patient.

He or she may prescribe other medications, such as pain management medications or probiotics after antibiotic treatment. You should trust the doctor’s opinion and follow his instructions. If you have doubts about his competence, you do not need to change the treatment regimen yourself; it is better to find another doctor whom you can completely trust.


For citation: Sheptulin A.A. BASIC DRUG THERAPY OF Peptic Ulcer // Breast Cancer. 1998. No. 7. S. 1

The concepts of “anti-ulcer treatment” and “anti-Helicobacter therapy” are not synonymous. Treatment of stomach and duodenal ulcers should be comprehensive; its goal is to relieve symptoms of exacerbation of peptic ulcer disease, to achieve (as possible short time) scarring of the ulcerative defect and prevention of relapse of the disease. The right combination Basic antiulcer drugs with eradication anti-Helicobacter therapy can successfully solve these problems.

The terms "antiulcerative treatment" and "antihelicobacter therapy" are not synonyms. The treatment of ulcerative lesions of the stomach and duodenum remains complex, its goal is to alleviate the symptoms of an exacerbation of peptic ulcer, to ensure ulcerative defect healing (in the shortest time) and to prevent recurrences. A correct combination of basic antiulcertaive agents and eradicative antihelicobacter therapy may solve these problems successfully.

A.A. Sheptulin, prof. Department of Propaedeutics of Internal Diseases of the Moscow Medical Academy named after. THEM. Sechenov
A.A. Sheptulin, prof. Department of Internal Propedeutics, I.M.Sechenov Moscow Medical Academy

D Advances in recent years in the study of the pathogenesis of peptic ulcer disease, associated primarily with the identification of Helicobacter pylori (HP), have forced a radical reconsideration of previously existing approaches to the pharmacotherapy of this disease. Thus, now no antiulcer treatment regimen can be considered scientifically valid if it does not require mandatory eradication of HP in the gastric mucosa. In the vast majority of works devoted to the problems of peptic ulcer pharmacotherapy, certain aspects of eradication therapy are affected. In this regard, some practitioners sometimes ask whether the concept of "anti-ulcer treatment" should be replaced by another - "anti-Helicobacter therapy".
Answering this question, we always emphasize that the concepts of "anti-ulcer treatment" and "anti-helicobacter therapy" are far from the same thing. Among the many tasks that have to be solved in the course of anti-ulcer treatment, the most important are the following: relief of symptoms of exacerbation of peptic ulcer (pain and dyspeptic disorders), achievement (as soon as possible) of scarring of the ulcer and prevention of subsequent occurrence of recurrence of the disease. Antihelicobacter therapy, for all its exceptional importance, solves only the third problem, contributing to a significant reduction in the frequency of recurrence of peptic ulcer during the year from 70 to 4-5%. Carrying out antihelicobacter therapy, we do not set the task of stopping pain and dyspeptic disorders(Moreover, the latter may arise in the course of its implementation). We are not
we strive to achieve healing of the ulcer through the eradication of HP, and to achieve this in 7 days (namely, this is the duration of many eradication treatment regimens, it is impossible even theoretically. The mentioned tasks are solved with the help of basic therapy, carried out not with anti-Helicobacter agents, but with anti-ulcer drugs.
The variety of different pathogenetic factors of peptic ulcer disease led at one time to the emergence of a large number of different drugs that, as originally assumed, acted on certain links in the pathogenesis of the disease. However, the effectiveness of many of them (for example, sodium oxyferriscarbon) has not been confirmed in clinical practice. Instead of drugs with wide range
With pharmacological effects on various organs and systems of the body, drugs have appeared that selectively affect only certain parts of the process of hydrochloric acid secretion. As a result, the extensive, if not exorbitantly expanded, arsenal of antiulcer drugs has undergone significant revision and radical reduction.
In 1990, W. Burget et al. published the results of a meta-analysis of 300 studies, which made it possible to establish a clear connection between the effectiveness of a particular antiulcer drug and the duration of the increase in pH in the gastric lumen during its use. The authors concluded that gastric ulcers heal in 100% of cases if intragastric pH can be maintained above 3.0 for about 18 hours per day. This fundamental conclusion, which is now referred to by the authors of almost all serious works on the pharmacotherapy of peptic ulcer disease, has made it possible to reduce the list of main antiulcer drugs used during exacerbation of peptic ulcer disease to relieve the clinical manifestations of the disease and achieve healing of the peptic ulcer defect to several main groups of drugs. These included antacids, selective anticholinergics, H blockers
2 -receptors and proton pump inhibitors.
Even in this much abbreviated form, the pharmacopoeia of antiulcer drugs confronts the practitioner with the need to decide which drug to choose. There is still no unequivocal answer to this question in the literature, and the specific recommendations proposed in the works
often differ significantly from each other.

The severity of the course of peptic ulcer is also not the same in different patients, and therefore they may require drugs that are different in severity of the antisecretory effect. At favorable course peptic ulcer, rare and short exacerbations, small ulcers, a moderate increase in acid production, the absence of complications, drugs that do not have pronounced antisecretory activity may well be used as basic therapy drugs. and when prescribed in medium therapeutic doses, they are able to maintain the level of intragastric pH at a level above 3.0 for only a relatively short time (up to 8-10 hours per day), - antacids and selective M-anticholinergics.
With frequent and prolonged exacerbations of peptic ulcer, large (more than 2 cm in diameter) size of the ulcer, severe hypersecretion of hydrochloric acid, the presence of complications (including history), concomitant erosive esophagitis, N
2 - blockers and inhibitors of the proton pump, which maintain the necessary indicators of intragastric pH for a much longer time (up to 12-18 hours per day).
Antacids. Traditionally, this group of drugs includes absorbable (sodium bicarbonate, calcium carbonate, magnesium oxide) and non-absorbable (aluminum hydroxide and aluminum phosphate, magnesium hydroxide and magnesium trisilicate) antacids. Drugs of the first subgroup cause serious adverse reactions (release carbon dioxide, the “rebound” phenomenon, the development of alkalosis and “milk-alkali syndrome”), and therefore are not currently used in clinical practice.
The acid neutralizing activity of antacids (ANA) is determined by their ability to neutralize H+ ions and is expressed in milliequivalents of neutralized hydrochloric acid. In addition, antacids reduce the proteolytic activity of gastric juice (both through the adsorption of pepsin and by increasing the pH of the environment, as a result of which pepsin becomes inactive), have good enveloping properties, and bind lysolecithin and bile acids.
In recent years, data have been published on the cytoprotective effect of antacids containing aluminum hydroxide, their ability to prevent in experiments and clinical conditions the occurrence of damage to the gastric mucosa caused by ethanol and non-steroidal anti-inflammatory drugs. It was found that this cytoprotective effect is associated with an increase in the content of prostaglandins in the gastric wall when taking antacids. In addition, antacid preparations containing aluminum hydroxide stimulate the secretion of bicarbonates and increase the production of gastric mucus, have the ability to bind epithelial growth factor and fix it in the area of ​​the ulcer, thereby stimulating cell proliferation, development vascular network and tissue regeneration.
In the treatment of peptic ulcers, antacids are usually recommended as adjuvant drugs in addition to other antisecretory drugs, the main ones being
way as a symptomatic remedy (for the relief of pain and dyspeptic disorders). The attitude of many gastroenterologists to the possibility of using antacids in the treatment of peptic ulcers as the main drugs remains skeptical to this day: it is believed that these drugs are significantly inferior in their effectiveness to other antiulcer drugs. In addition, the opinion was expressed that for a course of treatment of exacerbation of peptic ulcer disease, very high doses of antacids and their frequent use are necessary.
Works published in recent years have allowed us to reconsider this point of view. Representative symposia on the clinical aspects of antacid therapy, held in Bermuda (1991) and Budapest (1994), showed the unfoundedness of the concerns expressed. The healing rate of duodenal ulcers after 4 weeks of treatment with antacid drugs averaged 73%, which significantly exceeded the effectiveness of placebo.
In addition, it was found that the doses of antacids required for healing of ulcers were not as high as previously thought, and that during a course of therapy, the daily ANA of antacids may not exceed 200 - 400 mEq. The results obtained make it possible to use antacids for basic treatment exacerbations of peptic ulcer disease as monotherapy, but only in mild cases of the disease. An important advantage of antacids here is that after taking a single dose they relieve pain and dyspeptic disorders much faster than antisecretory drugs (including N
2-blockers and omeprazole). In more severe cases, antacids can be used as symptomatic agents against the background of basic therapy carried out by other, more powerful antisecretory drugs.
Pirenzepine. It is a selective anticholinergic drug. It selectively blocks predominantly M-cholinergic receptors of the fundic glands of the gastric mucosa and does not affect the cholinergic receptors of the cardiovascular system. Unlike anticholinergics with a systemic mechanism of action, it does not cause side effects (tachycardia, accommodation disturbances, urinary retention, etc.).
The leading mechanism of the antiulcer effect of pirenzepine is associated with the suppression of hydrochloric acid secretion. When taken orally, the maximum antisecretory effect of the drug is observed after 2 hours and persists (depending on dose taken) from 5 to 12 hours. Recent work has shown that this drug also has a cytoprotective effect, which is believed to be associated with the ability of pirenzepine to dilate the blood vessels of the stomach.
The use of pirenzepine in a dose of 100 - 150 mg allows achieving healing of duodenal ulcers within 4 weeks in 70 - 75% of patients, which can be considered a fairly good result
.Not having such high antisecretory activity as omeprazole and H blockers 2 -receptors, it still gives a lower frequency of relapses compared to the above-mentioned drugs. This fact is due, in particular, to the fact that when using pirenzepine there is no increase in the level of gastrin in the blood, as is the case, for example, when using proton pump blockers. There have already been recommendations to prescribe pirenzepine after treatment with omeprazole in order to reduce the concentration of serum gastrin.
N
2 -blockers. H blockers 2 -receptors are among the most common antiulcer drugs currently used. Several generations of these drugs have now been used in clinical practice. After cimetidine, which for a number of years was the only representative of H 2 -blockers, ranitidine, famotidine, and a little later - nizatidine and roxatidine were sequentially synthesized.
High antiulcer activity H
2 -blockers is primarily due to their powerful inhibitory effect on the secretion of hydrochloric acid. In this case, the antisecretory effect after taking cimetidine lasts for 4 - 5 hours, after taking ranitidine - 8 - 9 hours, after taking famotidine, nizatidine and roxatidine - 10 - 12 hours.
H blockers
2 -receptors not only have an antisecretory effect, but also suppress basal and stimulated pepsin production, increase gastric mucus production, bicarbonate secretion, improve microcirculation in the mucous membrane of the stomach and duodenum, normalize gastroduodenal motility.
When using N
2 -blockers for 2 weeks, pain in the epigastric region and dyspeptic disorders disappear in 56 - 58% of patients with exacerbation of gastric and duodenal ulcers. After 4 weeks of treatment, scarring of duodenal ulcers is achieved in 75 - 83%, after 6 weeks - in 90 - 95% of patients. Frequency of scarring of gastric ulcers after 6 weeks of treatment N 2 -blockers is 60 - 65%, after 8 weeks of treatment - 85 - 70%. In this case, a single dose of the entire daily dose of N 2-blockers at bedtime (ie, for example, 300 mg ranitidine or 40 mg famotidine) are as effective as taking half doses twice (morning and evening).
The accumulated experience with the use of cimetidine has shown that this drug causes a variety of side effects. These include an antiandrogenic effect, hepatotoxic effect, various cerebral disorders, increased creatinine levels in the blood, changes in hematological parameters, etc. Ranitidine and famotidine, significantly superior to cimetidine in antisecretory activity, give less pronounced side effects. As for H 2 -blockers of subsequent generations (nizatidine and roxatidine), then they, while also noticeably superior to cimetidine, do not have any special advantages over ranitidine and famotidine and therefore are not widely used.
Proton pump inhibitors. Proton pump inhibitors (H inhibitors)
+ , K + -ATPases of the parietal cell) currently occupy, perhaps, a central place in the range of antiulcer drugs. This is explained by the fact that their antisecretory activity (and, accordingly, clinical effectiveness) significantly exceeds that of other antiulcer drugs. In addition, proton pump inhibitors create favorable conditions for anti-Helicobacter therapy, and therefore they are now included as a mandatory component in most eradication regimens. Of the drugs in this group, omeprazole, pantoprazole and lansoprazole are currently used in clinical practice.
Being benzimidazole derivatives, proton pump inhibitors, accumulating in the secretory tubules of the parietal cell, are converted into sulfenamide derivatives, which form covalent bonds with cysteine ​​H molecules
+ , K + -ATPases and thereby inhibit the activity of this enzyme.
When taking an average therapeutic dose of these drugs once a day, gastric acid secretion throughout the day is suppressed by 80 - 98%. Essentially, proton pump blockers are currently the only drugs that can maintain intragastric pH levels above 3.0 for more than 18 hours a day and thus satisfy the requirements formulated by D. Burget et al. for ideal antiulcer agents.

Multicenter and meta-analytic studies have shown that proton pump inhibitors are by far the most effective antiulcer drugs. In 69% of patients with duodenal ulcers, scarring of the ulcer occurs within 2 weeks of therapy. After 4 weeks of treatment with proton pump inhibitors, the rate of scarring of duodenal ulcers is 93 - 100%. These drugs also have a good effect in patients with peptic ulcers who are resistant to therapy with H 2 blockers.
Omeprazole, pantoprazole and lansoprazole differ in chemical structure, bioavailability, half-life, etc., but their results clinical application turn out to be almost identical.
The safety of proton pump inhibitors during short (up to 3 months) courses of therapy is very high. With long-term (especially for several years) continuous use of these drugs, hypergastrinemia occurs in patients, and the symptoms progress atrophic gastritis, and some patients may develop nodular hyperplasia of endocrine cells (ECL cells) of the gastric mucosa, which produce histamine.
For an objective analysis of the results of antiulcer treatment great importance has strict adherence to the protocol for the treatment of exacerbation of peptic ulcer disease, which includes the prescription of the selected drug in the appropriate dose, a certain duration of treatment, certain terms of endoscopic monitoring, and standard criteria for assessing the effectiveness of treatment.
For example, during exacerbation of a peptic ulcer, ranitidine is prescribed at a dose of 300 mg/day, famotidine at a dose of 40 mg/day, omeprazole at a dose of 20 mg/day, etc. The duration of treatment is determined by the results of endoscopic monitoring, which is carried out at two-week intervals . To assess the effectiveness of a particular antiulcer drug, they calculate not the average time (as is practiced in many domestic works), but the frequency of scarring of ulcers over 4, 6, 8 weeks, etc. Compliance with the protocol makes it possible to conduct multicenter and meta-analytic studies that combine dozens and hundreds of studies carried out in different countries, which allows us to evaluate with a high degree of reliability (since the number of patients reaches tens and hundreds of thousands of people) the effectiveness of the drug and the influence of certain factors on it.
Important feature Modern pharmacotherapy for peptic ulcer disease is the absence of fundamental differences in approaches to the treatment of gastric and duodenal ulcers. Previously, it was believed that duodenal ulcers required the use of antisecretory drugs, and stomach ulcers required drugs that stimulate regeneration processes. It is now generally accepted that after confirmation of the benign nature of gastric ulcers, the treatment of these patients is carried out in exactly the same way as the treatment of patients with duodenal ulcers. The only difference is the duration of the course of pharmacotherapy. Considering that gastric ulcers scar more slowly than duodenal ulcers, the results of scarring of gastric ulcers are monitored not after 4 and 6 weeks of treatment, as with duodenal ulcers, but after 6 and 8 weeks.
An important issue is the tactics of pharmacotherapy for patients with hard-to-heal ulcers of the stomach and duodenum. Gastroduodenal ulcers that do not scar within 12 weeks are usually called hard-to-heal (or long-term non-healing). Their frequency, which previously reached 10–15%, decreased to 1–5% after the introduction of proton pump inhibitors into clinical practice.
In cases of insufficient effectiveness H 2 -blockers (ranitidine, famotidine), it is currently considered most appropriate to increase their dose by 2 times or transfer the patient to take proton pump inhibitors. If the patient initially received the usual doses of proton pump inhibitors (for example, 20 mg omeprazole), then they are increased by 2- 3 times (i.e., adjusted to 40 - 60 mg/day). This scheme makes it possible to achieve healing of the ulcer in approximately half of the patients with difficult-to-scar ulcers.
The high frequency of relapses of gastroduodenal ulcers after cessation of course treatment served as the basis for the development of maintenance regimens of antiulcer drugs.
Maintenance therapy H2 remains the most common currently. -blockers, including daily administration of 150 mg of ranitidine or 20 mg of famotidine before bedtime. This makes it possible to reduce the frequency of relapses of peptic ulcer disease within a year after the main course to 6 - 18%, and within 5 years - to 20 - 28%.
Later, continuous maintenance administration of antisecretory drugs was replaced by intermittent maintenance therapy regimens. These include “yourself treatment” or “on demand” therapy, when patients themselves determine the need to take medications based on their well-being, and the so-called “weekend treatment”, when the patient remains without treatment from Monday to Thursday and takes antisecretory drugs from Friday to Sunday. Intermittent maintenance therapy is less effective than daily medication, however, this method of maintenance treatment is better tolerated by patients.
Currently, when anti-Helicobacter therapy is recognized as the basis for anti-relapse treatment of peptic ulcers, the indications for maintenance therapy with basic antisecretory drugs have narrowed significantly. It is considered necessary for patients whose peptic ulcer is not accompanied by contamination of the gastric mucosa with HP (i.e. for 15 - 20% of patients with gastric ulcers and about 5% of patients with duodenal ulcers), for patients who have at least two attempts at anti-Helicobacter therapy were unsuccessful, also for patients with a complicated course of peptic ulcer disease (in particular, with a history of perforation of ulcers).
Thus, modern pharmacotherapy for peptic ulcer disease still remains complex. The correct combination of basic antiulcer drugs with eradication anti-Helicobacter therapy allows one to successfully solve the main tasks facing a doctor when treating a patient with an exacerbation of a peptic ulcer: relief of clinical symptoms, achieving scarring of the ulcer, preventing relapses after a course of treatment.

