V.I. KASYANENKO, Doctor of Medical Sciences, Leading Researcher, Central Research Institute of Gastroenterology, Moscow
Symptomatic erosive ulcerative lesions stomach and twelve duodenum– a fairly common group of diseases, united by a common feature (changes in the mucous membrane in response to the influence of various ulcerogenic factors), aggravating the underlying disease, leading to serious complications and requiring the appointment of additional drug treatment.
The term “symptomatic erosive and ulcerative lesions of the stomach and duodenum (SEUD)” refers to acute or chronic focal destruction of the mucous membrane (SM) of these organs, etiologically and pathogenetically different from peptic ulcer(JB). Symptomatic erosions and ulcers are some of the local manifestations pathological condition organism, occurring in seriously ill patients against the background of burns, severe injuries, sepsis, multisystem organ failure, hemorrhagic shock and other critical conditions.
SEYAPZhDK are described in the literature under different names: erosive or hemorrhagic gastritis, medicinal ulcers, stress ulcers, symptomatic ulcers (US), stress-related mucosal damage, stress-related mucosal damage, etc.
The question of in what cases gastroduodenal ulcerative lesions occur in diseases internal organs should be classified as SY, remains quite debatable. It must be remembered that the presented conditions can not only cause the formation of acute stress ulcers, but also contribute to the exacerbation of pre-existing ulcers. Characteristic Features SEYAPZhiDK are:
Pathogenetic dependence of the occurrence on the underlying disease,
atypical clinical picture (erasure pain syndrome, lack of seasonality, etc.),
enough fast healing and remission as the underlying disease improves.
For the course of ulcer of the stomach and duodenum (DC), in contrast to EPGIDC, it is natural:
indication in the anamnesis of the presence of gastroduodenal ulcers,
presence of signs of ulcer (etiological factors, typical clinical picture, seasonality of exacerbation, etc.),
development of the disease regardless of the underlying disease.
Based on the etiopathogenetic mechanisms, the following are classified as SEJAPGID:
1. Symptoms that arose against the background of chronic diseases of internal organs (digestion, lungs, cardiovascular system, kidneys, etc.).
2. Medications (when taking non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, indole derivatives, histamine, etc.).
3. Endocrine (for hyperparathyroidism, ulcerogenic tumor of the pancreas (Zollinger-Ellison syndrome)), etc.
4. Stressful (with myocardial infarction, burn disease, stroke, in postoperative period etc.).
SEJPGIDK, like PU, can be complicated by bleeding, perforation, and penetration.
Symptoms arising from chronic diseases of internal organs
A wide range of chronic diseases can be accompanied by erosive and ulcerative lesions of the gastric mucosa and DC. In gastroenterological practice, SAEs identified in patients with chronic diseases liver (usually cirrhosis, less often chronic hepatitis), are called hepatogenic ulcers. The mechanism of occurrence of these ulcers may be an increase in the content of histamine and gastrin in the blood due to a decrease in the inactivation of these compounds in the liver, impaired blood flow in portal system with the subsequent occurrence of hypoxia of the gastroduodenal zone, a disorder of gastric mucus formation. The causes of pancreatogenic ulcers occurring in patients with chronic pancreatitis are a decrease in the active secretion of bicarbonates by the pancreas due to inflammatory changes in the organ, as well as alcohol abuse, duodenogastric reflux bile, increased release of kinins, etc.
Lesions of the mucous membranes of the upper gastrointestinal tract, which developed during long-term lung diseases, are associated with prolonged hypoxia, leading to a decrease in resistance, impaired microcirculation, including in the mucous membranes of the gastroduodenal zone. SEYAPZhiDK with widespread atherosclerosis, especially with damage to the abdominal aorta, are of a trophic nature and are caused by CO ischemia. SAs of atherosclerotic origin are close to the so-called. senile stomach ulcers that occur in elderly and senile patients. Hypergastrinemia plays a role by reducing the destruction of gastrin in the kidneys, uremic intoxication, as well as the effect of drugs (primarily steroid hormones, used in large doses after transplantation).
Medicinal SEYAPZhiDK
Symptoms that have developed against the background of rheumatoid arthritis are caused, perhaps, not so much by the underlying disease as by the use of NSAIDs in its treatment, which, on the one hand, cause acute ulcers, and on the other, provoke an exacerbation of pre-existing ulcers.
Among the drugs that cause SEJPC, one of the first places is occupied by NSAID drugs, widely used in the treatment of many diseases manifested by inflammatory reactions and pain (arthritis, arthralgia, neuritis, neuralgia, collagenosis, etc.). To prevent thrombosis and thromboembolism during different situations(IHD, thrombophlebitis, etc.) drugs are widely used acetylsalicylic acid. When prescribing glucocorticosteroids, it is necessary to take into account their effect on CO. These drugs have a direct toxic effect on the mucous membranes of the gastroduodenal zone and often only gastrointestinal tract, and also inhibit the activity of cyclooxygenase, prostaglandins (PGE2).