Literature:

1. Misiewicz G., Harris A. Clinicians’ manual on Helicobacter pylori in peptic disease. Science Press London 1995; 1-42.
2. Burget D.W., Chiverton K.D., Hunt R.H. Is there an optimal degree of acid suppression for healing of duodenal ulcers? A model of the relationship between ulcer healing and acid suppression. Gastroenterology 1990; 99:345-51.
3. Tytgat G.N.J., Janssens J., Reynolds J.C, Wienbeck M. Update on the pathophysiology and management of gastro-oesophageal reflux disease: the role of prokinetic therapy. Eur J Gastroenterol Hepatol 1996; 8:603-11.
4. Rosch W. (Hrsg) Der Einsatz von Antacida in der Gastroenterologie. Braunschweig-Wiesbaden 1995; 1-64.
5. Classen M., Dammann H.G., Schepp W. The ulcer patient in general practice. Hoechst AG, 1991; 84.


By modern ideas, the leading link in the pathogenesis of peptic ulcer disease is an imbalance between the factors of acid-peptic aggression of the gastric contents and the elements of protection of the gastric mucosa.

The aggressive part of ulceration includes:

    a) hypersecretion of hydrochloric acid due to an increase in the mass of parietal cells, hyperfunction of gastrin, disturbances of nervous and humoral regulation;

    b) increased production of pepsinogen and pepsin;

    c) disturbance of the motor function of the stomach and duodenum (delay or, conversely, acceleration of evacuation from the stomach).

In recent years, Helicobacter pyloricus has been recognized as the most important aggressive factor in ulcer formation ( Helicobacter pylori) a microorganism capable of colonizing the gastric mucosa and metaplastic mucous membrane of the duodenum.

Various factors can lead to a weakening of the protective properties of the mucous membrane of the stomach and duodenum:

    a) decreased production and/or disruption of the qualitative composition of gastric mucus (for example, due to alcohol abuse);

    b) decreased secretion of bicarbonates (with chronic pancreatitis);

    c) decreased regenerative activity of epithelial cells;

    d) deterioration of blood supply to the gastric mucosa;

    e) decrease in the content of prostaglandins in the stomach wall (for example, when taking non-steroidal anti-inflammatory drugs).

The variety of different pathogenetic factors of peptic ulcer disease led to the emergence of a large number of drugs that selectively acted, as originally assumed, on certain pathogenetic mechanisms of the disease. However, the effectiveness of many of them, for example, sodium oxyferriscorbone, has not been further confirmed.

In 1990, W. Burget et al. published data from a meta-analysis of 300 studies, in which they established a correlation between the effectiveness of antiulcer drugs and the duration of maintaining an elevated pH in the stomach, achieved with their use. The authors concluded that gastric and duodenal ulcers are scarred in 100% of cases if intragastric pH levels >3 can be maintained for about 18 hours during the day. Therefore, the list of antiulcer drugs used in the treatment of exacerbations of the disease to relieve clinical symptoms and achieve scarring of the ulcer has been reduced and currently includes 4 groups of drugs: antacids, selective anticholinergics, histamine H2 receptor blockers, proton pump inhibitors. A separate “niche” was occupied by cytoprotectors, bismuth preparations, antibiotics and some other drugs, for the use of which special indications have been formulated.

CLINICAL CLASSIFICATION OF MODERN
ANTI-ULCER DRUGS

Taking into account that the severity of the antisecretory effect of drugs used for the purpose of basic therapy peptic ulcer (that is, for the treatment of exacerbations of diseases and maintenance administration), are not the same, they from the standpoint of practical use can be divided into first- and second-stage drugs. It is advisable to include antacids and selective M-anticholinergics in the first group, and H 2 blockers and proton pump inhibitors in the second group.

An independent group consists of drugs used for special indications: cytoprotective agents (sucralfate, synthetic analogues of prostaglandins), prescribed mainly for the treatment and prevention of lesions of the mucous membrane of the stomach and duodenum caused by taking ulcerogenic drugs; drugs that normalize motor function stomach and duodenum (antispasmodics, prokinetics); anti-helicobacter agents (antibiotics, bismuth preparations) ().


Table 1. Classification of antiulcer drugs

A drug Night secretion (%) General secretion (%) Duration of action (hour)
Cimetidine 50-65 50 4-5
Ranitidine 80-95 70 8-9
Famotidine 80-95 70 10-12
Nizatidine 80-95 70 10-12
Roxatidine 80-95 70 10-12

In addition to inhibiting the secretion of hydrochloric acid, H2 blockers have a number of other effects. They suppress basal and stimulated production of pepsin, increase the production of gastric mucus and bicarbonates, enhance the synthesis of prostaglandins in the stomach wall, and improve microcirculation in the mucosa. In recent years, H2 blockers have been shown to inhibit degranulation mast cells, reduce the content of histamine in the periulcerous zone and increase the number of DNA-synthesizing epithelial cells, thereby stimulating reparative processes.

Pharmacokinetics

When taken orally, H 2 -blockers are well absorbed in the proximal small intestine, reaching peak blood concentrations after 30-60 minutes. The bioavailability of cimetidine is 60-80%, ranitidine 50-60%, famotidine 30-50%, nizatidine 70%, roxatidine 90-100%. Excretion of drugs occurs through the kidneys, with 50-90% of the dose taken unchanged. The half-life of cimetidine, ranitidine and nizatidine is 2 hours, famotidine 3.5 hours, roxatidine 6 hours.

Clinical efficacy and indications for use

15 years of experience in the use of H 2 blockers has convincingly proven their high effectiveness. After their introduction into clinical practice, the number surgical interventions for peptic ulcer disease in many countries has decreased by 6-8 times.

When using H2 blockers for 2 weeks, pain in the epigastric region and dyspeptic disorders disappear in 56-58% of patients with exacerbation of gastric and duodenal ulcers. After 4 weeks of treatment, scarring of duodenal ulcers is achieved in 75-83% of patients, after 6 weeks in 90-95% of patients. Stomach ulcers heal somewhat more slowly (as with the use of other drugs): the frequency of their scarring after 6 weeks is 60-65%, after 8 weeks 85-90%.

Comparative multicenter randomized studies have shown that the effectiveness of double and single doses of cimetidine, ranitidine, famotidine, nizatidine is approximately the same. Comparing individual generations of H2 blockers, it should be noted that although ranitidine and famotidine are superior to cimetidine in antisecretory activity, convincing evidence of their higher clinical effectiveness has not been obtained. The main advantage of the latter is better tolerance by patients. Nizatidine and roxatidine do not have any special advantages over ranitidine and famotidine and therefore are not widely used.

For the treatment of ulcerative lesions of the stomach and duodenum in patients with Zollinger-Ellison syndrome, H 2 blockers are prescribed in very high doses (4-10 times higher than the average therapeutic ones), for ulcerative bleeding - parenterally.

H 2 blockers are used for anti-relapse therapy, for the treatment and prevention of erosive and ulcerative lesions of the stomach and duodenum caused by taking non-steroidal anti-inflammatory drugs, as well as “stress” ulcers.

Adverse reactions

Characteristic mainly for cimetidine:

  • antiandrogenic effect, observed with long-term use (especially in high doses), is manifested by an increase in the level of prolactin in the blood, the occurrence of galactorrhea and amenorrhea, a decrease in the number of sperm, the progression of gynecomastia and impotence;
  • hepatotoxicity: deterioration of hepatic blood flow, increased levels of transaminases in the blood, in rare cases - acute hepatitis;
  • penetrating the blood-brain barrier, the drug causes cerebral disorders (especially in the elderly): headaches, anxiety, fatigue, fever (caused by the drug’s effect on the hypothalamic thermoregulation centers), depression, hallucinations, confusion, sometimes coma;
  • hematotoxicity: neutropenia, thrombocytopenia;
  • cardiotoxicity: sick sinus syndrome, rhythm disturbances;
  • nephrotoxicity: increased serum creatinine levels.

Subsequent generation H2 blockers, ranitidine, famotidine, nizatidine and roxatidine, are much better tolerated. They do not have antiandrogenic or hepatotoxic effects, do not penetrate the blood-brain barrier and do not cause neuropsychiatric disorders. When using them, only dyspeptic disorders (constipation, diarrhea, flatulence) and allergic reactions (mainly in the form of urticaria), which are relatively rare (1-2%), can be observed.

With long-term use of H2 blockers (more than 8 weeks), especially in high doses, one should keep in mind the potential for the development of hypergastrinemia with subsequent hyperplasia of enterochromaffin cells in the gastric mucosa.

With abrupt withdrawal of H2 blockers, especially cimetidine, the development of “rebound syndrome”, accompanied by secondary hypersecretory reactions, is possible.

Drug interactions

Cimetidine is one of the most potent inhibitors of the microsomal cytochrome P-450 system in the liver. Therefore, it slows down metabolism and increases the concentration in the blood of a number of drugs: theophylline, diazepam, propranolol, phenobarbital, indirect anticoagulants and others. The weak inhibition of cytochrome P-450 by ranitidine has no clinical significance. Other H 2 blockers do not have a similar effect at all.

H 2 blockers may reduce the absorption of ketoconazole, which depends on the presence of hydrochloric acid in the stomach.

Cimetidine(altramet, histodil, neutronorm, primamet, tagamet) for exacerbation of ulcers, usually prescribed 200 mg 3 times a day before meals and 400 mg at night (1000 mg per day). In case of renal failure, the dose is reduced to 400-800 mg per day. The maintenance dose is 400 mg at night. For ulcerative bleeding: 200 mg intramuscularly or intravenously 8-10 times a day. Available in tablets of 200 and 400 mg, ampoules of 200 mg/2 ml.

Ranitidine(Zantac, Raniberl, Ranisan, Gistak, Ulcodine) is used in a therapeutic dose of 150 mg 2 times a day (morning and evening) or 300 mg at night. Maintenance dose 150 mg at night. For chronic renal failure, the therapeutic dose is reduced to 150 mg, maintaining up to 75 mg per day. For bleeding: 50 mg intramuscularly or intravenously every 6-8 hours. Available in tablets of 150 and 300 mg, ampoules of 50 mg/2 ml.

Famotidine(gastrosidin, quamatel, lecedil, ulfamide) is prescribed 20 mg 2 times a day or 40 mg at bedtime. Maintenance dose 20 mg at night. For chronic renal failure, the therapeutic dose is reduced to 20 mg per day or the intervals between doses are increased (up to 36-48 hours). Intravenously 20 mg every 12 hours (per 5-10 ml of isotonic sodium chloride solution). Available in tablets of 20 and 40 mg, ampoules of 20 mg.

Nizatidine(axid) 150 mg 2 times a day or 300 mg at night. Maintenance dose 150 mg per day. For chronic renal failure, 150 mg per day or every other day. For bleeding intravenous drip for a long time at a rate of 10 mg/hour or 100 mg for 15 minutes. 3 times a day. Available in capsules of 150 and 300 mg, bottles of 100 mg/4 ml.

Roxatidine(Roxane) 75 mg 2 times a day or 150 mg at night, with maintenance therapy 75 mg per day. For chronic renal failure 75 mg 1 time per day or every other day. Available in 150 mg tablets.

PROTON PUMP INHIBITORS

Proton pump inhibitors (PPIs) occupy a central place among antiulcer drugs. This is due, firstly, to the fact that in terms of antisecretory activity (and therefore clinical effectiveness) they are significantly superior to other drugs. Secondly, PPIs create a favorable environment for the anti-Helicobacter action of antibacterial agents, and therefore they are included as an integral component in most Helicobacter pyloric eradication schemes. Of the drugs in this group, the ones currently used in the clinic are: omeprazole, as well as less known in our country, but widely used abroad, pantoprazole And Lansoprazole

Pharmacodynamics

Inhibition of the proton (acid) pump is achieved by inhibiting the H + K ± -ATPase of parietal cells. The antisecretory effect in this case is realized not by blocking any receptors (H2-histamine, M-cholinergic) involved in the regulation of gastric secretion, but by a direct effect on the synthesis of hydrochloric acid. The functioning of the acid pump is the final stage of biochemical transformations inside the parietal cell, which results in the production of hydrochloric acid (). By influencing this stage, PPIs cause maximum inhibition of acid formation.



Rice. 2.

PPIs do not initially have biological activity. But, being weak bases by chemical nature, they accumulate in the secretory tubules of parietal cells, where, under the influence of hydrochloric acid, they are converted into sulfenamide derivatives, which form covalent disulfide bonds with cysteine ​​H + K ± ATPase, inhibiting this enzyme. To restore secretion, the parietal cell is forced to synthesize a new enzyme protein, which takes about 18 hours.

The high therapeutic effectiveness of PPIs is due to their pronounced antisecretory activity, 2-10 times higher than that of H 2 blockers. When taking an average therapeutic dose once a day (regardless of the time of day), gastric acid secretion during the day is suppressed by 80-98%, while when taking H2 blockers it is suppressed by 55-70%. As such, PPIs are currently the only drugs capable of maintaining intragastric pH above 3 for more than 18 hours, and thus meet the requirements formulated by Burget for ideal antiulcer agents.

PPIs do not directly affect the production of pepsin and gastric mucus, but according to the law " feedback" increase (1.6-4 times) the level of gastrin in the serum, which quickly normalizes after stopping treatment.

Pharmacokinetics

When taken orally, PPIs of the proton pump, getting into the acidic environment of the gastric juice, can prematurely turn into sulfenamides, which are poorly absorbed in the intestine. Therefore, they are used in capsules that are resistant to gastric juice. The bioavailability of omeprazole in this dosage form is about 65%, pantoprazole 77%, for lansoprazole it is variable. The drugs are rapidly metabolized in the liver, excreted through the kidneys (omeprazole, pantoprazole) and the gastrointestinal tract (lansoprazole). Elimination half-life of omeprazole 60 minutes, pantoprazole 80-90 minutes, lansoprazole 90-120 minutes. In diseases of the liver and kidneys, these values ​​do not change significantly.

Clinical efficacy and indications for use

Multicenter and meta-analytic studies have confirmed the higher effectiveness of PPIs in the treatment of exacerbations of peptic ulcer disease compared to H 2 blockers. Thus, within 2 weeks, clinical remission (disappearance of pain and dyspeptic disorders) is achieved in 72% of patients with duodenal ulcers and 66% with gastric ulcers. In 69% of patients, the ulcerative defect of the duodenum is scarred within the same period. After 4 weeks, healing of duodenal ulcers is observed in 93-100% of patients. Stomach ulcers heal after 4 and 8 weeks, on average, in 73% and 91% of patients, respectively.

A special indication for the use of PPIs are gastroduodenal ulcers resistant to therapy with H2 blockers. This resistance occurs in 5-15% of patients receiving H2 blockers. With 4 weeks of use of PPI, duodenal ulcers heal in 87%, and gastric ulcers in 80% of such patients, after 8 weeks in 98 and 94% of patients, respectively.

For hard-to-heel ulcers, which are often localized in the stomach, an increased effect is observed with a doubling of the dose. The frequency of scarring after 4 weeks increases to 80%, and after 8 weeks to 96%.

PPIs are also used for anti-relapse therapy of peptic ulcers, for the treatment of ulcerative lesions caused by taking NSAIDs. For gastroduodenal ulcers in patients with Zollinger-Ellison syndrome, PPIs are prescribed in doses 3-4 times higher than the average therapeutic ones.

As already indicated, PPIs are included in many anti-Helicobacter therapy regimens.

Adverse reactions

The safety profile of PPIs during short (up to 3 months) courses of therapy is very high. The most common symptoms are headache (2-3%), fatigue (2%), dizziness (1%), diarrhea (2%), constipation (1% of patients). In rare cases, allergic reactions such as skin rash or bronchospasm. With intravenous administration of omeprazole, isolated cases visual and hearing impairments.