Endocrine SEYAPZhiDK
EPLD of endocrine origin (with an ulcerogenic tumor of the pancreas - Zollinger-Ellison syndrome, hyperparathyroidism, etc.) have a unique clinical picture, and the acid-peptic factor plays a decisive role in their formation due to increased gastrin production.
Stress ulcers are usually acute, often superficial and multiple ulcerative lesions of the stomach and DC that occur in some extreme conditions.
The first description of stress ulcers apparently belongs to J. Swan (1823), who discovered ulcers in the gastric mucosa of children who died from widespread burns (“spots and stripes similar to scabs, very deep and completely black”), and associated them origin with skin burn. Subsequently, B. Curling (1842) cited 12 cases of gastroduodenal ulcers in patients with extensive burns. Since that time, these ulcerative lesions of the stomach and DC began to be called Curling ulcers. In 1867 T. Billroth described new look stress ulcers acutely occurring after thyroidectomy. He was also the first to suggest the existence of a relationship between sepsis and the subsequent development of gastric ulcers. In 1932, H. Cushing, having described the possibility of ulcer formation in the stomach in patients with cerebral hemorrhage, thereby discovered new variety gastroduodenal stress ulcers that occur after traumatic brain injuries, neurosurgical operations, with brain tumors and are called Cushing's ulcers in the literature.
In addition to the mentioned Curling and Cushing ulcers, gastroduodenal ulcerative lesions that have developed after major operations (especially those associated with organ transplantation), severe wounds, multiple injuries, against the background of sepsis and others serious illnesses.
Symptomatic, especially stressful, EJV&DC can be a source of bleeding in 20–60% of all bleedings from upper section gastrointestinal tract. Since the 70s An increase in the frequency of stress ulcers has been observed all over the world, which is explained by: an increase in severe injuries; the development of surgical techniques and anesthesiology, which made it possible to carry out extensive, previously impossible operations; improvement of resuscitation and intensive treatment of patients in critical conditions; improved diagnosis of gastroduodenal ulcers as a result of the widespread use of modern endoscopes.
Pathogenetic aspects of the development of SEYAPZhiDK
Main pathogenetic mechanisms The development of erosive and ulcerative lesions of the gastric mucosa is a violation of the interaction of factors of aggression and protection of the gastric mucosa and DC. Factors of aggression begin to prevail over factors of defense. Stress and surgery provoke the release of stress hormones, glucocorticosteroids and catecholamines, into the blood. On the one hand, stimulated secretion occurs hydrochloric acid as a damaging aggressive agent, on the other hand, a decrease in protective factors against the background of CO ischemia due to hypoperfusion, leading to an imbalance of oxidative processes. The activity of gastric mucus production as a protective mechanism also sharply decreases. Moreover, restoration of blood circulation after prolonged hypoperfusion leads to non-occlusive disruption of the mesenteric circulation, which further aggravates the damage to the mucous membrane. The microcirculation system is a factor determining the degree of compensation or decompensation metabolic processes in CO. The result of ischemia is a decrease in the ability to neutralize hydrogen ions, which induces massive cell death and causes the formation of ulcers. .
Studies have shown that the formation of a blood clot in the gastric cavity is more efficient, and its dissolution by proteolytic enzymes is slowed down under conditions of high pH values. In the development of gastroduodenal ulcerative bleeding(GDYAK) has great value the total time during which the pH inside the stomach is less than 4; as this interval increases, the frequency of such changes decreases. To prevent HDYAC and in a comprehensive manner intensive care There is experience in the use of drugs that are used in the treatment of ulcers, i.e. antacids, histamine H2 receptor blockers, proton pump inhibitors (PPIs).
Prevention and treatment of EJPC
The basic principles of preventing the development of erosive and ulcerative lesions of the mucous membrane are:
1) maintaining gastric Ph > 4 (this results in a decrease in proteolytic activity gastric juice due to inhibition of the conversion of inactive pepsinogen to active pepsin);
2) normalization of blood supply and oxygenation of CO;
3) support for CO protection systems.
Since the main goal of prevention and treatment of EPGI, regardless of etiology, is to reduce the factors of aggression on the gastric mucosa, the basis of therapy is adequate suppression of acid production. The leading place here belongs to drugs that block the production of hydrochloric acid by the parietal cells of the gastric mucosa. This effect is inherent in histamine H2 receptor blockers and PPIs (H+/K+-adenosine triphosphatase - ATPase). However, when choosing drugs, the following points must be taken into account:
1. Widely used in the 70s. antacids (reduce acidity by chemical interaction with hydrochloric acid in the stomach) do not affect the secretion of hydrochloric acid, they must be taken frequently to achieve the optimal pH (almost 1-2 hours) and only orally, due to their consistency, they can cause occlusion of the nasogastric tube, lead to disturbance of water-electrolyte balance, development of diarrhea, affect the absorption of a significant amount of medications that are necessary in crisis situations ( ACE inhibitors, antiepileptic drugs, indirect anticoagulants, NSAIDs, cardiac glycosides, etc.). On the other hand, oral administration of drugs in a patient in critical condition (artificial ventilation, condition after operations on the gastroduodenal zone, gastrointestinal paresis) is technically very problematic. The release of carbon dioxide during the interaction of hydrochloric acid and carbonates can lead to distension of the stomach and regurgitation of gastric contents into the trachea and bronchi (Mendelssohn syndrome, aspiration pneumonia).