With long-term (especially for several years) continuous use of PPIs in high doses (40 mg omeprazole, 80 mg pantoprazole, 60 mg lansoprazole), hypergastrinemia occurs, atrophic gastritis progresses, and sometimes nodular hyperplasia of enterochromaffin cells of the gastric mucosa. The need for long-term use of such doses is usually only in patients with Zollinger-Ellison syndrome and in severe cases of erosive-ulcerative esophagitis.

Drug interactions

Omeprazole and lansoprazole moderately inhibit cytochrome P-450 in the liver and, as a result, slow down the elimination of certain drugs - diazepam, warfarin, phenotoin. At the same time, the metabolism of caffeine, theophylline, propranolol, and quinidine is not affected. Pantoprazole has virtually no effect on cytochrome P-450.

Dosage and forms of release of drugs

Omeprazole(losec, omeprol, omez) is usually prescribed orally at a dose of 20 mg once a day in the morning on an empty stomach. For hard-to-heel ulcers, as well as during anti-helicobacter therapy, 20 mg 2 times a day. During maintenance therapy, the dose is reduced to 10 mg per day. For ulcer bleeding, for “stress” ulcers: 42.6 mg of omeprazole sodium (corresponding to 40 mg of omeprazole) intravenously in 100 ml of 0.9% sodium chloride solution or 5% glucose solution. Available in capsules of 10 and 20 mg, in bottles of 42.6 mg of omeprazole sodium.

Pantoprazole 40 mg orally 1 time per day before breakfast. For anti-helicobacter therapy 80 mg per day. Intravenous drip of 45.1 mg of pantoprazole sodium (corresponding to 40 mg of pantoprazole) in an isotonic sodium chloride solution. Available in capsules of 40 mg, bottles of 45.1 mg of pantoprazole sodium.

Lansoprazole(lanzap) orally 30 mg 1 time per day (morning or evening). For anti-helicobacter therapy 60 mg per day. Available in 30 mg capsules.

CYTOPROTECTERS

Cytoprotectors include drugs that increase the protective properties of the gastric mucosa and its resistance to the action of various ulcerogenic factors (primarily NSAIDs). This group includes synthetic analogues of prostaglandins ( misoprostol), sucralfate and bismuth preparations. However, the antiulcer effect of the latter is currently associated mainly with anti-Helicobacter activity, so they are discussed in the corresponding chapter.

Misoprostol

Misoprostol (Cytotec) is a synthetic analogue of prostaglandin E1.

Pharmacodynamics

The drug stimulates the production of glycoproteins in gastric mucus, improves blood flow in the gastric mucosa, and increases the secretion of bicarbonates. It also has fairly high antisecretory activity, dose-dependently suppressing basal and stimulated production of hydrochloric acid. It has been established, however, that misoprostol exhibits an antiulcer effect in doses that are insufficient to suppress acid secretion.

Pharmacokinetics

Rapidly absorbed from the gastrointestinal tract. The maximum concentration in the blood serum is reached after 15 minutes. When taken with food containing a large number of fats, absorption slows down. When deesterified, it turns into misoprostolic acid, which then undergoes the metabolism characteristic of prostaglandins and fatty acids. The half-life of misoprostol is 30 minutes. With chronic renal failure, the peak blood concentration and half-life increase slightly.

Clinical efficacy and indications for use

Misoprostol is quite effective in the treatment of exacerbations of peptic ulcers: within 4 weeks healing occurs in 76-85% of patients with duodenal ulcers, and after 8 weeks in 51-62% of patients with gastric ulcers.

However, indications for its use are currently limited to the treatment and prevention of gastroduodenal erosive and ulcerative lesions caused by NSAIDs, since one of the main mechanisms of their ulcerogenic action is to suppress the synthesis of endogenous prostaglandins in the stomach wall. In terms of effectiveness in these cases, it is superior to H2>-blockers and is approximately equivalent to omeprazole. When prescribed together with NSAIDs, misoprostol reduces the incidence of gastric ulcers from 7-11% to 2-4%, and duodenal ulcers from 4-9% to 0.2-1.4%. At the same time, the risk of developing ulcer bleeding is significantly reduced. Prescribed for the treatment of drug-induced gastroduodenal ulcers, misoprostol allows most patients to achieve healing without discontinuing NSAIDs.

Adverse reactions

Dyspeptic disorders, cramping abdominal pain, and skin rashes are noted. Most often (in 11-33% of patients), diarrhea develops due to increased intestinal motility. It is usually mild and usually goes away within a few days.

Misoprostol increases the tone of the myometrium, which may result in pain in the lower abdomen and spotting from the vagina. Therefore, it can only be taken starting 2-3 days after menstruation. The drug is contraindicated during pregnancy.

Dosage and release forms

Orally 200 mcg 4 times a day (3 times a day after meals and at night) for the entire period of taking NSAIDs. With severe chronic renal failure, the dose is reduced by 2 times. Available in tablets of 200 mcg. Included in the drug arthroteka(tablets: 50 mg diclofenac sodium, 200 mcg misoprostol), which is prescribed 1 tablet 2-3 times a day to patients with rheumatoid arthritis or osteoarthritis.

Sucralfate

Sucralfate (Alsukral, Venter, Sucramal, Sucrafil) is the main aluminum salt of sucrose sulfate. It is insoluble in water and, when taken orally, is almost not absorbed from the gastrointestinal tract.

Pharmacodynamics

In the acidic environment of the stomach, it dissociates into aluminum hydroxide and sucrose hydrogen sulfate. Despite the formation of aluminum hydroxide, sucralfate has very weak antacid activity, using only 10% of its potential acid-neutralizing properties. Sucrose hydrogen sulfate forms a complex with necrotic masses in the area of ​​the ulcer, which persists for about 3 hours and creates a barrier to the action of hydrochloric acid, pepsin and bile acids.

Reduces the absorption of phosphates in the intestine.

Clinical efficacy and indications for use

The frequency of scarring of stomach and duodenal ulcers while taking sucralfate reaches 70-80%. However, at present it is used not for course therapy of exacerbations of peptic ulcers, where it has given way to more powerful antisecretory drugs, but mainly for the prevention and treatment of gastroduodenal ulcers caused by taking ulcerogenic drugs.

Can be used to prevent stress bleeding in patients with severe injuries and burns. At the same time, as controlled studies have shown, the risk of developing hospital-acquired pneumonia is less than with the use of antacids, since sucralfate, unlike the latter, does not cause an increase in the pH of the gastric contents and the associated proliferation of gram-negative bacteria in the stomach.

It is also used for erosive and ulcerative lesions of the stomach caused by taking large quantities spicy food or alcohol, but there is no objective clinical evidence of its effectiveness in such situations.

A special indication for the use of sucralfate is hyperphosphatemia in patients with uremia who are on dialysis.

Adverse reactions

The most common are constipation (in 2-4% of patients); Dizziness and urticaria are less common. Caution must be exercised when using the drug in patients with severe renal failure.

Drug interactions

Sucralfate reduces the absorption of many drugs in the gastrointestinal tract (tetracyclines, fluoroquinolones, H 2 blockers, digoxin, long-acting theophyllines), so the intervals between their doses should be at least 2 hours.

Antacids, by reducing stomach acidity, reduce the degree of dissociation of sucralfate and weaken its activity, so they should be used at least 30 minutes before or no earlier than 30 minutes after taking sucralfate

Dosage and release forms

Orally 1 g 3 times a day 0.5-1 hour before meals (or 2 hours after meals) and at night. Another option is 2 g 2 times a day. Available in tablets of 1 g, in sachets containing 1 g of sucralfate granules. The tablets can be swallowed whole with water, or just like the granules, stir in half a glass of water and drink.

ANTI-HELICOBACTER DRUGS

Antibiotics

Of the large number of antibiotics previously used for eradication H. pylori, amoxicillin, clarithromycin, tetracycline and nitroimidazoles are currently retained.

Amoxicillin(flemoxin solutab) semi-synthetic penicillin with an extended spectrum of activity. Stable in the acidic environment of the stomach, well absorbed in the intestines. Bioavailability is about 94%. Partially metabolized in the liver, excreted by the kidneys (60-80% unchanged). Half-life 1-1.5 hours.

Amoxicillin is highly active in vitro against H. pylori However, in patients with peptic ulcer it has an anti-helicobacter effect only in combination with antisecretory drugs, primarily with proton pump inhibitors, which potentiate its bactericidal activity. When combined with nitroimidazole derivatives, amoxicillin prevents the development of resistance H. pylori to these drugs.

When conducting anti-Helicobacter eradication therapy, amoxicillin is prescribed 0.5 g 3-4 times a day or 1.0 g 2 times a day.

Clarithromycin(clacid) semi-synthetic 14-membered macrolide. By activity against H. pylori superior to other macrolides and nitroimidazole derivatives. Anti-Helicobacter action of clarithromycin in vitro amoxicillin enhances. Well absorbed from the gastrointestinal tract. Metabolized in the liver to form 14-hydroxyclarithromycin, which also has an antibacterial effect. Excreted through the kidneys and intestines. Half-life 3-7 hours.

In combination with antisecretory drugs (omeprazole, ranitidine), nitroimidazole derivatives, amoxicillin, bismuth preparations, clarithromycin exhibits a pronounced anti-Helicobacter effect and is included in the main eradication therapy regimens. However, it should be borne in mind that 5-10% of patients may experience resistance H. pylori to clarithromycin.

Prescribed 0.25 or 0.5 g 2 times a day, in some schemes 0.5 g 3 times a day. Available in tablets of 0.25 g.

Data have emerged on the possibility of including some other macrolides (roxithromycin, azithromycin) in anti-helicobacter therapy regimens.

Tetracycline has a wide spectrum of activity. Well absorbed from the gastrointestinal tract when taken on an empty stomach, excreted through the kidneys and intestines. The half-life is approximately 8 hours.

Tetracycline was one of the first antibiotics that was used to eradicate Helicobacter as part of the “classical” triple combination. Currently, it is considered as a component of a reserve quadruple therapy regimen, used when traditional treatment regimens are ineffective. In anti-helicobacter therapy regimens, tetracycline is prescribed in a daily dose of 2.0 g.

TO nitroimidazolam include metronidazole and tinidazole. Empirically, they began to be used for peptic ulcer disease even before it was discovered H. pylori, since it was believed that these drugs stimulate regeneration processes in the gastric mucosa.

Nitroimidazoles are well absorbed when taken orally. Metabolized in the liver, excreted through the kidneys and intestines.

They are used as part of many eradication schemes, although a serious problem, as it has recently become clear, is the resistance of microorganisms to nitroimidazoles, which occurs in 30% of patients in developed countries, and in almost 70-80% of patients in developing countries. The development of resistance is due to the widespread and often uncontrolled use of nitroimidazoles for the treatment of intestinal and urogenital infections. Nevertheless, nitroimidazoles retain their place in anti-Helicobacter therapy regimens. This is partly due to the fact that, having high activity against anaerobic flora, they, when prescribed in combination with another antibiotic, reduce the risk of developing pseudomembranous colitis.

Metronidazole(Trichopol, Flagyl, Efloran) is prescribed 0.25 g 4 times a day or 0.5 g 2 times a day. Available in tablets of 0.25 g.

Tinidazole(phasizhin), which has a longer half-life, is used 0.5 g 2 times a day. Available in tablets of 0.5 g.

Bismuth preparations

Bismuth preparations were widely used in the treatment of peptic ulcers back in the last century. The emphasis then was on the astringent and antiseptic properties of bismuth. After identifying the role H. pylori It has been shown that bismuth preparations have a pronounced anti-Helicobacter effect, which is bactericidal in nature. Precipitated on the surface of bacterial cells, bismuth particles then penetrate into their cytoplasm, leading to structural damage and death of microorganisms.

Currently, bismuth preparations are used in the treatment of peptic ulcers in the form of a short course as part of various Helicobacter eradication regimens.

When using bismuth preparations, dyspeptic disorders (nausea, diarrhea), allergic reactions ( skin rash). It is necessary to remember the appearance of a dark color in the stool due to the formation of bismuth sulfide. When taking normal doses of bismuth preparations, its level in the blood increases extremely slightly. Symptoms of overdose and intoxication can only be observed in patients with chronic renal failure with long-term (several months) use of high doses.

Bismuth subcitrate(de-nol, ventrisol, tribimol) colloidal tripotassium bismuth dicitrate, which in the acidic environment of the stomach forms a protective film on the surface of ulcers that prevents the action of hydrochloric acid and pepsin. Enhances mucus formation, stimulates the secretion of bicarbonates and the synthesis of prostaglandins in the stomach wall.

Previously, bismuth subcitrate was prescribed in 4-week courses as an independent antiulcer drug. Currently, it is used as a component of the classical triple eradication regimen and the backup quadruple therapy regimen. Prescribed 120 mg 4 times a day. Available in 120 mg tablets.

Bismofalk combination drug. Available in tablets, each of which contains 50 mg of basic bismuth gallate and 100 mg of basic bismuth nitrate. Prescribed 2 tablets 3 times a day before meals.

Ranitidine bismuth citrate(pylorid) combines the antisecretory properties of H 2 blockers and the bactericidal effect of bismuth. Suppresses basal and stimulated production of hydrochloric acid and has an anti-Helicobacter effect. One of the goals of creating the drug was to reduce the total number of tablets that patients with peptic ulcer disease are forced to take daily during a course of eradication therapy. Ranitidine-bismuth citrate is prescribed in combination with an antibiotic (amoxicillin or clarithromycin) 400 mg 2 times a day for 2 weeks, after which treatment continues with only ranitidine-bismuth citrate for another 2 weeks until the ulcer is completely healed. Available in 400 mg tablets.


2000-2009 NIIAKh SGMA

Peptic ulcer- a chronic recurrent disease of the gastroduodenal region, in which relapses of stomach or duodenal ulcers occur.

In the treatment of patients with peptic ulcer there are two main period(two tasks):

Treatment of the active phase of the disease (newly diagnosed peptic ulcer or its exacerbation);

Prevention of relapse (preventative treatment).

Treatment in the active phase of the disease (i.e. during the exacerbation period) includes the following main directions:

1. Etiological treatment.

2. Treatment regimen.

3. Medical nutrition.

4. Drug treatment.

5. "Herbal medicine.

6. Use of mineral waters.

7. Physiotherapeutic treatment.

8. Local treatment long-lasting ulcers.

1. Etiological treatment

Etiological treatment is an important section in the complex therapy of peptic ulcer and includes:

Elimination of chronic duodenal disorders that exist in some cases
dental patency;

stopping smoking and alcohol abuse;

elimination of factors damaging the mucous membrane of the stomach and duodenum (medicines - acetylsalicylic acid and other non-steroidal anti-inflammatory drugs, reserpine, glucocorticoids, occupational hazards, etc.).

2. Treatment regimen

The first stage of active antiulcer treatment (especially for newly diagnosed ulcers) is most appropriate to carry out in a hospital. During the period of exacerbation of the disease, the patient must be provided with mental and physical rest. It is advisable to recommend relaxed bed rest for 7-10 days, followed by replacing it with free rest. Bed rest has a beneficial effect on intra-abdominal pressure and blood circulation in the gastrointestinal tract, promotes rapid healing of ulcers. However, prolonged rest negatively affects the functional state of the body. Therefore, after eliminating acute manifestations diseases, it is necessary to gradually introduce patients to exercise therapy. With mild exacerbation of peptic ulcer disease, small size of the ulcer, outpatient treatment of patients is possible.

The criteria for discharge of a patient from the hospital are the disappearance of symptoms of exacerbation, healing of ulcers and erosion, reduction in the severity and prevalence of the inflammatory process in the esophagogastro-duodenal mucosa. Extending the duration of hospital treatment until the onset of complete endoscopic remission is not justified, since limited gastroduodenitis, and sometimes distal esophagitis with moderate degree inflammation can persist for three or more months. After discharge from the hospital, treatment is continued on an outpatient basis without release from work.

2.1. Estimated duration of inpatient treatment, outpatient treatment and temporary disability due to peptic ulcer disease

2.1.1. peptic ulcer of the stomach and duodenum,
first identified

Inpatient treatment - 29-25 days.

Outpatient treatment after inpatient treatment - 3-5 days.

The total period of temporary disability is 23-30 days.

2.1.2. Mediogastric ulcer

Inpatient treatment - 45-50 days.

Outpatient treatment after inpatient treatment - 4-10 days.

The general period of temporary disability is 50-60 days.

2.1.3. Peptic ulcer of the stomach and duodenum
(chronic flow)

Mild exacerbation

Outpatient treatment - 20-25 days

or hospital treatment- 18-20 days.

The general period of temporary disability is 18-25 days.

Moderate exacerbation

Inpatient treatment - 30-35 days.

The general period of temporary disability is 30-35 days.

Severe exacerbation

Inpatient treatment 40-45 days.

The general period of temporary disability is 40-45 days.

2.2. Working capacity of patients with peptic ulcer

Stomach and duodenal ulcers (newly identified): exemption from heavy physical labor for 2 weeks.

Mediogastric ulcer:

exemption from heavy physical labor for 3 months.

Peptic ulcer of the stomach and duodenum (chronic course).

Mild exacerbation:

liberation from hard physical labor. Exacerbation medium degree severity and severe course:

liberation from hard physical labor. For very frequent exacerbations:

release from work of moderate intensity.

3. Medical nutrition

Clinical studies in recent years indicate that mechanically and chemically gentle anti-ulcer diets No. 1a and No. 16 (in the chapter "Treatment" chronic gastritis") are indicated only for severe symptoms of exacerbation, they are prescribed only for 2-3 days, and then patients are transferred to diet No. 1. This diet stimulates the repair processes of the affected mucous membrane, prevents the development of constipation, restores appetite and has positive influence on the general well-being of the patient. Food is given boiled, but not mashed.

The diet includes white stale bread, soups from cereals, vegetables, well-cooked porridges, mashed potatoes, lean varieties of meat, poultry, fish (boiled, in pieces), ripe fruits, baked or boiled berries, berry and fruit juices, cottage cheese, milk, omelettes, puddings and cottage cheese pancakes.

You need to eat 5-6 times a day. Diet No. 1 contains proteins - 110-120 g, fats - 110-120 g, carbohydrates - 400-450 g. It is not recommended to eat spicy foods, pickled and smoked foods.

During the period of remission, there are no major dietary restrictions, but frequent meals are recommended, which have a buffering effect and prevent duodenogastric reflux. In the scarring phase of the ulcer, patients can be transferred to a general diet.

In recent years, the need to prescribe special therapeutic nutrition for patients with peptic ulcer disease has been questioned, since the effect of diet therapy on the healing time of ulcers has not been proven. In addition, modern pharmacotherapeutic agents allow sufficiently block acid formation stimulated by food intake.

In the diet of patients with peptic ulcers, it is necessary to provide an optimal amount of protein (120-125 g) in order to meet the requirements

nosgey of the body in plastic material and strengthening of regeneration processes. In addition, complete protein supplied to sufficient quantity with food, reduces the excitability of glandular cells, reduces the production of hydrochloric acid and pepsin, has a neutralizing effect on acidic contents (binds hydrochloric acid), which creates peace for the stomach and leads to the disappearance of pain. X. X. Mansurov (1988) proposed adding soy flour to the diet of patients 5 g 3 times a day 30 minutes before meals for 4-6 weeks as vegetable fiber, which reduces the production of hydrochloric acid and pepsin, normalizes the motor function of the gastrointestinal tract.

4. Pharmacotherapy

Drug therapy for patients with peptic ulcer disease (PU) is one of the most important components of conservative treatment.

Main groups of drugs for the treatment of ulcers

I. Drugs that suppress Helicobacter pylori infection (de-nol, trichopolum, furazolidone, oxacillin, ampiox and other antibiotics).

II. Antisecretory agents (suppressing the secretion of hydrochloric acid, pepsin and increasing intragastric pH or neutralizing and adsorbing hydrochloric acid and pepsin).

1. M-anticholinergics:

Non-selective (atropine, platyphylline, metacin);

Selective (gastrocepin, pirenzepin).

2. H2-histamine receptor blockers:

Tsimetvdin (histodil, tagamet);

Ranitvdin (ranisan, acelok E, zantac, pentoran);

Famotidine (ulfamide);

Nizatidine (Axid);

Roxatidine.

3. H + K + -ATPase (proton pump) blockers - omeprazole (omez, losec, timoprazole).

4. Gastrin receptor antagonists (proglumide, milid).

5. Antacids (sodium bicarbonate, magnesium oxide, calcium carbonate, almagel, phosphalugel, maalox, gaviscon, bismuth).

III. Gastrocytoprojectors (increasing the resistance of the mucous membrane of the stomach and duodenum).

1. Cytoprotective agents that stimulate mucus formation:

Carbenoxolone;

Synthetic prostaglandins - enprostil, cytotec.

2. Cytoprotectors that form a protective film:

Sucralfate;

Colloidal bismug - de-nol;

3. Enveloping and astringent agents:

Bismuth preparations - Vikalin, Vikair.

IV. Drugs that normalize the motor function of the stomach and duodenum (cerucal, raglan, metoclopramide, eglonil, sulpiride), antispasmodics (no-spa, papaverine).

V. Reparants (solcoseryl, obleggikh oil, anabolics, acemin, gastrofarm).

VI. Facilities central action(dalargin, eglonil, sedatives, tranquilizers).

4.1. Agents that suppress Helicobacter pylori infection

Currently Helicobacter pylori(HP) is recognized as the leading etiological factor in gastric and duodenal ulcers. HP is found in the mucous membrane of ulcers in almost 100% of cases; its role in the development of inflammation, the formation of erosions and ulcers in the mucous membrane of the stomach and duodenum has been proven. Exacerbation of Helicobacter pylori infection is also the most common cause of exacerbation of ulcerative disease.

In this regard, the main modern principle of treatment of ulcer and the accompanying chronic active gastroduodenitis associated with HP is the destruction of bacteria infecting the gastric mucosa and duodenum.

For this purpose, drugs are used that suppress the activity of HP, which contributes to the rapid onset of remission and the prevention of relapses.

De-nol(colloidal bismuth subcitrate), available in tablets of 0.12 g. When taken orally, the drug gradually forms a colloidal mass distributed over the surface of the mucous membrane of the stomach and duodenum. The ulcer becomes covered with a foamy white coating, which persists for several hours and is easily detected endoscopically.

In a de-nol solution, the pH is approximately 10.0. Lowering the pH to 4.0 or lower by exposure to hydrochloric acid causes precipitation of insoluble bismuth oxychloride and citrate. When exposed to gastric juice, a precipitate forms at pH 3.5.

Maximum precipitation occurs at pH values ​​ranging from 2.5 to 3.5. The pH of gastric acidity is usually below this limit, which, however, is achieved by combining hydrogen ions with amino acids at the ulcer site.

The drug causes the formation of chelate compounds of bismuth and proteins of ulcerative exudate, which protect ulcers and erosions from the further destructive effects of gastric juice. De-nol forms a complex with gastric mucus, which is more effective against hydrogen ions than normal gastric mucus.

In addition, de-nol reduces the activity of pepsin and has a gastrocytoprotective effect (increases the quantity and quality of gastric

mucus, increases the production of gastric mucin). De-nol destroys HP infection in the stomach and duodenum.

De-nol take 1 tablet half an hour before breakfast, lunch and dinner and before bed for 4-6 weeks. The drug should not be taken with milk; half an hour before taking it and for half an hour after it, you should refrain from drinking drinks, solid food and antacids (so as not to increase the pH of gastric juice and reduce the activity of the drug).

There is another method of treatment with de-nol: 2 tablets half an hour before breakfast and 2 hours after dinner, washed down with water.

The drug has virtually no side effects or contraindications; nausea occurs occasionally. De-nol causes darkening of stool.

During a course of treatment with de-nol in the form of monotherapy (4-8 weeks), an average of up to 50% of HP is destroyed. De-nol has direct cytotoxicity and destroys both dividing and dormant bacteria, preventing the formation of strains resistant to therapy. To increase the effectiveness of treatment, de-nol must be combined with other antibacterial agents(metronidazole, ampicillin, clarithrimycin, amoxicillin, tetracyclines) and omeprazole(Ch. "Treatment of chronic gastritis").

Optimal combinations for course therapy of peptic ulcer disease associated with HP (P. Ya. Grigoriev, A. V. Yakovenko, 1997).

1. De-nol 0.12 g 4 times a day for 14 days + metronidazole(Trichopolum) 0.25 g 4 times a day for 14 days + gastrocepin 0.05 g 2 times a day for 8 weeks for duodenal ulcer and 12 weeks for gastric ulcer.

2. Gastrostatpo 1 tablet 5 times a day for 10 days + omeprazole(Losec) 20 mg 2 times a day for 10 days and 20 mg 1 time a day for 4 weeks for duodenal ulcer and 6 weeks for gastric ulcer.

Gastrostat is a combined preparation containing 108 mg of colloidal bismuth subcitrate, 200 mg metronidazole, 250 mg tetracycline.

3. Omeprazole (Losec) 20 mg 2 times a day for 7 days and 20 mg 1 time a day for 4 weeks for duodenal ulcer and 6 weeks for gastric ulcer +metronidazole amoxicillin 500 mg 4 times a day for 7 days or clarithrimycin

4. Ranitidine 150 mg 2 times a day for 7 days and 300 mg 1 time a day for 8 weeks for duodenal ulcer and 16 weeks for gastric ulcer + metronidazole 250 mg 4 times a day 7 days + amoxicillin 500 mg 4 times a day or clarithrimycin 250 mg 2 times a day for 7 days.

5. Ftotidt(kvamatel, ulfamid) 20 mg 2 times a day for 7 days and 40 mg 1 time a day for 8 weeks for duodenal ulcer and 16 weeks for gastric ulcer + metronidazole 250 mg 4 times a day 7 days + amoxicillin 0.5 g 4 times a day or clarithrimycin 250 mg 2 times a day for 7 days.

With the first combination of agents, HP infection is eliminated in 80% of cases, with the 2nd, 3rd, 4th, 5th combinations - in 90% of cases or more.

Of interest are the data from Khulusi et al. (1995) that bile acids inhibit HP growth by damaging bacterial walls. The same authors established a reliable inhibitory effect of linoleic acid

you on the growth of Helicobacter, which is associated with its active incorporation and accumulation in them. It has been shown that the incidence of duodenal ulcer inversely correlates with the consumption of unsaturated fatty acids.

The number of relapses in patients with peptic ulcer after combination anti-Helicobacter pylori therapy is less than with de-nol monotherapy.

To consolidate remission, it is advisable to carry out repeated courses of antibacterial therapy de-nol, oxacimin, trichopolom with possible replacement of the last two drugs furazhodon, tetracycline, amoxicimine or erythromycin.

N. E. Fedorov (1991) showed high efficiency in HP tari vida(ofloxacin) at a dose of 0.2 g 2 times a day after meals for 10-14 days, as well as cephalexin in capsules of 0.25-0.5 g 4 times a day for 7-14 days, regardless of food intake.

4.2. Antisecretory agents

Antisecretory agents have a different mechanism of action: they suppress the secretion of hydrochloric acid and pepsin, or neutralize or adsorb them.

One of the most important factors of ulcer formation is acid-pegging. The production of hydrochloric acid is controlled by three types of receptors located on the basement membrane of parietal cells - Ngistamine, gastrin and M-cholinergic receptors.

Inside the cell, the effect of stimulation of H 2 -Histamine receptors is realized through the activation of adenylate cyclase and an increase in the level of cAMP, and gastrin and M-cholinergic receptors - through an increase in the level of free Ca ++.

The final stage of intracellular reactions is the activation of H + K + -ATPase, leading to an increase in the secretion of hydrogen ions into the lumen of the stomach.

Thus, the production of hydrochloric acid can be reduced with the help of Ngistamine and M-cholinergic receptor blockers, as well as H + K + -ATPase inhibitors (6)

Somatosgatin and prostaglandin E 2 have an antisecretory effect by inhibiting adenozyme enzyme.

4.2.1. M-anticholinergics

M-anticholinergics have the ability to block M-cholinergic receptors; they become insensitive to acetylcholine formed in the area of ​​the endings of postganglionic parasympathetic (cholinergic) nerves. There are two subtypes of M-cholinergic receptors (M and M2), which differ in density in different organs.

Non-selective M-anticholinergics block M and Mg cholinergic receptors and reduce the secretion of hydrochloric acid, bronchial, sweat glands, pancreas, cause tachycardia, and reduce the tone of the GLAD-muscular organs.

Selective M, -CholInalithias1 selectively block M, -CHOLIN receptors of the stomach and reduce its secretory and motor activity, with virtually no effect on M-cholinergic receptors of other organs (heart, bronchi, etc.).

Non-selective M^ and M 2 -anticholinergics

Atropine - used in VVD 0.1% solution orally 5-10 drops or subcutaneously 0.5-1 ml 30 minutes before meals and at night.

Metacin - taken orally in tablets of 0.002 g 3 times a day 30 minutes before meals and 0.004 g before bedtime or 1-2 ml of a 0.1% solution subcutaneously 1-3 times a day.

Platifillin - applied orally 0.003-0.005 g 3 times a day before meals and at night or 1-2 ml of a 0.2% solution subcutaneously 2-3 times a day.

Platiphylline and metacin, unlike atropine, are better tolerated by patients and cause dry mouth to a lesser extent.

Belladonna extract - taken orally 0.015 g 3 times a day before meals and at night. Belladonna is also included in the composition of the tablets becarbon, by-lastezin, belmeti etc. .

Non-selective M-cholinolytics cause the following side effects: dry mouth, decreased visual acuity, increased intraocular pressure, tachycardia, urinary retention, atonic constipation, often bile stasis, sometimes mental agitation, hallucinations, euphoria, dizziness occur.

Contraindications: glaucoma, prostate adenoma, bladder atony, constipation, hypokinetic dyskinesia biliary tract, reflux esophagitis, esophageal achalasia.

Non-selective M-holinolytics give a short antisecretory effect. It is advisable to combine them with antacids (this potentiates their effect); this combination quickly eliminates hyperkinetic disorders of motility of the stomach and intestines, and quickly relieves pain and dyspeptic disorders.

Non-selective M-anticholinergics are usually prescribed 30-40 minutes before meals (or 1.5 hours before the onset of pain) and before bedtime. For severe pain in the first 5-7 days, it is advisable to administer the drugs parenterally. The course of treatment lasts 2-3 weeks, if necessary it is increased to 4-6 weeks, taking a break of 2-3 days every 10 days to avoid overdose.

Non-selective M-cholinolytics are more indicated for pilorhoduodenal ulcer. The possibility of using drugs of this group for monotherapy has not been proven. They are used mainly during exacerbation.

Selective M-anticholinergics

Gastrocepin (pireiaapt)- tablets of 0.025 and 0.05 g, ampoules of 2 ml (10 ml of dry preparation) with the addition of a solvent. Selectively blocks Mg cholinergic receptors of the stomach, significantly suppresses the secretion of pepsin and hydrochloric acid, quickly reduces pain, dyspeptic symptoms, and shortens the healing time of ulcers.

The drug is well tolerated, has virtually no side effects (only dry mouth is possible), and can be prescribed in cases where non-selective M-anticholinergics are contraindicated. The drug penetrates the blood-brain barrier poorly and does not affect the central nervous system.

Gastrocepin is used to treat duodenal and gastric ulcers (with preserved secretion). Prescribed orally 25-50 mg in the morning before breakfast and 50 mg in the evening before bed; for duodenal ulcer, the daily dose can be 125 mg (50 mg before breakfast and 100 mg before bed). Can be used intramuscularly at 10 mg 2-3 times a day.

Healing of duodenal ulcers is usually observed at 3-4 weeks, gastric ulcers - at 4-6 weeks. With long-term use at night at a dose of 50 mg, a decrease in the frequency of relapses was noted, less pronounced than with the use of H2-histamine receptor blockers.

At a dose of 100-150 mg/day, Gastrocepin caused ulcer healing in 60-90% of patients.

Telenzepin - a new analogue of gastrocepin, but 10-25 times more active than it, it binds more selectively to M.-cholinergic receptors.

Among anticholinergics, telenzepine is the most potent inhibitor of hydrochloric acid secretion. The drug is administered intravenously for 15-20 days; 3-5 mg can be taken orally before breakfast and in the evening before bed.

Selective Mr. Anticholinergic blockers can be recommended for monotherapy of patients with peptic ulcer of the stomach and duodenum, but, according to Yu. B. Belousov, only in cases of mild disease. In cases of mild to moderate peptic ulcer disease and the absence of pronounced hypersecretion of hydrochloric acid, selective M,-CHOLINOLYTICS can be considered as an alternative to H2-histamine receptor blockers; in particular, Gastrocepin can be used if the latter are ineffective.

4.2.2. Blockers of Shch-histamine receptors

The stimulating effect of histamine on gastric secretion is carried out through the Hg receptors of the parietal cells of the stomach. By blocking these receptors, H2-histamine receptor blocking drugs have a pronounced antisecretory effect. In the therapeutic doses used, they reduce the basal secretion of hydrochloric acid by 80-90%, inhibit the production of pepsin, and reduce nighttime gastric acid secretion (by 70-90%).

Blockers of H 2 -histamine receptors were created in the mid-70s. This major achievement in medicine of the 20th century was awarded the Nobel Prize in 1988.

Hg histamine receptor blockers are the most effective and frequently used antiulcer drugs - the “gold standard” of antiulcer therapy.

Drugs in this group also affect the motility of the gastrointestinal tract and regulate the function of the gastric and esophageal sphincters. There are 5 generations of H2-histamine receptor blockers.

Hg blockers of histamine receptors of the 1st generation

Cimetidine(histodil, belomet, tagamet, acylok) is available in tablets of 0.2 g, ampoules of 2 ml of 10% solution.