2. Before active implementation in clinical practice PPIs that were most effective in suppressing acid production were representatives of the group of histamine H2 receptor blockers. And although it is possible to use drugs intravenously (an advantage compared to antacids), the tachyphylaxis they cause ( rapid decline therapeutic effect with repeated use) makes it difficult to maintain the pH of gastric juice above 4. H2 blockers do not inhibit the secretion of hydrochloric acid caused by an increase in vagal tone, which makes them less effective in patients with cerebral disorders, interact with wide range medications (hypnotics, neuroleptics, antiarrhythmics, opioid analgesics, etc.). Often when using them there is headache, diarrhea, intestinal dyspepsia, and since the drugs are excreted by the kidneys, their dose should be adjusted in patients with reduced creatinine clearance.
Most effective drugs inhibitors are currently used to suppress the formation of hydrochloric acid proton pump(IPP). Among all the antisecretory drugs PPIs that are currently available (omeprazole, rabeprazole, esomeprazole, lansoprazole, pantoprazole), they most effectively suppress basal and stimulated production of hydrochloric acid by inhibiting H+/K+-ATPase, the proton pump of the parietal cell.
For the prevention and treatment of ovarian cancer, PPIs must have the following properties:
Have a spectrum dosage forms(intravenous, orally or via nasogastric tube),
increase intragastric pH (above 4) long time,
interact slightly with others medicines,
have a favorable safety profile, allowing use in patients with multiple organ failure.
All PPIs have oral forms; intravenous forms include omeprazole, pantoprazole, esomeprazole, and lansoprazole.
According to the study, pantoprazole (the drug Controloc), unlike omeprazole and esomeprazole, does not accumulate in the body after taking repeated doses. The pharmacokinetics of pantoprazole in serum/plasma is linear and does not depend on the route of administration when using 20, 40 and 80 mg; The pH level in the stomach increases in proportion to the dose of the drug. The linearity of the values of the pharmacokinetics of pantoprazole is maintained even with intravenous administration at a dose of 240 mg. These pharmacokinetic properties differ significantly from those observed with intravenous administration of omeprazole. When the dose of the latter increases in the same range, the AUC changes disproportionately, and the half-life increases after a single dose. intravenous administration. During the first 3 days of treatment with pantoprazole (40 mg), a more rapid onset of action and a more pronounced decrease in gastric acid secretion (up to 46 hours) was observed than with treatment with omeprazole 20 mg (28 hours), esomeprazole (28 hours), as well as stable first dose and upon re-appointment.
In a randomized, double-blind study, it was proven that in patients with HDAC with endoscopic hemostasis (1:10,000 injections of adrenaline 8–15 mg) with additional administration of the drug Controloc (80 mg intravenous bolus, then as a drip infusion 8 mg/hour) over the course of 3 days, compared with the administration of the same dose of omeprazole, the risk of recurrent HDAC is reduced by 3 times, the need for surgical intervention by 4 times, and mortality and length of hospitalization by 2 times.
All PPIs are metabolized in the liver with the participation of cytochrome P450 and its isoenzymes - CYP2C19, CYP3A4. The interaction of individual representatives of the PPI group with other drugs varies significantly when the first dose is administered and when it is re-administered.
Compared to other PPIs, pantoprazole weakly inhibits the cytochrome P450 system, which clearly reduces the possibility of its influence on the metabolic elimination of concomitantly taken drugs compared to omeprazole or lansoprazole. In particular, it does not interact clinically with drugs used in intensive care such as caffeine, metoprolol, theophylline, metronidazole, amoxicillin, clarithromycin, diclofenac, naproxen, diazepam, carbamazepine, digoxin, nifedepine, warfarin, cyclosporine, etc. At the same time, there are restrictions when taking omeprazole.
In patients with severe renal failure, including patients on hemodialysis (creatinine clearance 0.48–14.7 ml/min), there is no need to reduce the dose of pantoprazole; its daily dose should not exceed 40 mg/day.
In patients with liver cirrhosis, the half-life of pantoprazole is slightly increased, but no dosage adjustment is required. In case of severe liver dysfunction, the dose can be reduced to 40 mg once every 2 days. In such patients, liver enzyme levels should be monitored. In the elderly, no dose adjustment is required. The daily dose of omeprazole (20 mg) should not be exceeded in patients with impaired renal or liver function, as well as in elderly patients.
Pantoprazole (the drug Controloc) is the only PPI that has characteristic properties that contribute to the management of EPJCD, creating convenience not only for patients, but also for doctors. These properties include rapid, effective control of acid production (which promotes faster healing and immediate relief of symptoms), ease of use and transfer from intravenous treatment on taking tablets, good tolerability by patients and safety, stability and predictability of the effect, absence of potential drug interactions and positive attitude of patients towards the chosen treatment strategy.
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For some reason, various types of damage can occur in the stomach. In some cases they are minor, in others they are very dangerous. Let's look at two types of serious defects, or rather, let's find out how erosion differs from an ulcer.