During an exacerbation of peptic ulcer, cimetidine is prescribed 200 mg 3 times immediately after meals or during meals and 400 mg at night or 400 mg after breakfast and before bed for 4-8 weeks or more, and then 400 mg before bed for a long time (from 6 to 12 months). This distribution of the drug during the day is due to the fact that from 11 pm to 7 am, 60% of hydrochloric acid is released, and from 8 am to 10 pm - only 40% of hydrochloric acid.

Cimetidine can also be used intramuscularly or intravenously at 200 mg every 4-6 hours.

In recent years, cimetidine has been prescribed once at night in a dose of 800 mg (this method of administration gives the same antacid effect as twice the use of the drug 400 mg).

Cimetidine has a healing effect on duodenal ulcers and gastric ulcers with high acidity. At the same time, the drug is not very effective for stomach ulcers with low secretion of hydrochloric acid and does not prevent its recurrence. But, according to some data, cimetidine is effective for mediogastric localization of ulcers due to the ability to reduce dysrhythmia in the activity of the neuromuscular apparatus of the antrum of the stomach and normalize the reparative processes of the mucous membrane of the gastroduodenal zone.

Cimetidine causes the following side effects:

Hyperprolacganemia, which causes persistent galactorrhea syndrome in women and gynecomastia in men;

Antiandrogenic effect (loss of libido, impotence), to a certain extent associated with hyperprolainemia;

Impaired liver and kidney function, and in case of severe renal and hepatic failure and large doses of the drug - side effects from the central nervous system: drowsiness, depression, headache, agitation, periods of apnea;

“rebound syndrome” is the possibility of a rapid relapse of peptic ulcer disease, often with complications in the form of gastroduodenal bleeding when the drug is abruptly discontinued, which is associated with hyperplasia of gastrin-producing cells and the preservation of their activity while taking cimetidine. To avoid this syndrome, it is necessary to reduce the dose of the drug very gradually and combine for

1.5-2 months of therapy with cimetidine with anticholinergics or antacids. It is recommended to take β-blockers for a long time, which prevent degranulation of mast cells, inhibit the activity of endocrine cells and the release of gastrin;

Cardiac arrhythmias, lowering blood pressure (when administered intravenously); neutropenia, thrombocytopenia;

Formation of antibodies to cimetidine long-term treatment;

Skin rashes, itching.

Cimetidine is a powerful inhibitor of microsomal oxidation due to inhibition of the activity of cytochrome P 45 o enzymes and increases the concentration of many drugs in the blood - theophylline, oral anticoagulants, diazepam, lidocaine, propranolol and metoprolol.

Cimetidine also increases the absorption of ethanol and inhibits its breakdown, which is due to inhibition of microsomal oxidation of ethanol.

According to Yu. B. Belousov (1993), during treatment with cimetidine compared to placebo, duodenal ulcers are scarred in the majority of patients: in 82.6% during treatment with cimetidine compared to 48% during placebo.

In approximately half of the patients, the duodenal ulcer heals in the first 2 weeks, in 67% - after 3 weeks, in 89% - after 4 weeks. Gastric ulcers heal in 57-64% of patients after 4 weeks, in 91% - after 8 weeks.

It should be noted that 10-25% of ulcers are resistant to treatment with cimetidine, even if it is used in a daily dose of 1-1.2 g.

If after 4-6 weeks of treatment with cimetidine in an adequate dose the ulcer has not healed, you can proceed as follows (P. Ya. Grigoriev):

1. add gastrozepin to the therapy with cimetidine at a dose of 50-75 MG at night;

2. replace cimetidine with more powerful ranitidine or famotidine;

3. switch to treatment with other drugs (omeprazole, De-nol, sucral-fat).

Resistance of ulcers to treatment with cimetidine may be due to the formation of antibodies to it during long-term use and, to a certain extent, continued smoking during treatment with cimetidine.

Cimetidine extended release neutronorm-retard Available in tablets of 0.35 g, take 1 tablet with each meal, for maintenance therapy - 1 tablet at night.

II generation histamine receptor blockers

Ranitidine Available in tablets of 0.15 g. Synonyms: ranisan, acylok E, zantac, ranigast.

Compared with cimetidine, ranitidine has a 4-5 (according to some data, 19) times more pronounced antisecretory effect and lasts longer (10-12 hours), while the drug causes almost no side effects (rarely headache, constipation , nausea).

In the mechanism of action of ranitiDIN, in addition to the blockade of H2-histamine receptors, its ability to enhance the inactivation of hisgamine, which is associated with an increase in the activity of taegamin methyltransferase, is also important.

Pharmacokinetic studies have shown that ranitidine is sufficient to prescribe at a dose of 150 mg 2 times a day or 300 mg once a day.

night, i.e. its effective dose is 3-4 times less than that of cimetidine. The effectiveness of two-time use of ranitidine and a single dose at night is almost the same, but a single dose of the drug at night is more convenient in outpatient practice.

According to P. Ya. Grigoriev, after 4 weeks of treatment with ranitvdin, gastric ulcers scar in 80-85% of patients, duodenal ulcers - in 90%, with 6-week treatment, scarring of gastric ulcers is observed in 95% of patients, duodenal ulcers - almost in 100% of patients.

Ranitidine does not have the side effects of cimetidine, does not affect the metabolism of other drugs, since it does not inhibit the activity of liver monooxygenase enzymes. Treatment with ranitidine can be continued for several months or even years. Long-term (for 3-4 years for duodenal ulcers and 2-3 years for mediogastric ulcers) maintenance, continuous or intermittent therapy with ranitidine at a dose of 150 mg at night reduces the frequency of relapses of peptic ulcer disease.

Ranitidine bismuth citrate(pylorid) - complex drug, combining in its structure the H2-histamine receptor blocker ranitidine and bismuth citrate. The drug inhibits gastric secretion, has anti-Helicobacter and gastrocytoprotective effects. Available in 400 mg tablets.

Treatment regimen for duodenal ulcers with HP infection: for the first 2 weeks, ranitidine-bismuth citrate is taken 400 mg 2 times a day in combination with clarithromyctomus at a dose of 250 mg 4 times a day or 500 mg 3 times a day or amoxicymin at a dose of 500 mg 4 times a day. After 2 weeks, antibiotics are stopped, and treatment with ranitidine-bismuth citrate is continued for another 2 weeks. For duodenal ulcers without HP infection, take ranitidine bismuth citrate 400 mg 2 times a day for 4 weeks. For stomach ulcers, the drug is used in the same dose, but for 8 weeks.

III generation Hg histamine receptor blockers

Famotidine(ulfamide, pepcid) is available in tablets of 0.02 and 0.04 g and ampoules (1 ampoule contains 20 mg of the drug) and wafers containing 20 or 40 mg of the drug. The antisecretory effect is 9 times greater than ranitidine and 32 times greater than cimetidine.

In case of exacerbation of peptic ulcer, famotidine is prescribed 20 mg in the morning and 20-40 mg in the evening before bedtime or 40 mg before bedtime for 4-6 weeks; to prevent relapse, the drug is prescribed 20 mg once at night for 6 months or more.

The drug is well tolerated and causes almost no side effects.

IV generation Ngistamine receptor blockers

Nizatidine(axid) is available in tablets of 0.15 g. Prescribed 0.15 g 2 times a day or 0.3 g at night for a long time for the treatment of ulcers and 0.15 g at night to prevent exacerbation of ulcers. In 4-6 weeks, gastroduodenal ulcers heal in more than 90% of patients.

V generation ff2-histamine receptor blockers

Roxacidin - Available in tablets of 0.075 g, prescribed 150 mg per day in 2 or 1 dose (in the evening before bedtime). It is believed that drugs of the IV and V generations are practically free of side effects.

H2-histamine receptor blockers are the most active antisecretory agents; in addition, they also stimulate the production of protective mucus (i.e., they also have a gastroprotective effect).

eat), normalize motor function gastroduodenal zone, effective for duodenal and gastric ulcers with high acidity, both to relieve exacerbations and to prevent relapses of peptic ulcer disease. At the same time, there is an opinion that H2-histamine inhibitors receptors for symptomatic ulcers are ineffective, in this situation it is more advisable to use antacids, as a prophylactic, or de-nol, as well as synthetic analogues pro-staglandins (Cytotec and etc.).

4.2.3. Blockers H + K + -ATPase (proton pumps)

Enzymes H+K+-ATPases participate in the functioning "proton pump" of secretory tubules lining stomach cells, which provides the synthesis of hydrochloric acid.

Omeprazole(losec, timoprazole, omez) - available in tablets of 0.02 g, is a derivative benzimidazole and blocks the enzyme N + K + - ATPase, involved in the final stage of the synthesis and excretion of hydrochloric acid.

Omeprazole suppresses both basal, and stimulated secretion of hydrochloric acid, since it acts on the intracellular enzyme, and not on receptor device and, in addition, does not cause side effects, since it exists in active form only in the parietal cell.

After 7 days of treatment omeprazole at a dose of 30 mg per day basal and stimulated secretion is blocked 100% (London, 1983).

A single dose of 80 mg of omeprazole leads to complete inhibition of secretion for 24 hours. By changing the dose and time of administration of this drug, you can set the desired pH value in the gastric lumen.

Omeprazole is the most powerful antisecretory drug; with a monthly course, it promotes scarring of duodenal ulcers in almost 100% of cases. It caused scarring of stomach and duodenal ulcers when ranitidine-resistant ulcers in 94.4% of patients.

After discontinuation of omeprazole, there is no “rebound” increase in gastric secretion. Omeprazole is the only drug that is superior in effectiveness H2-histamine blockers receptors in patients with peptic ulcer disease.

When treated with omeprazole, persistent achlorhydria leads to increased production gastrin and hyperplasia enterochromaffin cells (ECL) of the stomach (in 10-20% of patients), but not to dysplasia or neoplasia. In connection with this effect, treatment with omeprazole is recommended to be prescribed only for exacerbation of peptic ulcer for 4-8 weeks, mainly for severe cases. leptic ulcers that cannot be treated with other antiulcer drugs (H 2 -gastamine blockers).

The drug is prescribed orally. The usual doses for peptic ulcer of the duodenum and stomach are 20-40 mg 1 time per day before breakfast (20 mg 2 times a day is possible), for the syndrome Zollinger-Ellison the daily dose can be increased to 60-80 mg per day (in 2 divided doses). There is also a method of using omeprazole 30 mg orally in the evening (after dinner), the dose can be increased to 60 mg after dinner.

4.2.4. Antagonists gastrin receptors

This group of antiulcer drugs blocks gastrinaceae receptors, reduces the secretion of hydrochloric acid and increases resistance gastric mucosa.

Proglumide(mtsh)- tablets of 0.2 and 0.4 g, glutamic acid derivative. Used orally in a daily dose of 1.2 g in 4-5 doses. The duration of treatment is 4 weeks.

In terms of effectiveness, the drug does not differ from Hg histamine receptor blockers, it significantly reduces acid formation, has a local protective effect, strengthening the mucous barrier of the stomach and duodenum. After 4 weeks of treatment, ulcer scarring occurs in 83% of cases; 6 months after treatment, relapses are noted in 8%, after 2 years - in 35% (Bergman, 1980).

4.2.5. Antacids and adsorbents

Antacids and adsorbents neutralize hydrochloric acid in the stomach without affecting its production. By reducing the acidity of gastric juice, these drugs have a beneficial effect on tone (eliminate muscle spasm) and the mountain-evacuation function of the gastroduodenal zone.

Antacids are divided into three groups:

absorbable (easily soluble, short but fast acting);

non-absorbable (insoluble, long-acting);

adsorbent.

Absorbable antacids

Absorbed antacids dissolve in gastric juice (and sodium bicarbonate - in water), have a high acid-binding ability, act quickly, but for a short time (from 5-10 to 30 minutes). In this regard, soluble antacids are used to relieve pain and heartburn; pain and heartburn are most quickly relieved by taking sodium bicarbonate.

Sodium bicarbonate(soda) - used in a dose of 0.5-1 g 1 and 3 hours after meals and at night. In case of prolonged use, it may cause alkalosis. When taken orally, carbon dioxide molecules are formed in the gastric cavity when hydrochloric acid is neutralized and this leads to secondary hypersecretion of gastric juice (however, this effect is low). 1 g of sodium bicarbonate neutralizes 11.9 mmol of hydrochloric acid.

Magnesium oxide(burnt magnesia) - prescribed in a dose of 0.5-1 g 1 and 3 hours after meals and at night. Neutralizes hydrochloric acid of gastric juice, without the release of carbon dioxide and therefore the antacid effect is not accompanied by secondary hypersecretion of gastric juice. Passing into the intestines, the drug causes a laxative effect. 1 g of magnesium oxide neutralizes 49.6 mmol of hydrochloric acid.

Magnesium carbonate basic(magnesii subcarbonas) is prescribed 0.5-1.0 g 1 and 3 hours after meals and at night. Has a slight laxative effect. It is also included in the Vikalin and Vikair tablets.

Calcium carbonate(precipitated chalk) - has a pronounced antacid activity, acts quickly, but after the cessation of the buffering effect it increases the secretion of gastric juice. Has a pronounced antidiarrheal effect. Prescribed orally 0.5-1 g 1 and 3 hours after meals and at night. 1 g of calcium carbonate neutralizes 20 mmol of hydrochloric acid.

Gafter mixture: calcium carbonate, bismuth subnitrate, magnesium hydro-CSID in a ratio of 4:1:1. Prescribed 1 teaspoon per ½ glass of water 1.5-2 hours after meals.

Rent - antacid preparation containing 680 mg of calcium carbonate and 80 mg of magnesium carbonate. Take 1-2 tablets 4 times a day (1 hour after meals and at night), if necessary, you can increase the daily dose to 16 tablets. The drug has a pronounced neutralizing effect on the hydrochloric acid of gastric juice (the pH of gastric juice increases to 4.3-5.7), quickly relieves heartburn. Rennie is well tolerated. The use of the drug is contraindicated in case of renal failure and hyperkalydemia. The onset of action of reHNi is 5 minutes after administration, the duration of action is 60-90 minutes.

Non-absorbable antacids

Non-absorbable antacids have slow neutralizing properties, adsorb hydrochloric acid and form buffer compounds with it. The drugs of this group are not absorbed and do not change the acid-base balance.

Aluminum hydroxide(alumina) - has antacid, adsorbing and enveloping properties. The drug neutralizes hydrochloric acid (1 g of the drug neutralizes about 250 ml of 0.1 N solution of hydrochloric acid) with the formation of aluminum chloride and water; The pH of gastric juice gradually increases to 3.5-4.5 and remains at this level for several hours. At this pH value, the peptic activity of gastric juice is also inhibited. In the alkaline contents of the intestine, aluminum chloride forms insoluble and non-absorbable aluminum compounds. Available in powder form, used orally as a 4% suspension in water, 1-2 teaspoons 4-6 times a day 30 minutes before meals or 1 hour after meals and at night.

It is advisable to combine aluminum hydroxide with magnesium oxide (burnt magnesia). Magnesium oxide reacts with hydrochloric acid to form magnesium chloride, which has laxative properties. In order to prolong the angacid effect of magnesium oxide, it is used in a dose of 0.5-1 g 1-3 hours after meals. Magnesium oxide is included in many other antacid medications.

Protab contains aluminum hydroxide, magnesium hydroxide, methylpolyxylosane (absorbs gas bubbles and eliminates symptoms of flatulence).

Alfogy - aluminum phosphate gel, envelops the mucous membrane. Prescribed 1-2 packets of 16 g 3 times a day in 1/2 glass of water before meals or 2 hours after meals.

Almagel - bottles of 170 ml. A combined preparation, every 5 ml of which (1 dosage spoon) contains 4.75 ml of aluminum hydroxide gel and 0.1 g of magnesium oxide with the addition of D-sorbitol. It has antacid, enveloping, and adsorbing properties. D-sorbitol has a laxative and choleretic effect. The dosage form (gel) creates conditions for uniform distribution of the drug throughout the gastric mucosa and a longer lasting effect.

Almagel A - bottles of 170 ml. This is an almagel containing an additional 0.1 g of anesthesin for every 5 ml of gel. Almagel A is used if a hyperacid state is accompanied by pain, nausea, and vomiting.

Almagel and Almagel A are prescribed orally 1-2 teaspoons (dosage) 4 times a day (morning, afternoon, evening 30 minutes before

meals or 1-1.5 hours after meals) and before bedtime. To avoid dilution of the drug, do not take liquid in the first half hour after taking it. After taking the drug, it is recommended to lie down and turn from side to side several times every 2 minutes (to improve the distribution of the drug on the gastric mucosa). The duration of treatment is 3-4 weeks. With long-term treatment, hypophosphatemia and constipation may develop.

Phosphalugel - available in sachets of 16 g. The drug contains aluminum phosphate (23%) in the form of a colloidal gel, as well as pectin and agar-agar. The drug has an antacid and enveloping effect, protects the gastric mucosa from the effects of aggressive factors.

It is taken orally undiluted (1-2 sachets) with a small amount of water or diluted Chg a glass of water (you can add sugar) 30 minutes before a meal or 1.5-2 hours after a meal and at night.

Lini - tablets containing 0.45 g of aluminum hydroxide in combination with magnesium carbonate and magnesium oxide (0.3 g). The drug has a high antacid effect. Take 1-2 tablets 1 hour after meals 4-6 times a day.

Compensated - 1 tablet contains 0.5 g of aluminum silicate and 0.3 g of sodium bicarbonate. Take 1 tablet 1-1.5 hours after meals 3 times a day and at night.

Alugastrj - sodium salt of dischdroxyaluminum carbonate, has an antacid, astringent, enveloping effect. Produced in bottles of 250 ml and sachets of 5 and 10 ml. It is taken orally 0.5-1 hour before or 1 hour after meals and at night, 1-2 teaspoons of the suspension or the contents of 1-2 sachets (5 or 10 ml) with a small amount of warm boiled water or without it.

Maadox (maalokat) - is issued in the form of suspension in bags on 10 and 15 ml, in tablets, bottles on 100 ml. It is a well-balanced combination of aluminum hydroxide and magnesium hydroxide, which provides a high neutralizing ability and a gastrocytoprotective effect.

10 ml of suspension contains 230 mg of aluminum hydroxide, 400 mg of magnesium hydroxide, as well as sorbitol and mannitol. 15 ml of suspension neutralizes 40.5 meq HC1, one tablet - 18.5 meq. The gastroprotective effect of the drug is due to the stimulation of mucus formation and the synthesis of PgE 2 .

The drug is prescribed 1 hour after eating and immediately before bedtime 1-2 sachets or 1-2 tablets.

Shalox-70 tablets, sachets of 15 ml, vials of 100 ml of suspension. Is different increased content active ingredients, which provides acid-neutralizing activity up to 70 meq. One tablet contains 400 mg aluminum hydroxide and 400 mg magnesium hydroxide. 15 ml suspension in a sachet contains 523.5 mg of aluminum hydroxide and 598.5 mg of magnesium hydroxide. The drug is used 1 hour after meals and immediately before bedtime 1-2 sachets or 1-2 tablets.

Magnesium tishkat - antacid, adsorbent and enveloping agent, 1 g of magnesium tilicate binds 155 ml of 0.1 N. hydrochloric acid solution. The drug is a slow-acting antacid. The colloid formed as a result of the interaction of magnesium tilicate and hydrochloric acid has a high adsorption capacity and protects the gastric mucosa from the aggressive effects of hydrochloric acid and pepsin. Magnesium tilicate is taken orally 0.5-1.0 g 3-4 times a day 1-3 hours after meals.

Gaviscon - combined antacid and an enveloping agent. Available in packages, containing 0.3 g sodium bicarbonate, 0.2 g aluminum hydroxide, 0.05 g magnesium tilicata and 1 g of basic magnesium carbonate. The contents of the package are dissolved in 80-100 ml of water and taken 4-6 times a day during the inter-digestive period (1 and 3 hours after meals and at night).

Telusil-varnish - a combination drug, available in tablets. One tablet contains 0.5 g of aluminum silicate, 0.5 g of magnesium silicate and 0.3 g of skimmed milk powder. Is non-absorbable antacid long-acting. Prescribed 1 tablet 1.5-2 hours after meals and at night.

Pee-hoo (Finland) - a combined preparation consisting of aluminum hydroxide, magnesium carbonate, calcium carbonate, burnt magnesia. Available in tablets of 0.8 g and bottles of 500 ml. It is prescribed 2 tablets or 10 ml 4 times a day (1.5 hours after meals and at night). The course of treatment is 20-30 days. The drug has a pleasant taste.

clay white(bolus alba) - aluminum silicate with a small admixture of calcium and magnesium silicates. Available in powder form. Possesses antacid, enveloping and adsorbing effect. Applicable inside 30 each G V 1/2 a glass of warm water 1.5 hours after eating. Currently, it is rarely used to treat peptic ulcers.

Side effects with long-term use of antacids containing aluminum

Aluminum-containing antacids form insoluble aluminum phosphate salts in the small intestine, disrupting the absorption of phosphates. Hypophos- fatemia manifests itself as malaise, muscle weakness, and with a significant deficiency of phosphates, osteoporosis and osteomalacia, brain damage, nephropathy.

With long-term use aluminum-containing antacids develops "Newcastle bone disease" - aluminum directly affects bone tissue, disrupts mineralization, toxic effect on osteoblasts, disrupts the function parathyroid glands, inhibits the synthesis of the active metabolite of the vitamin D3- 1,25-dihydroxycholecalciferol.

to the occurrence of aluminum intoxication appears when its concentration in the blood is more than 100 µg/ml, and clear signs of aluminum intoxication develop when its concentration in the blood is more than 200 µg/ml. The maximum permissible daily dose of aluminum is 800-1000 mg.

Severe side effects from the use of aluminum-containing antacids are often irreversible, especially in children and the elderly. That's why you should use the recommended doses of these drugs and do not use them for a very long time. IN THE USA aluminum-containing Antacids are not recommended for use for more than 2 weeks.

Adsorbent antacids

To adsorbent angacids relate bismuth nitrate basic(Bismuth!subnitras) and combination preparations containing it. The name of this subgroup (adsorbent antacids) is to some extent conditional, since the action of bismuth goes beyond only the adsorbing effect, in addition, non-absorbable antacids also have adsorbing properties to a certain extent.

Bismuth nitrate basic(Bismuthi subnkras) - the drug has an astringent, partially antiseptic effect, in addition, it is an adsorbent, enhances the separation of mucus, forms a protective layer over the gastric mucosa; The neutralizing (antacid) ability of bismuth is low. Available in powders and tablets of 0.25 and 0.5 T. It can be used for gastric and duodenal ulcers, regardless of the state of acidity of gastric juice, 0.25-0.5 g 2 times a day after meals.

Bismuth is a component of vikhalin and vikair.

Vikalin - Available in tablets. One tablet contains 0.3 g of bismuth subnitrate, 0.4 g of basic magnesium carbonate, 0.2 g of sodium bicarbonate, 0.025 g of calamus rhizome and buckthorn bark powder, 0.005 g of rutin and kellin.

Bismuth subnitrate, sodium bicarbonate and magnesium carbonate provide antacid and astringent action, buckthorn bark - laxative effect, rutin - some anti-inflammatory, kellin - antispasmodic effect. Take 1-2 tablets 3 times a day after meals in 2 glasses of water (it is advisable to crush the tablets). The stool turns dark green or black while taking the pills.

Vikair - tablets that have the same effect as vikalin, but unlike it do not contain kellin and rutin, the remaining components are the same as in vikalin. Take 1-2 tablets 3 times a day, 1-1.5 hours after meals, with a small amount of water.

De-nol(Tribimol, Ulceron) - colloidal bismuth subcitrate, has an antacid and enveloping effect. Available in tablets of 0.12 g. When tablets are taken orally, a colloidal mass is formed, which is distributed over the surface of the gastric mucosa and envelops the parietal cells, thus the drug also has a cytoprotective effect. In addition, de-nol has an anti-Helicobacter effect. The drug is taken 1-2 tablets 1 hour before meals 3 times a day and before bedtime. The course of treatment is 4-8 weeks. When treated with de-nol, stool turns black.

Ventol - Available in tablets of 0.12 g, contains bismuth oxide, the mechanism of action is the same as that of do-nol. It also has anti-helicobacter activity and is also used as de-nol.

IN medical practice Combinations of various antacids are widely used:

Bourget's mixture: sodium bicarbonate - 4 g, sodium phosphate - 2 g, sodium sulfate - 1 g; take 1/2 teaspoon per 2 glasses of water 1 and 3 hours after meals;

Magnesium oxide (burnt magnesia) and sodium bicarbonate - 15 g each, bismuth subnitrate - 6 g; take 2 teaspoons 1 and 3 hours after meals;

Sodium bicarbonate - 0.2 g, magnesium carbonate - 0.06 g, calcium carbonate - 0.1 g, magnesium tilicate - 0.15 g; take 1 powder 1 and 3 hours after meals;

Calcium carbonate and bismuth subnitrate - 0.5 g each; take 1 powder 3 times a day 1 hour after meals;

"calcium carbonate, bismuth subnitrate, magnesium oxide 0.5 g each;

take 1 powder 3 times a day 1 hour after meals.

Thus, antacids reduce the activity of hydrochloric acid and pepsin, normalize the motor function of the stomach and duodenum due to faster opening of the pylorus and expulsion of gastric contents into the cavity of the duodenum, which reduces intragastric and intraduodenal pressure, and eliminates pathological reflexes. The same mechanism explains the analgesic effect. Along with this, antacids also have gasgrocytoprotective properties due to stimulation of the production of protective prostaglandins, astringent and enveloping effects (magnesium tilicate, bismuth preparations), and binding of bile acids (aluminum compounds).

The anti-relapse activity of antacids in patients with peptic ulcer disease when taken long-term has not been proven in randomized controlled trials. In addition, there are reports that long-term administration of antacids can lead to an increase in gastric acid formation (acid rebound), which in turn is caused by the resulting hypersecretion of gastrin. Therefore, antacids are used, as a rule, during the period of exacerbation of the ulcer, for 4-6 weeks.

In descending order of antisecretory effect, the drugs can be arranged as follows: omeprazole, ranitidine, cimetidine, phosphalugel and almagel, gastrocepin, peripheral M-anticholinergics. Drugs such as cimetidine, ranitidine, famotidine, gastrocepin, omeprazole can be used for monotherapy of peptic ulcer disease; they not only accelerate the healing of ulcers, but are also used to prevent relapses and complications. Antacids and anticholinergics are used mainly in complex therapy during exacerbations.

4.3. Gastrocytoprotectors

Gastrocytoprotectors have the ability to increase the resistance of the mucous membrane of the stomach and duodenum to aggressive factors of gastric juice.

Misoprostol(Cytotec, Cytotec) - a synthetic analogue of PgE. Available in tablets of 0.2 and 0.4 mg. The drug causes gastrocytoproteority (increased production of bicarbonates and mucus by the gastric mucosa; formation epithelial cells stomach surfactant-like compounds - phospholipids; normalization of blood flow in the microvessels of the gastric mucosa; trophic effect on the mucous membrane of the stomach and duodenum) and antisecretory effects (suppresses the release of hydrochloric acid and pepsin, reduces the reverse diffusion of hydrogen ions through the gastric mucosa).

The cytoprotective effect is manifested in doses lower than those necessary to suppress the secretion of hydrochloric acid and pepsin.

Misoprostol and other prostaglandin derivatives are successfully used to treat gastroduodenal erosions and ulcers, especially in patients who smoke and abuse alcohol, as well as in those who are refractory to treatment with H2-histamine receptor antagonists. In addition, Misoprostol is used to prevent ulcers and erosions in people taking non-steroidal anti-inflammatory drugs.

Misoprostol is prescribed 0.2 mg 4 times a day immediately after meals for 4 to 8 weeks. O. S. Radbil (1991) recommends taking 1 tablet 2 times a day for duodenal ulcers, and 1 tablet 4 times a day for stomach ulcers.

Side effects of the drug: transient diarrhea, mild nausea, headache, abdominal pain. The drug is contraindicated during pregnancy.

Enprostil - synthetic analogue of PgEj. Analogs: arbaprosgil, rio-prosgil, tamoprostil. Available in tablets and capsules of 35 mg. Used in the form of capsules of 35 mg 3 times a day after meals for 4-8 weeks.

The mechanism of action is similar to that of misoprostol. Side effects are mild, usually transient diarrhea.

Sodium carbenoxolone fiotasgro")- obtained from an extract of licorice root, from glycyrrhizic acid, which is part of it. The drug stimulates the secretion of mucus, increases the content of sialic acids in it, increases the lifespan of the integumentary epithelium of the mucous membrane and its regenerative abilities, and prevents the reverse diffusion of hydrogen ions. The positive effect of carbenoxolone on ulcer healing is manifested primarily when it is localized in the stomach; when the ulcer is localized in the duodenum, the effect is less pronounced. Available in tablets of 0.05 and 0.1 g, in capsules of 0.15 g.

The drug is used in a daily dose of 300 mg in the first week of treatment (i.e., 0.1 g 3 times a day before meals), then 150 mg per day (0.05 g 3 times a day) for 5 weeks Since carbenoxolone is quickly absorbed in the stomach, it is advisable to use carbenoxolone in capsules - duogastron - when treating duodenal ulcers.

Side effects of the drug: hypokalemia, sodium and fluid retention, edema, increased blood pressure. These side effects are due to the structural similarity between sodium carbenoxolone and aldosterone and, thus, the manifestation of the mineralocortacoid effect of the drug. When treated with carbenoxolone simultaneous administration antacids and anticholinergics are inappropriate. Contraindications to treatment with sodium carbenoxolone: arterial hypertension, heart and kidney failure, pregnancy, childhood.

Sucralfate(venter) - aluminum salt of sucrose-octahydrogen sulfate. The mechanism of action of the drug is based on the binding of the drug with the proteins of the damaged mucous membrane into complex complexes that form a strong barrier, in the form of a protective film, which has protective properties at the site of localization ulcerative lesion. In addition, sucralfate locally neutralizes gastric juice without affecting the pH of the entire stomach, slows down the action of pepsin, absorbs bile acids (they are thrown into the stomach during duodenogastric reflux), increases the resistance of the gastric mucosa, and inhibits the reverse diffusion of hydrogen ions. At low pH, sucralfate dissociates into aluminum and sucrose sulfate, which are fixed on the surface of the ulcer for 6 hours. The drug does not affect the physiological processes in the stomach and duodenum, is absorbed very poorly (3-5% of the administered dose), does not have a systemic effect, 90% of sucralfate is excreted unchanged in the feces. Increases mucus secretion.

Sucralfate is available in tablets of 1 g or in sachets of 1 g of the drug. Use 1 g 40 minutes before meals 3 times a day and before bed for 4-8 weeks.

The drug can be used in monotherapy, as well as in combination with M-anticholinergics and H2-histamine receptor blockers. It is not recommended to prescribe it together with antacids. If necessary, apply

If antacids are not accepted, they should be prescribed no earlier than behind half an hour before taking sucral-fat.

When treated with sucralfate, side effects are possible: constipation, nausea, gastric discomfort.

Treatment with sucralfate for 4-6 weeks leads to healing of gastric and duodenal ulcers in 76-80% of cases. After a course of treatment, maintenance therapy can be carried out orally at a dose of 0.5-1 g 30 minutes before breakfast and in the evening before bed (P. Ya. Grigoriev).

Gastrocytoprotectors should also include colloidal bismuth subcitrate - de-nol (forms a protective film on the surface of the gastric mucosa), as well as preparations containing bismuth subnitrate - vicalin, vikair (enveloping effect).

Smecta(dioctahedral replace) - medicine natural origin, characterized high level fluidity of its components and thus excellent enveloping ability. It is a mucosal stabilizer, forms a physical barrier that protects the mucosa from the negative effects of ions, toxins, microorganisms and other irritants. Use 1 sachet 3 times a day for 3-4 weeks.

4.4. Drugs that normalize the motor function of the stomach and duodenum

Yaerukal (metoclopramide, Raglan) is a derivative of orthoprocainamide. The mechanism of action of the drug is associated with the blockade of dopamine receptors and suppression of the release of acetylcholine. Cerucal suppresses vomiting reflex, nausea, hiccups, increases the tone of smooth muscles in the lower parts of the esophagus, in the area of ​​\u200b\u200bthe entrance to the stomach, stimulates gastric emptying and petalsis in the upper sections of the small intestine. Does not significantly affect the secretory functions of the digestive organs.

The drug is used in the complex therapy of gastric ulcer and duodenal ulcer, reduces duodenogastric and gastroesophageal reflux, is administered orally at 5-10 mg 4 times a day before meals or intramuscularly at 10 mg 2 times a day. Available in tablets of 1 mg and ampoules of 2 ml (one ampoule contains 5 mg of the drug).

When treated with cerucal, side effects are possible: galactorrhea due to hyperprolactinemia, headache, skin rashes, increased aldosterone in the blood plasma, feeling of weakness. At joint use cerucal and cimetidine may reduce absorption of the latter by 20%.

Domtridon(motilium) - a dopamine antagonist, stimulates and restores normal motor activity of the upper gastrointestinal tract, accelerates gastric emptying, eliminates gastroesophageal and duodenogastric reflux, nausea. Use 0.01 g 3 times a day for 3-4 weeks. Available in 10 mg tablets.

Sul/sh/>CD (eglonil, doshatal) is a central anticholinergic and antipsychotic drug, as well as a selective dopamine receptor antagonist. It has an antiemetic effect, has an inhibitory effect on the hypothalamus, which helps normalize the increased activity of the vagus nerve, inhibits the secretion of hydrochloric acid and gastrin. In addition, sulyshrid has an antidepressant effect and normalizes the motor function of the gastrointestinal tract. The drug is used in the complex therapy of gastric and duodenal ulcers (eliminates spasms of the pylorus, accelerates

prevents evacuation, reduces secretion and acidity), combined with antacids and separators.