Gastric erosion– a pathology that affects the mucous membrane of the corresponding organ.
Ulcer- a defect that is characterized by deep penetration into the stomach tissue.
The two phenomena in some cases represent stages of a single destructive process. Moreover, the difference between erosion and ulcer is that the first of them is formed on early stage, and the second – after some more time.
Initially occurs negative impact one or more factors. Abnormalities in the stomach can occur, for example, due to irregular eating habits, constant use hot liquids or taking irritating medications. All this, and much more, can lead to the destruction of mucosal cells and the occurrence of erosion.
It represents more light form diseases, since it affects only the superficial layer. The damaged area has a round or jagged shape and differs in color from the surrounding healthy tissue. The integrity of the mucous membrane during erosion can be impaired in several places at the same time, which aggravates the situation.
The development of erosion is indicated by spasms, discomfort when ingested by food, as well as bloody inclusions in stool or vomit. Fortunately, such a defect does not always degenerate into an ulcer. The pathogenic process may stop at this stage, especially if it has been necessary treatment. With a favorable outcome, the tissues are completely restored, not even a scar remains.
But if provoking factors continue to operate and the person is in no hurry to see a doctor, there is a risk of earning more dangerous defect- ulcer. With it, in addition to the mucous membrane, the deeper layers of the organ are also corroded. Unlike erosion, this damage is detected not only by endoscopic examination, but also by x-ray examination.
What is the difference between erosion and ulcer regarding symptoms? The fact is that the last one for obvious reasons feels stronger. Pain occurs here both during and after eating. The stomach may not accept the food consumed, and vomiting occurs. The ulcer is often accompanied by severe heartburn and periodic bowel movements.
The disease takes a long time to treat and tends to periodically worsen. The diet is prescribed in both cases, but with an ulcer it is more strict. In case of successful healing, a scar remains at the site of such a deep defect.
Epidemiology . Over the last decade in Ukraine, the number of patients with erosive and ulcerative lesions (EAL) of the gastrointestinal tract has increased. For example, only the number of patients with peptic ulcer of the stomach (G) and duodenum (DU) increased by 38%, and the prevalence of these diseases reached 150 cases per 100 thousand population. There is also an increase in the complications of ulcers - the number of ulcer bleedings has doubled over the same time, which is associated with an increase in the prevalence of not only ulcers, but also symptomatic ulcers, especially those caused by taking non-steroidal anti-inflammatory drugs (NSAIDs).
Damage to the coolant and duodenum, leading to the development of erosions and ulcers, can be associated with both the action of endogenous (hypersecretion, bile reflux) and exogenous ( Helicobacter pylori, NSAIDs, alcohol) aggressive factors, and a decrease in protective factors (decreased secretion of bicarbonates and synthesis of prostaglandins, impaired microcirculation).
Classification . EJPs are usually classified according to etiology into infectious (primarily HP-associated, as well as tuberculosis, syphilis); medicinal (most often NSAID-associated, and also associated with the use of glucocorticosteroids, reserpine, cytostatics); hemodynamic (for shock, vasculitis); endocrine (gastrinoma, hyperparathyroidism, pheochromocytoma, diabetes mellitus); neoplastic (cancer and lymphoma of the stomach); granulomatous (Crohn's disease, sarcoidosis). According to the depth of the lesion, EJPs are divided into erosions (superficial, complete) and ulcers; according to the nature of the process - acute (symptomatic) and chronic; by prevalence - single and multiple; by localization - gastric (cardiac, body, pylorus, antrum), duodenal (bulb, subbulb) and erosions and ulcers of the gastroenteroanastomosis (postoperative). Traditionally, PU is divided into active and inactive; into uncomplicated and complicated by perforation, penetration, bleeding, stenosis, malignancy.
Clinical manifestations Dyspepsia syndrome with EJP is not very specific. Its main manifestation may be pain in the upper abdomen. It is localized in the epigastrium or pyloroduodenal zone, much less often in the left or right hypochondrium. The nature of the pain can be varied: burning, aching; sometimes the patient is only bothered by the feeling of hunger. The pain is most often periodic, usually lasting several weeks, disappearing on its own or when taking antacids or antisecretory drugs. Relapses are associated with stress or changes in seasons (spring, autumn). When the pathology is localized in the stomach, pain occurs immediately after eating, and with a duodenal ulcer, “hungry” and night pain are characteristic.
Ulcers of the pyloric canal are very often accompanied by symptoms of a transient disturbance of gastric evacuation - heaviness in the epigastrium, rapid satiety, belching, vomiting. If the ulcer is located in the cardial part of the stomach, the patient may be bothered by chest pain, aggravated in a horizontal position, which often requires differential diagnosis with heart disease.
In many patients, the pain may be mild or absent altogether, while other manifestations of the dyspepsia syndrome may come to the fore - heaviness in the epigastrium, nausea, vomiting, heartburn. Unfortunately, some patients, especially those with symptomatic ulcers, the disease can only manifest itself with its complications - perforation or bleeding. At the same time, the uncomplicated course of EJP is often clinically completely asymptomatic.