In case of peptic ulcer, sulpiric is first applied intramuscularly at a dose of 0.1 g 2-3 times a day, after 7-15 days - in capsules daily inside, 1-2 pieces 3 times a day for 2-7 weeks. Available in capsules of 50 and 100 MG, in tablets of 0.2 g and ampoules of 2 ml of a 5% solution.

Possible side effects: increased blood pressure, galactorrhea, gynecomastia, amenorrhea, sleep disturbance, allergic reactions, dizziness, dry mouth.

Antispasmodics -(no-shpa or papaverine, 2 ml of a 2% solution 1-2 times a day intramuscularly) are used for peptic ulcer of the stomach and duodenum in the presence of spastic phenomena from the stomach (pylorospasm).

4.5. Reparants

Reparants - a group of drugs that can improve the regenerative processes in the mucous membrane of the gastroduodenal zone and thus accelerate the healing of the ulcer.

Solcoseryl - large blood extract cattle(calves), freed from protein, devoid of antigenic properties. 1 ml of solcoseryl contains about 45 mg of dry matter, 70% of which are inorganic and organic compounds, including amino acids, OXIKeto acids, deoxyribonucleotides, purines, polypeptides. Active beginning Solcoseryl has not yet been identified or isolated. The drug improves capillary circulation, oxidative metabolic processes in pathologically altered tissues and the action of tissue enzymes (cytochrome oxidase, succindehydrogenase, etc.), accelerates granulation and epithelialization, increases oxygen uptake in tissues. Between the healthy tissue and the necrotic zone, there is a perinecrotic zone, the metabolic processes in which are reversibly disturbed. Solcoseryl has a positive effect at the level of this zone.

The drug is administered intramuscularly, 2 ml 2-3 times a day until the ulcer heals, and then 2-4 ml 1 time per day for 2-3 weeks. Available in ampoules of 2 ml.

Sea buckthorn oil - has anti-inflammatory and stimulating the healing of tissue defects, including the healing of ulcers. The drug contains an antioxidant tocopherol, which suppresses the processes of lipid peroxidation, which promotes faster healing ulcers It is prescribed orally before meals for "/g tablespoon 3 times a day for 3-4 weeks. Available in 100 ml vials.

Etaden - participates in the metabolism of nucleic acids, stimulates reparative processes in epithelial tissue, which accelerates the healing of ulcerative defects. The drug is administered intramuscularly at a dose of 0.1 g (i.e. 10 ml) once a day for 4-10 days. Available in ampoules of 5 ml of 1% solution.

Caleflon - purified extract from marigold flowers has an anti-inflammatory effect and stimulates reparative processes in the gastroduodenal zone. In recent years, the antacid effect of caleflon has also been established. Take 0.1-0.2 g 3 times a day after meals for 3-4 weeks. Available in tablets of 0.1 g.

Sodium oxyfercorbone complex ferrous salt of gulonic and alloxonic acids. Stimulates repair and healing processes

ulcers, mainly of the stomach, has an anti-inflammatory effect. 30-60 ml is administered intramuscularly daily for 1 month; after a month, the course of treatment can be repeated (for stomach ulcers). For duodenal ulcers, treatment lasts 6-8 weeks, repeated courses of treatment of 10-15 injections are prescribed for 2 years. Available in ampoules of 30 mg of dry substance with the addition of a solvent (3 ml of isotonic sodium chloride solution).

Side effects: skin itching, possible increase in glycemia.

Gastrofarm - contains dried bacterial bodies of lactic acid bulgaric bacillus - the main component of the drug. Stimulates repair processes in the gastroduodenal zone. Prescribed orally 1-2 tablets 3 times a day 30 minutes before meals for 30 days. Available in tablets of 2.5 g.

Anabolic steroid(retabolil - 1 ml 5% solution intramuscularly 1 time per week 2-3 injections or methandrostenolone - 5 mg 2-3 times a day for 3-4 weeks) can be recommended for patients with significant weight loss. Anabolic steroids improve the state of protein metabolism and increase protein synthesis, but do not have a significant healing effect on the ulcer. It should also be taken into account that under their influence it is possible to increase the level of carbonic acid in the gastric contents.

The effectiveness of previously widely used B vitamins, methyluracil, biogenic stimulants(aloe, bioseda, etc.) is currently considered doubtful.

4.6. Central acting agents

Sedatives and tranquilizers(diazepam, elenium, seduxen, relanium in small doses, infusion of valerian, motherwort) may be included in complex therapy peptic ulcer disease, taking into account the role of cortico-visceral disorders in the genesis of this disease, as well as taking into account the fact that in many patients an exacerbation of the disease occurs after exposure to psycho-emotional stress. However, these drugs do not play a significant role in the healing of ulcers.

Dalargin - opioid pjsapeltide, a synthetic analog of enkephalin. The drug has an analgesic effect, inhibits hydrochloric acid (hydrochloric acid production), and has protective effect on the gastric mucosa, promotes the healing of ulcers, improves psycho-emotional status.

The drug is administered intravenously or intramuscularly, 1 mg in 10 ml of isotonic sodium chloride solution 2 times a day. The total dose of the drug for the course of treatment is 30-60 mg. Ulcer healing occurs by the 28th day in 87.5% of patients. In recent YEARS, it has been proven that the drug increases the number of cells producing somatostatin, which inhibits the production of hydrochloric acid. With intravenous administration, a feeling of heat is possible. Produced in ampoules of 1 mg of powder.

4.7. Differentiated prescribing of drugs for peptic ulcer disease

1. For antropyloroduodenal ulcers occurring with gastric hypersecretion, gastroduodenal dyskinesia of the hypermotor type, the following options for the use of drugs are recommended:

a) antisecretory agents (gasgrocepin, metacin, or H2-histamine receptor blockers - cimetidine, famotidine) + antacid (almagel, phosphalugel, maalox, gastal, vikalin);

b) antisecretory agent (gastrocepin, metacin, cimetidine, ranitidine or famotidine) + cytoprotector (sucralfate, sichgek or misoprostol);

c) omeprazole;

d) sucralfate;

d) de-nol.

In table 32 (P. Ya. Grigoriev, A. V. Yakovenko, 1997) provides a comparative assessment of combinations of antiulcer drugs used to treat exacerbation of ulcer disease.

2. With mediogastric ulcers (including ulcers of lesser curvature.
stomach) regardless of the state of gastric secretion, it is advisable
use the following options:

a) antisecretory agent (ranitvdin or famotidine) + eglonil (sulpiride) + gastrocytoprotector (Venter) + reparants (solcoseryl, sea buckthorn oil);

b) eglonil (or sulpiride, or cerucal) + cytoprotector (venter, sucralfate);

c) eglonil (sulpiride or cerucal) + de-nol;

d) sucralfate (Venter);

e) de-nol;

f) eglonil + antacid (vikalin or almagel).

Thus, in traditional therapy for relapse, antisecretory agents are more often used, often in combination with antacids and adsorbents, as well as cytoprotectors and reparatives.

Currently, a point of view has emerged that, due to the availability of modern effective antiulcer drugs (de-nol, omep-razole, famotidine, ranigidine, cytotec, venter, etc.), monotherapy for patients with peptic ulcer disease is advisable. However, when treating a relapse of ulcer in the same patient, it is necessary to change drugs, since antibodies are formed to some drugs (to gastrocepin, cimetidine, etc.) and their effectiveness is significantly reduced.

Combination therapy is indicated for a very persistent course of recurrence of PU.

The main type of anti-relapse drug therapy for ulcerative disease is intermittent (course) drug treatment, usually including the use of a full dose of one antisecretory drug (ranitidine, famotidine, gastrocepin, etc.), often in combination with an antacid (gasgal, almagel, etc.) , and if HP is detected in the inflamed anthropopyroduodenal mucosa, therapy includes at least 3 antibacterial drugs (de-nol, trichopolum, oxaTSSHSHIN or tetracycline, furazolvdon).

Treatment tactics are adjusted depending on the location of the ulcer, the state of the secretory function of the stomach, and the effectiveness of previously administered therapy.

Usually within 3-4 weeks it is possible to achieve jushno-endoscopic remission of the disease (“healing”, “scarring” of the ulcer). If during this period the ulcer does not heal, the attending physician must exclude malignancy of the ulcer, its penetration, periulcerous sclerosing changes (callous ulcer), analyze the rationality, validity of therapy, discipline of the patient, review the treatment regimen with a possible replacement of the drug, physiotherapeutic procedures (if no contraindications).

In case of a long-lasting gastric ulcer, despite intensive treatment, it is advisable to repeat a targeted multiple biopsy and, in the absence of signs of malignancy, continue treatment by replacing drugs. It is better to switch to treatment with omeprazole, sucralfate or de-nol in combination with anti-Helicobacter drugs, if the latter have not been used previously and a connection between ulcerative disease and HP cannot be ruled out.

In addition, for long-term non-healing ulcers, local treatment through an endoscope is added to drug treatment (intragastric laser therapy, sealing the ulcer with special adhesives, injecting the ulcer with reparants, etc.).

Upon the onset of clinical and endoscopic remission of ulcer and negative test in case of HP, it is advisable to stop the course of drug therapy and determine its type to prevent possible exacerbation of the disease and relapse of the ulcer (course of treatment “on demand” or continuous maintenance therapy).

Indications for continuous maintenance drug therapy for ulcerative disease

1. Unsuccessful use of intermittent course treatment, when after its completion there were frequent relapses(three or more times a year).

2. Complicated course of peptic ulcer (history of bleeding or perforation).

3. Concomitant erosive reflux gastritis, reflux esophagitis.

4. The patient’s age is over 50 years.

5. The presence of concomitant diseases requiring constant use of non-steroidal anti-inflammatory drugs and other drugs that damage the gastroduodenal mucosa.

6. The presence of gross cicatricial changes in the walls of the affected organ with symptoms of perivisceritis.

7. Ulcers resistant to treatment with histamine H2 receptor blockers, when in order to achieve an effect it is necessary to lengthen the treatment period and resort to combined treatment.

8. "Heavy smokers."

9. Persons with diseases contributing to the development of peptic ulcers (chronic obstructive pulmonary diseases, liver cirrhosis, rheumatoid arthritis), chronic renal failure.

10. The presence of active gastroduodenitis and Helicobacter bacteria of the mucous membrane.

1. cimetidine - 400 mg or ranitidine - 150 mg or famotidine 20 mg once before bedtime;

2. gastrocepin - 50 mg (2 tablets) after dinner;

3. misoprostol (Cytotec, Cytotec) - 200 mcg after breakfast and dinner;

4. omeprazole -20 mg after dinner;

5. sucralfate (Wenger) - 1 g 30 minutes before breakfast and before bed;

6. peritol - 2-4 mg after dinner in combination with sucralfate (both drugs in the indicated doses simultaneously);

7. metacin - 0.004 g after dinner in combination with sucralfate (two drugs at the same time in the indicated doses);

8. Eglonil or Raglan (cerucal, perinorm, bimaral, etc.) - 1-2 times a day simultaneously with sucralfate or antacids(vikalin, vikair, almagel, phosphalugel, gastal, gelusik-varnish, acidrinmaloxy, etc.).

The duration of the prolonged course varies from 2-3 weeks to several months and even years.

A. A. Krylov, L. F. Gulo, V. A. Marchenko, L. M. Yazovitskaya, S. G. Borovoy (1987) recommend year-round preventive treatment regimens for peptic ulcer disease (Table 33, 34).

The following preventive treatment regimens use the following fees: medicinal plants.

Note. Bourget's mixture: sodium sulfate - 0.1 g, sodium phosphate - 0.1 G, sodium bicarbonate - 4 g dissolved in 250 ml of water. Belpap (composition of 1 powder): papaverine hydrochloride - 0.1 g, belladonna extract - 0.015 g, phenobarbital - 0.015 g, sodium bicarbonate - 0.25 g, burnt magnesia - 0.25 g, basic bismuth nitrate - 0.25 Bish- pan: no-shpa- 0.06 g + anticholinergic isopropamide- 0.005 G(combined tablets).

If you are prone to constipation, you can add rhubarb root or buckthorn bark, dill seeds, joster fruits, 1 weight each, to collection No. 1 Ch., and also reduce the dose of St. John's wort by 2 times, which, due to the presence of tannins, can cause a fixing effect.

Indications for intermittent on-demand treatment:

Newly diagnosed duodenal ulcer;

Uncomplicated course of duodenal ulcer with a short history (no more than 4 years);

The frequency of relapses of duodenal ulcers is no more than 2 per year;

The presence of typical pain and ulcerative defect during the last exacerbation without gross deformation of the wall of the affected organ;

Absence of active gastroduodenitis and Helicobacteria in the mucosa
shell.

Indications for a course of treatment “on demand” are peptic ulcer disease with an uncomplicated course, a short history (no more than 4 years), with a history of no more than 2 relapses per year, with the presence of typical pain and an ulcer defect without gross deformations of the wall at the last exacerbation of the affected organ, as well as rapid attack remission under the influence of course treatment and the patient’s consent to actively follow the doctor’s instructions.

The essence of the course of treatment “on demand” is that when the first subjective manifestations of an exacerbation of the disease appear, the patient immediately independently resumes taking one of the antiulcer drugs in the full daily dose (cimetvdine, ranitvdine, famotidine, omeprazole, gastrocepin, misoprostol, sucralfate) . If subjective symptoms stop completely within 4-6 days, the patient independently switches to maintenance therapy and stops treatment after 2-3 weeks, and if there is no effect in the first days, the patient should consult a doctor.

Patients undergoing a course of treatment “on demand” should be advised to exclude risk factors (smoking, taking non-steroidal anti-inflammatory drugs and other ulcerogenic drugs) and carefully follow the doctor’s instructions.

Treatment "on demand" can be prescribed for up to 2-3 years.

P. Ya. Grigoriev names the following advantages of “treatment on demand”:

The patient is responsible for the effectiveness of treatment and therefore takes it seriously;

This treatment has a positive effect psychological impact on the patient, he does not consider himself doomed, hopeless;

the effectiveness of on-demand therapy is not inferior to the effectiveness of continuous maintenance therapy with H2-histamine blockers, the cost of treatment is lower, and the quality of life of patients is higher.

Regardless of the type of preventive treatment, if a relapse occurs against the background of chronic active gastroduodenitis associated with HP, a 2-week course of anti-Helicobacter therapy is justified (above).

Anti-Helicobacter therapy is also indicated for patients with antropyloroduodenal ulcer, if they have recurred again 2-4 months after the end of the course of treatment of the previous relapse. typical symptoms exacerbations. At the same time, Helicobacter bacteria can always be detected in the gastroduodenal mucosa.

5. Herbal medicine

The use of medicinal plants for peptic ulcers is based on the use of anti-inflammatory, enveloping, laxative, astringent, analgesic, carminative, antispasmodic and hemostatic effects. Herbal medicine improves the trophism of the mucous membrane of the gastrointestinal tract and promotes regeneration processes.

In herbal medicine for peptic ulcers, plants with anti-inflammatory properties (oak, St. John's wort, plantain, calendula, elecampane, yarrow), antispasmodic (chamomile, licorice, mint, oregano, dill, fennel), antispastic (calendula, St. John's wort, chamomile, plantain, elecampane) are used. , antiallergic (licorice), laxatives (rhubarb, buckthorn, trefoil watch, zoster).

In addition, for peptic ulcers with preserved and increased secretion of gastric juice, the following fees are recommended:

The following medicinal plants can be added to the above fees or taken separately from them:

Calamus root powder(on the tip of a knife) - take 3-4 times a day 20-30 minutes before meals for heartburn for 2-3 weeks.

Fresh cabbage juice - significantly accelerates the scarring of gastric ulcers and duodenal ulcers. Freshly prepared cabbage juice is taken at "/G glass or 1 glass 3-4 times a day 20-40 minutes before meals. The course of treatment is 1.5-2 months. Not all patients tolerate cabbage juice well.

Some patients successfully take potato juice(especially for duodenal ulcers), it neutralizes well

acidic gastric juice Prescribe 2 glasses 3-4 times a day before meals for 1.5-2 months.

A good analgesic and enveloping agent is flax seed(brew at the rate of 2 tablespoons per 0.5 liter of boiling water, you can boil for 3-4 minutes over low heat, then pour into a thermos and leave overnight). Take 7g glass 3-4 times a day before meals.

When treating patients with callous, long-lasting ulcers, the components (or increase the amount) of those herbs that contribute to scarring of the ulcer (celandine, plantain, shepherd's purse, burdock root, chicory, calendula, fireweed, etc.).

Treatment with medicinal preparations continues for 5-6 weeks As the exacerbation subsides, you can use phytoapplications on the anterior abdominal wall and lumbar region for 20 minutes (10-15 sessions, every other day). For phytoapplications you can use the following fee:

Swamp dry grass (grass) 5 tsp.

Calendula flowers 5 tsp.

Elecampane grass 2 hours.

Celandine herb 1 tsp.