Diagnostics . If EJP is suspected, an endoscopic examination is indicated to confirm the diagnosis. Previously widely used X-ray methods diagnostics turned out to be little informative, especially in the presence of erosions and acute ulcers. Currently X-ray examination carried out if endoscopy is impossible, if the malignant nature of the ulcerations is suspected (more informative modern techniques– NMR and X-ray tomography and/or intragastric sonography) and, if necessary, assessment of the evacuation function of the stomach. However, identifying erosions and ulcers in the stomach or duodenum requires further clarification of the etiological causes of the disease listed above.
Etiology . The most common cause of EJP is Helicobacter pylori infection. As large-scale studies conducted in many countries around the world have shown, 70-80% of duodenal ulcers and up to 50-60% of gastric ulcers are associated with this infection. HP is a unique microorganism that has adapted to life in the highly aggressive environment of the stomach, using the ability to break down urea to form ammonia, a substance that has an alkaline environment, to protect against hydrochloric acid. This microorganism can cause various options stomach lesions: acute and chronic gastritis, peptic ulcer, MALTOMA (Mucosa-associated lymphoid tissue lymphoma) and carcinoma. Helicobacter pylori infection is transmitted through the fecal-oral and oral-oral routes, so children living in large families are most easily infected, especially in poor living conditions. This is more typical for developing countries, which to some extent can include our country. In Ukraine, many people are infected with HP in childhood, and in adults it reaches 70-90%. In industrialized countries, the incidence of HP infection is much lower - 0.5-1% per year.
The mechanisms of damage to the coolant and duodenum during Helicobacter pylori infection include both a decrease in resistance and an increase in aggressiveness. After adhesion to epithelial cells, NR immediately causes an increase in the synthesis of pro-inflammatory interleukins and the attraction of leukocytes from the bloodstream. A typical inflammatory reaction occurs, leading to varying degrees of damage to the CO. Toxins produced by HP also damage the mucous membrane, activate inflammation and impair microcirculation, which aggravates the resulting changes. In patients with helicobacteriosis, gastric secretion initially increases, i.e., the aggressiveness of gastric juice increases. This is due to the predominant damage to D-cells that produce somatostatin (a histamine antagonist), which stimulates histamine-mediated gastric secretion. It should be noted that only 10% of people infected with HP develop EJP, while the rest experience chronic non-erosive gastritis. ENP is most often caused by strains that produce a vacuolating toxin and a cytotoxic protein. The characteristics of the human immune response and the hereditarily determined mass of the gastric glands and the presence of receptors for HP adhesins on epithelial cells are important.
Diagnosis of HP infection carried out using a variety of tests. The materials for the study can be biopsies of CO, blood, feces, saliva, and dental plaque. Depending on the method of obtaining biological materials, non-invasive tests are distinguished (urease breath test, serological determination of antibodies to HP in saliva and stool, polymerase chain reaction [PCR] in saliva, stool and dental plaque) and invasive (determination of urease activity and fragments in biopsies of the gastric mucosa Microorganism DNA by PCR, direct HP microscopy, detection of antibodies to HP in blood serum).
Usually first diagnostic test on HP in our country is the determination of urease activity of gastric mucus during an endoscopic examination and microscopic identification of the pathogen in biopsies of the mucus. Non-invasive diagnostic methods are most often used to assess the completeness of HP eradication no earlier than 4 weeks after completion of anti-Helicobacter therapy.
In case negative tests In case of HP, it is necessary to exclude other causes of EP. Most often this turns out to be gastroduodenopathy associated with NSAID use. The mechanism of damage to the coolant and duodenum when taking these drugs is both inhibition of cyclooxygenase-1 (COX-1) with a subsequent decrease in the synthesis of prostaglandins, and direct damage to the mucosa by the drugs themselves. As is known, COX-1 is present in all tissues of the body, including the gastrointestinal tract. Here it stimulates the production of prostaglandins E 2, I 2, F 2, which increase the mucosal resistance to damage. The protective effect of prostaglandins is to stimulate the secretion of mucus bicarbonates, increase blood flow and cell proliferation, and stabilize cellular lysosomes and membranes. Depending on the chemical structure of NSAIDs, the risk of developing gastropathy ranges from 4% for diclofenac to 74% for ketoprofen. Ultrastructural changes in the mucous membrane can develop within a few minutes after taking NSAIDs, macroscopic changes - after a few days.
More selective COX-2 inhibitors - nimesulide, meloxicam ( movalis), celecoxib, roficoxib.
Factors that increase the risk of EJP when taking NSAIDs are:
· age over 65 years;
history of peptic ulcer;
· large doses and/or simultaneous use of several NSAIDs;
· treatment with glucocorticosteroids;
· long duration therapy;
· female gender;
· smoking;
· drinking alcohol;
· presence of HP.
To diagnose NSAID gastropathy, esophagogastroduodenoscopy is indicated, which must be performed in all patients taking these drugs and having increased risk complications, regardless of the presence of any complaints. Repeated endoscopic examinations are produced every 6 months. Unlike peptic ulcers, in patients with NSAID gastropathy, ulcerations are often multiple, they are localized in the body of the stomach, and periulcerous inflammation is less pronounced.
In patients with long-term non-scarring ulcers, it is necessary to exclude primary ulcerative form of stomach tumors– carcinoma, much less often lymphoma. Risk factors for the development of gastric cancer include severe dysplasia and metaplasia of the epithelium, developing against the background of long-standing atrophic gastritis, which in most cases is associated with HP. Gastric polyposis is also of great importance. The previously existing opinion (in the “pre-endoscopic era”) about the high frequency (up to 50%) of malignancy in primary benign gastric ulcer was not confirmed by subsequent studies; in reality it does not exceed 2%. Quite often, against the background of active antiulcer therapy with modern antisecretory drugs, epithelization of even malignant ulcerations occurs. In this regard, all patients with an ulcer localized in the stomach need morphological verification of it before starting treatment. benign in nature, which requires gastrobiopsy from both the periulcerous zone and the scar zone. If the diagnosis of a stomach tumor is confirmed, the patient should be treated by surgeons and oncologists.
Detection of multiple erosive and ulcerative lesions of the gastric mucosa is very often a manifestation symptomatic non-Helicobacter lesions. In this situation, it is necessary to think about the so-called rare diseases: Zollinger-Ellison syndrome (gastrinoma), hyperparathyroidism, systemic vasculitis. Somewhat more often, such changes in the mucous membrane are associated with systemic or local violation blood circulation (stress ulcers). Classic examples of such ulcerations are Cushing's and Curling's ulcers associated with burns, acute disorder cerebral circulation, shock due to myocardial infarction or acute blood loss. Shock ulcers are usually difficult to diagnose, since there are practically no symptoms of dyspepsia, and signs of shock come to the fore. Very often, the first and only manifestation of such ulcers are symptoms of complications - bleeding or perforation.
Over the past two decades, approaches to treatment of peptic ulcer , because the principle “without acid there is no ulcer”, proposed more than 90 years ago, was replaced by the principle “without Helicobacter and acid there is no ulcer.” Therefore the development effective methods elimination of HP infection and the emergence of new antisecretory drugs have led to the fact that what was previously considered chronic, i.e. incurable, PU can now be completely cured.
Much less importance is now given to diet therapy. Numerous studies have shown that with adequate drug therapy There is no significant difference in the timing of ulcer scarring depending on whether patients follow or fail to comply with a strict diet. It is considered advisable to eliminate alcohol, caffeine-containing drinks and individually intolerant foods, as well as quit smoking. Most patients with uncomplicated ulcers can be treated on an outpatient basis and do not require mandatory hospitalization.
It is well known that for successful scarring of an ulcer it is necessary to increase the intragastric pH level to 3 or higher and maintain it for at least 18 hours a day. In this regard, antacids have almost completely lost their importance, since it turned out that in order to adequately reduce gastric secretion, their very frequent use in large doses is necessary. The M-anticholinergic drugs that replaced them also turned out to be insufficiently effective. Type 2 blockers remain important in antisecretory therapy histamine receptors- ranitidine, famotidine ( kvamatel), nizatidine. However, due to insufficient antisecretory activity, they are not recommended for the treatment of ulcers as first-line drugs; They are used with great effect in patients with ulcer-like forms of FD.
The main group of antisecretory drugs currently are PPIs - drugs that act on the final link of gastric secretion and suppress the release of hydrochloric acid by 90% or more. There are several generations of these drugs, but the most common in our country include omeprazole (1st generation) and lansoprazole (2nd generation). As our research confirms, they make it possible to achieve high frequency scarring of ulcers (over 80%) within 10 days of taking even without anti-Helicobacter drugs. Due to their higher cost, rabeprazole, pantoprazole, and esomeprazole belonging to subsequent generations are used much less frequently in Ukraine, although esomeprazole today ranks first in the world in terms of sales among all PPIs.
Based on multicenter data clinical trials(GU-MACH, 1997 and DU-MACH, 1999) numerous recommendations have been developed for the treatment of diseases associated with HP. In September 2000, the second Maastricht Agreement was adopted, providing for mandatory anti-Helicobacter therapy for peptic ulcer and duodenum (both active and inactive), MALToma, atrophic gastritis; It is also recommended to treat HP-positive patients after gastric resection for cancer and their 1st degree relatives. Treatment regimens have also been developed. Regimen that eliminate (eradicate) HP in at least 80-85% of patients are considered effective, preferably with minimal side effects.
TO first line therapy (triple therapy) refers to a combination of a PPI or ranitidine bismuth citrate (not registered in Ukraine) with two antibacterial drugs: clarithromycin and amoxicillin or clarithromycin and metronidazole for at least 7 days. Second line therapy (quad therapy) involves prescribing a PPI in combination with a bismuth drug, metronidazole and tetracycline for at least 7 days.