Licorice root 2 tsp.

Coltsfoot leaves 4 hours.

Lungwort herb 3 tsp.

Chamomile flowers 5 hours.

Phytoapplications are applied mainly to the epigastric region. For phytoapplication with a layer thickness of 4-6 cm for each square centimeter body requires up to 50 g of medicinal plant collection.

To prepare the phytocollection, the calculated amount of medicinal raw materials is carefully crushed, mixed, poured into 0.5 l of boiling water in an enamel bowl and steamed for 15-20 minutes (under the lid). Next, the infusion is filtered into a separate container (it can be used for baths), and the medicinal plants are squeezed out so that they remain slightly moist. Then they are wrapped in gauze, folded in four layers, or in linen cloth and placed on the epigastric region. Cellophane or oilcloth is placed on top and wrapped in a woolen blanket. Optimal temperature phytoapplications is 40-42 "WITH, procedure duration - 20 minutes.

Along with the use of medicinal plants inside and in the form of phytoapplications, therapeutic baths can also be used. For the preparation of therapeutic baths, 1-2 liters of infusion is used, which requires an average of 100-200 g of dry plant materials. Infusion is carried out for 1-2 hours in earthenware, enamel or glassware. The vessel must be tightly closed and additionally insulated with a cloth (wrapped in woolen cloth). The temperature of the water in the bath should be within 34-35 ° C. The duration of the procedure is 10-20 minutes, 2-3 times a week. Therapeutic baths can be alternated with herbal applications (prescribing these procedures every other day).

Contraindications for phytoapplication are periods of exacerbation of a febrile state, circulatory failure, tuberculosis, blood diseases, severe neuroses, bleeding, pregnancy (all periods).

6. Use of mineral waters

Mineral waters are used primarily for the treatment of gastric and duodenal ulcers with preserved and increased secretion of gastric function. Typically, low-mineralized mineral waters are recommended, without carbon dioxide or with minimal carbon dioxide content, with a predominance of hydrocarbonate and sulfate ions, having a slightly acidic or neutral, alkaline reaction. Such waters are “Borjomi”, “Essentuki” No. 4, “Smirnovskaya” No. 1, “Slavyanovskaya”, “Luzhanskaya”, “Berezovskaya”, “Jermuk”. Typically, slightly heated mineral waters (38-40 °C) without gas are used, which enhances their antispastic effect and reduces the carbon dioxide content. S. N. Golikov (1993) recommends taking mineral waters for duodenal ulcers 1.5-2 hours after meals, and for mediogastric ulcers - 1 hour after meals, i.e. the time of taking mineral water almost corresponds to the time of taking antacids for peptic ulcer. This method of taking mineral water enhances the antacid effect of food, lengthens the time of intragastric alkalization. With a stomach ulcer with low acidity, it is advisable to take water 20-30 minutes before meals.

First take small amounts of mineral water 0/y 1 / 2 glass, then gradually, with good tolerance, you can increase the amount of water to 1 glass per reception).

Patients tolerate different mineral waters differently. Especially often there is a poor tolerance of water "Essentuki" No. 17 (heartburn, nausea, diarrhea), which makes it necessary to be careful when prescribing it to patients with peptic ulcer.

In dispensaries and at home, bottled mineral waters can be prescribed. The average duration of a course of treatment with mineral waters is about 20-24 days.

7. Physiotherapy

The effectiveness of complex treatment of peptic ulcer increases with the use of physiotherapy methods. The choice of physical treatment factors is largely determined by the phase of the disease. Physiotherapy is carried out only in the absence of complications of peptic ulcer - pyloric stenosis, perforation and penetration of the ulcer, bleeding, malignancy of the ulcer.

In the acute phase may be appointed sinusoidal modulated currents(SMT), which have an analgesic and anti-inflammatory effect, improve blood and lymph circulation in the gastroduodenal zone. SMT is prescribed for the epigastric region, the duration of the procedure is 6-8 minutes, the course of treatment is 8-12 procedures, the tolerability is good. When using SMT, pain syndrome is stopped faster and ulcers heal in a shorter time. The same positive impact is also had dia-dynamic Bernard currents(10-12 procedures).

In the phase of exacerbation of peptic ulcer, it is also widely used microwave therapy, including decimeter waves, they are released by the "Volna-2" or "Romashka" devices with localization of the effect on the epigastric region for 6-12 minutes, the course of treatment is 10-12 procedures. This method is especially effective in the localization of the ulcer in the pyloroduodenal zone.

Impact can also be used ultrasound on epigastric after preliminary intake of 1-2 glasses of water in order for the gas bubble to move into upper divisions and did not interfere with the penetration of ultrasonic waves to the posterior wall of the stomach. During one procedure, 3 fields are sequentially affected: the epigastrium (0.4-0.6 W/cm2) and two paravertebral areas at the level of Th VII-XII (0.2 W/cm2) for 2-4 minutes per area. The course of treatment is 12-15 procedures, every other day.

Also widely used electrophoresis on the epigastric region of novocaine, papaverine (especially with severe pain).

An effective procedure that quickly relieves pain and promotes rapid healing of an ulcer is dalargin electrophoresis to the epigastric region. The technique is transverse, the anode is located in the projection of the pyloroduodenal zone, the pad is moistened with a solution of dalargin containing 1 mg of the drug. The current density in the first procedure was 0.06 mA/cm 2 , the duration was 20 min. Subsequently, every 5 procedures, the current density increases by 0.02 mA, the duration of exposure increases by 5 minutes. The course of treatment is 12-15 procedures.

It also has a positive effect intranual electrophoresis with dalargin.

In recent years, for the treatment of peptic ulcer has become widely used hyperbaric oxygenation, which reduces regional hypoxia of the gastroduodenal zone, stimulates metabolic and reparative processes in it, contributing to the fastest improvement in the patient's condition and the speedy healing of the ulcer. Treatment is carried out in a large therapeutic pressure chamber or in oxygen chambers such as "Oka", "Irtysh-MT", etc. Sessions are prescribed in the mode of 1.5-1.7 atm., Patients stay in the pressure chamber for 60 minutes, the course of treatment is 10-18 procedures.

In the presence of contraindications to the above procedures, as well as for the elderly, it is possible to recommend magnetic therapy, when an alternating magnetic field is used ("Pole-1"). This procedure reduces pain and is well tolerated by all patients. A continuous sinusoidal mode with a frequency of 50 Hz is used, the maximum magnetic induction is 20 mT, the duration of the procedure is 8-12 minutes, the course of treatment is 8-12 procedures every other day.

In the acute phase, you can also use galvanization - a positive electrode is applied to the epigastric region, a negative electrode is applied to the lower thoracic spine, the current density is 0.1 mA/cm*, the duration of the procedure is 10-20 minutes, the course of treatment is 8-10 procedures.

At home, in the acute phase, you can apply light heat in the form of a warming half-alcohol compress to the epigastric region.

In the decaying phase exacerbation thermal procedures are prescribed (mud, peat, ozocerite, paraffin applications, galvanic mud on the epigastric region) daily or every other day (10-12 procedures); UHF in pulse mode to the epigastric region; electrophoresis of medicinal substances(papaverine, novocaine, dalargan) on the epigastric region (12-15 procedures); hydrotherapy in the form of shared baths. A sedative effect is given by baths with mineral water of low concentration, at a temperature of 36-37 ° C, the duration of the bath is 10 minutes, the course of treatment is 8-10 procedures, every other day. Baths with mineral water are not indicated in the period of a pronounced exacerbation of the disease, as well as in the presence of complications. Valerian baths are also advisable.

IN phase remission, physiotherapy procedures are prescribed in order to prevent exacerbations. Ultrasonic and microwave therapy; diadynamic, sinusoidal modulated currents; electrophoresis of drugs; pine, pearl, oxygen, radon baths; local thermal procedures on the epigastric region (applications of paraffin or ozocerite, heated to 46 ° C, daily for 30-40 minutes, 12-15 procedures); mud applications(silt, sapropel, peat mud at a temperature of 42-44 ° C for 10-15 minutes every other day, 8-10 procedures per course).

Heat treatment has a positive effect on blood circulation in the gastro-duodenal zone, normalizes the motor-evacuation function of the stomach, and helps reduce intragastric pressure.

Preventive courses of physiotherapy are most conveniently carried out in dispensaries and sanatoriums, where they are combined with diet therapy and drinking mineral waters. Positive results were obtained when patients were included in complex treatment acupuncture(10-12 sessions).

8. Local treatment of long-term non-healing ulcers

For chronic non-healing ulcers of the stomach and duodenum, they resort to local gastric treatment. To do this, use targeted injection of the periulcerous zone with a solution of novocaine (1 ml of a 2% solution), tselnovocaine, solcoseryl, irrigation with sea buckthorn oil, and a solution of silver nitrate. Positive results were obtained when treating the ulcer and surrounding mucosa 2 times a week with solid ethyl. Recently, the application of film-forming agents (gastrozol, lifuzol) to the ulcerative surface and surrounding mucosa (1-2 cm) has become widespread. Aerosol film-forming adhesive is injected during endoscopic examination. Therapeutic gastroduodenoscopy is repeated after 2-3 days, the course of treatment is 8-10 procedures.

New method local impact on the ulcer is low-energy laser radiation. Irradiation of the ulcer and its edges is carried out through a light guide through the biopsy channel of the endoscope 2 times a week.

The most effective are helium-cadmium, argon and especially krypton lasers. On average, duodenal and gastric ulcers heal in 16-17 days.

When treating callous ulcers, first, to destroy the sclerosing formations blocking the reparative processes, the edges of the ulcer are treated with powerful radiation from an argon laser, then a soft helium-neon laser is used.

A new option for intragastric laser therapy is local therapy with pulsed-periodic yellow-green radiation from a copper vapor laser. In this case, 100% healing of the ulcer is observed (stomach ulcer heals after 1-8 sessions, duodenal ulcer - after 1-4 sessions).

9. Treatment of resistant gastric and duodenal ulcers

If during the 4-week treatment of duodenal ulcers and 8-week treatment of gastric ulcers there is no “healing effect” (scarring), the ulcer can be considered resistant to treatment. In this case, the attending physician must:

Determine the discipline of the patient (compliance with the regimen and rhythm of nutrition, medication, smoking cessation, alcohol abuse, etc.);

To analyze the rationality and validity of drug therapy and physiotherapy procedures;

Exclude malignancy or penetration of the ulcer, periulcerous sclerosing changes ("calcified" ulcer), Zollinger-Ellison syndrome, hyperparathyroidism, systemic mastocytosis;

Reveal possible factors, restraining scarring ulcers (medication for other diseases, undiagnosed cholecystolithiasis, CAH, intestinal dysbacteriosis, etc.);

When ascertaining the resistance of an ulcer to treatment, the following treatment tactics are recommended:

Increase the dose of the previously used antisecretory drug or replace it;

Add gastrocytoprotectors to the antisecretory drug (sucralfat 0.5-1.0 g 3 times 30 minutes before meals and at bedtime or Cytotec 250 mcg 4 times a day after meals);

If there is no effect, prescribe a "triple" antibiotic therapy (de-nol + metronidazole + antibiotic), since Helicobacter pylori infection often underlies resistant ulcers. It is advisable to use the combined preparation "gastrostat" containing bismuth subcitrate (108 mg), metronidazole (200 mg), tetracycline (250 mg). It is prescribed one tablet 5 times a day at regular intervals for 10 days;

In the absence of the effect of gastrostat, prescribe a combination of omeprazole, metronidazole and clarithromycin;

Actively use local methods treatment of long-term non-healing ulcers (above).

10. Spa treatment

Sanatorium-resort treatment of patients with peptic ulcer is important rehabilitation event. It includes a wide range of therapeutic measures aimed at normalizing the functions of not only the gastroduodenal zone, but also the body as a whole.

The following resorts are recommended for patients with peptic ulcer disease: Berezovsky Mineral Waters, Birshtonos, Borjomi, Goryachiy Klyuch, Darasun, Jermuk, Druskininkai, Essentuki, Zheleznovodsk, Izhevsk Mineral Waters, KraInka, Pärnu, Morshin, Pyatigorsk, Sairme, Truskavets, etc.

Contraindications for spa treatment are: peptic ulcer during a period of severe exacerbation, recent bleeding (within the last 6 months) and a tendency to bleed, pyloric stenosis, suspicion of malignant degeneration, the first 2 months after gastrectomy, severe exhaustion.

In addition to balneological resorts, treatment can also be carried out in local sanatoriums. In Belarus, these are the sanatoriums “Krinitsa”, “Narech”, “Porechye”.

11. Clinical examination

Medical examination tasks:

1. Timely (early) identification of patients with peptic ulcer
the active conduct of targeted preventive examinations.

2. Regular (at least twice a year, especially in spring and autumn) examination of patients with peptic ulcer disease to assess the dynamics of the ulcerative process, identify complications and concomitant diseases ( general analysis blood, urine, study of gastric secretion, FGDS).

3. Anti-relapse treatment.

5. Health education: promotion of a healthy lifestyle, rational nutrition, explaining the dangers of smoking, drinking alcoholic beverages.

6. Employment of patients is decided jointly with representatives of the administration and trade union organization.

Preventive (Anti-relapse) treatment is usually carried out in a clinic or in a sanatorium, and also, if possible, at a balneological or mud bath resort. The most important components preventive treatments are:

1. compliance with a therapeutic diet and nutrition regimen (at home, in a dietary canteen or in a sanatorium);

2. complete cessation of smoking and drinking alcohol;

3. prolongation of sleep time up to 9-10 hours;

4. exemption from shift work, especially at night, long and frequent business trips;

5. drug treatment;

6. physiotherapy;

7. sanitation of the oral cavity (treatment of caries, prosthetics);

8. treatment of concomitant diseases;

9. psychotherapeutic influences.

A) While eating; B) After 30 min. after meal; IN) 30 min. before meals; G) Only for the night; D) 1-2 hours after eating.

52. The rhythm of pain in peptic ulcers associated with food intake depends on:

A) The depth of the ulcer; B) Presence of Helicobacter pylori infection; IN ) Localization of the ulcer; G) Intestinal peristalsis; D) Biliary dyskinesia.

53. When studying the secretory function of the stomach, the following is used to stimulate gastric secretion:

A) Gastrocypin; B) Pentagastrin; IN) Adrenalin; G) Prostaglandin; D) Pepsin.

54. Which drug has a cytoprotective effect in the treatment of peptic ulcer?

A) Heptral; B) Vikalin; IN) Duspatalin; G) Sucralfate; D) Cholestyramine.

55. Factors of aggression of the gastric mucosa include all EXCEPT:

A) H. pylori; B) Hydrochloric acid; IN) Pepsin; G) Bile acids; D) Prostaglandins.

56. Symptomatic ulcers are characterized by the following signs:

A) Multiple, superficial ulcers; B) Blurred clinical picture; IN) Occurs under stress; G) Develop with the use of certain medications (NSAIDs); D) All of the above signs.

57. Diagnosis of H. Pylori eradication is carried out after completion of the course of anti-Helicobacter therapy through:

A) 1 week; B) 2 weeks; IN) 3 weeks; G) 4-6 weeks; D) 8-10 weeks.

58. Factors protecting the gastric mucosa include everything EXCEPT:

A) Stomach mucus; B) Prostaglandins; IN) Cytokines; G) Preserved blood supply ; D) Bicarbonates.

59. Diagnosis of gastric ulcer includes everything EXCEPT:

A) Detection of an ulcerative defect, B) Identification of H. pylori; IN) Studies of gastric secretory function ; G) Detection of anemic syndrome ; D ) Definitions of hyperbilirubinemia;

60. All of the following drugs are used to treat peptic ulcers, EXCEPT:

A) Bismuth containing preparations; B) Anticholinergics; IN) Amoxicillin, G) H 2 -histamine blockers; D) Sympathomimetics;

61. With IBS functional disorders continues:

A) No more than 12 weeks within 17 months; B) 10 weeks within 12 months; IN) 12 months within two years; G) 3 weeks throughout the year; D) At least 12 weeks throughout the year.

62. The following statement is true for IBS:

A ) Change in stool frequency; B) In severe cases, B 12 deficiency anemia may develop; IN) In the pathogenesis of the disease, deficiency of disaccharidases is important;

G) A history of dysentery is common; D) All of the above are true.

63. In the diet for IBS, everything should be excluded EXCEPT:

A) milk; B) Carbonated drinks; IN) Vegetables and fruits; G) Animal fats; D) Bobovykh.

64. IBS is characterized by all the signs EXCEPT:

A) Changes in stool frequency; B) Fever; IN) Changes in stool consistency; G) Discharge of mucus with feces; D) Flatulence.

65. Microscopy of feces in IBS is characterized by the presence of:

A) Remains of undigested fiber; B) Red blood cells; IN) Steatorrhea; G) Creatorrhea;

D) Dysbacteriosis.

66. As a drug for IBS with pain syndrome, use:

A) De-nol; B) Famotidine; IN) Drotoverin; G) Loperamide; D) Sulfosalazine.

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