Unfortunately, irrational use antibacterial drugs led to the emergence of HP strains resistant to metronidazole or clarithromycin. The true prevalence of such strains in Ukraine is unknown, but in some regions 70% of microorganisms turned out to be resistant to metronidazole. Clarithromycin-resistant strains are much less common, since due to the high cost and recent appearance of this antibiotic in our country, they simply did not have time to arise. Nitrofurans have been proposed as an alternative to metronidazole, and azithromycin may be a cheaper replacement for clarithromycin. There are reports of studies demonstrating the effectiveness of rifampicin and fluoroquinolones.
The therapeutic drug OMEZ, which belongs to the group of proton pump inhibitors, is prescribed for non-infected diseases of the gastrointestinal tract, as well as in the system complex therapy when the gastrointestinal tract is infected with the bacterium Helicobacter Pylori.
Prescriptions of drugs from the group of proton pump inhibitors are made only after a thorough diagnosis of the patient’s condition. In case of a confirmed diagnosis, the drug Omez is prescribed. Indications for the use of medicinal medication, are the following diseases:
Reflux esophagitis is best treated with a combination of complex anti-secretory therapy in combination with proton pump inhibitors (hereinafter referred to as PPIs). A significant increase in the sensation of heartburn caused by reflux esophagitis is provoked by the action of over-the-counter antacids. Their impact progresses due to the complex use of H2-blockers, as well as NSAIDs, which have always needed to be replaced with a drug with a lowering effect on gastric acidity. Since the cost of PPIs has decreased with the advent of Omez, the use of NSAID drugs is neither effective nor cost-effective. PPIs are considered as safe as H2 blockers but are more effective. Until PPIs were first introduced into Omez (omeprazole, Prilosec AstraZeneca, Wilmington, DE), the safety of antiulcer drugs was a concern.
The result was that Omez (omeprazole) plays a large role in deep decline secretion of gastric acid. The cells responsible for the stimulating secretory properties of producing the appropriate amount of acid increase the release of the stimulating hormone gastrin. Gastrin levels tend to be elevated in patients taking NSAIDs, but they are generally not clinically significant.
Animal studies, especially using mice as a model clinical trials, PPI data showed the spread of gastrin-secreting cells, and even the development of gastrinomamia as a specific condition of the body. Increased level gastrin (hypergastrinemia) is often observed in patients as an allergic reaction to PPIs, which over time poses a danger for this category of patients with the development of Gastrinomas.
Hypergastrinemia, or Zollinger-Ellison disease (ZES), is the most terrible diagnosis, caused allergic reaction on IPP. Normal level Gastrin in blood serum on an empty stomach is usually 110-150 mcg/ml. Antisecretory drugs can moderately increase gastrin levels in the range of 200-400 mcg/ml. However, in some study groups, approximately 5% of total number In patients taking PPIs, gastrin levels could exceed 400 mcg/ml. The only case recorded in the studies was in a patient with ZES with a fasting serum level of more than 1000 mcg/ml. But it is also necessary to take into account that about 10% of patients diagnosed with ZES have serum gastrins levels below 100 mcg/ml.
Zollinger-Ellison disease (ZES), as a rule, represents a sublimation of recurrent multiple lesions of the mucous membrane of a peptic ulcer, as a result of hypersecretion of the gastrointestinal tract. Approximately 90% of patients develop multiple ulcers. In most, these ulcers are located in the first part of the duodenum.
Zollinger-Ellison disease may be accompanied by diarrhea as the main symptom of the disease, since secretory excess acid in the gastric juice can lead to inactivation of pancreatic enzymes as a result of malabsorption and steatorrhea. Signs indicating acid hypersecretion, such as disseminated recurrent peptic ulcers, diarrhea, or a history of multiple endocrine neoplasia type I, should prompt the body to send out ZES. This includes fasting serum concentrations of gastrin while taking a PPI, and secretin as a stimulation test for gastric acid secretion.
In practice, two methods are used to facilitate the most accurate diagnosis of the disease, the location of ulcers, and to determine further methods of prescribed treatment. The first step is to measure fasting gastrin levels, excluding PPI use, for at least one week. As mentioned above, gastrin readings greater than 1000 mcg/ml are usually a direct symptom of ZES. This, however, is not an accurate diagnosis of the disease, as in patients with pernicious anemia, where a similar reading may also have serum gastrin levels in the same range. It is therefore important for the patient's clinical picture to be evaluated for gastrinoma.
For patients with serum gastrins values greater than 1000 mcg/mL, using a gastric tube and gastric pH alone may help differentiate chronic atrophic gastritis from other causes.
The second step is to measure the pH level. Elevated pH levels may be a precursor to pernicious anemia. For patients with gastrin levels between 110 mcg/mL and 1000 mcg/mL, a secretin stimulation test may help determine further diagnostics, and, consequently, therapy. This test is based on the fact that normal gastrin secreting cells will inhibit the formation of infustion secretin (usually an inhibitor of gastrin secretion).
Patients diagnosed with Zollinger-Ellison disease in the presence of gastrinoma, there is uncoupling of the secretin inhibitory receptor. Thus, these patients should have a persistent and significant increase in serum gastrin levels. After stimulation of secretin production, patients with other causes of hypergastrinemia do not experience an increase in serum gastrin levels. A decrease in any level should be recorded in the description of the progress of treatment of the patient’s disease and the clinical picture of the patient’s condition should be assessed.
If the patient's body does not respond to secretin-inhibiting methods, imaging should be performed to try to localize the tumors. This can be done by scanning using the OctreoScan parting, or using endoscopic ultrasound (EUS). OctreoScan shows more accurate results of studies of the metastatic form of the disease or lymph nodes. EUS endoscopy provides a more accurate image of the pancreas. The device is able to show with great accuracy the location of metastasis, and can allow finer tuning for the diagnosis of micro formations on the walls of the mucous membranes, which gives more full diagnostics during research.
Endosonographic studies show how the overall tumor mass is consistent with an islet cell tumor. Also, the data are the main indicator of the presence of gastrinsecreting cells in the immunostain, and how consistent they are with the level of gastrinoma. The best decision for the patient is to perform an endoscopy to evaluate his reflux and determine the diagnosis: his condition is associated with gastritis, or he is developing a stomach ulcer. Computed tomography, magnetic resonance imaging and EUS should be performed for imaging when gastrinoma is suspected.
Peptic ulcer disease has always been considered a classic example of psychosomatic interaction. But ulcers can be caused by household stress. Diagnosis in this area suffers from methodological limitations: insufficient documented diagnoses, as well as a lack of information about the main known risks and factors for the occurrence of ulcers.
“There are multiple doubts about the occurrence of ulcers as a disease. Mechanisms are still unknown and associations that may be associated with distortion and diagnostic bias against the background of the effect of stress as one of the symptoms of the disease have not been discovered,” said Professor of Psychiatry Dr. Susan Levenstein, MD, Dr. medical sciences Aventino Medical Group clinics in Rome, Italy. Psychological stress increases the risk of peptic ulcer disease, regardless of Helicobacter Pylori infection status or use of nonsteroidal anti-inflammatory drugs.
In an effort to resolve the controversy surrounding the question: how much does it contribute? psychological stress symptoms of peptic ulcer disease, Dr Susan Levenstein and colleagues obtained blood samples to test for the presence of antibodies and bacterial infection Helicobacter Pylori. The samples were obtained in addition to psychological, social, behavioral and medical data collected from 3379 eligible inpatient and laboratory patients in Danish healthcare settings. The World Health Organization (WHO) also took part in the research. Her research topic was to study the risk and development of peptic ulcers due to infection of the gastrointestinal tract. Stress was measured based on specific life stressors and various types of disasters and accidents using a 10-item stress index.
Ulcer as a diagnosis was confirmed by reviewing radiological and endoscopic reports and searching all participants in the Danish National Patient Registry.
There were a total of 76 confirmed ulcer incidents throughout the study period. The risk of ulcer was reported to have the highest rate of 3.5%, compared with the lowest tertile of 1.6. Adjustments for H. Pylori positivity, alcohol consumption, or insufficient sleep had no effect on the scores. However, the index fell significantly after adjusting for socioeconomic status, and continued to fall after adjusting for smoking, NSAID use, and lack of exercise.
Multivariate analysis showed that stress, socioeconomic status, smoking, H. pylori infections and NSAID use were independent predictors of the disease. From all of the above, brief conclusions can be drawn:
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Stress factors unhealthy image life and poor nutrition provoke the occurrence of many diseases of the gastrointestinal tract. Erosions and ulcers have a similar etiology and clinical picture, but their differentiation from each other plays a role important role in selection proper treatment and prevention of complications. Both diseases require immediate consultation with a doctor immediately after the first symptoms of the disease appear, as they can lead to serious pathological processes in the stomach.
Localized in the same organ, ulcer and erosion have common symptoms and the same etiological factors.
The ailments are characterized by a specific clinical picture, which is expressed by severe pain in the stomach, nausea, vomiting and general signs of indigestion. In addition, there is malaise, loss of appetite, and possible anemia due to bleeding. An ulcer is considered more serious illness, so her clinic is more extensive and pronounced. Both diseases occur due to the influence of the following etiological factors:
Erosion destroys the gastric mucosa. Common reasons The occurrence of erosive and peptic ulcer diseases is the same. However, it should be remembered that the first disease is limited to damage to the gastric mucosa, while the second also affects the muscle lining. The defect itself occurs after long-term exposure etiological factor on the digestive organs. As a result, there is a decrease in the barrier functions of the mucous membrane, which reduce the effect of gastric juice on the tissue. Defective areas are formed, which, if untimely and improper treatment deepen into the wall of the stomach and develop from erosions into ulcers.
Although both diseases have a number of common features, each of them is characterized by the presence of its own characteristics in pathogenesis and clinical picture, which makes it possible to differentiate them from each other and make the correct diagnosis. The difference between erosion and gastric ulcer lies in a number of factors, which are presented in the table:
| Factor | Erosive pathology | Peptic ulcer |
|---|---|---|
| Causes | Psychogenic factor | Circulatory disorders in the stomach wall |
| Long-term use of non-steroidal anti-inflammatory drugs | ||
| Availability pathogenic microflora(bacteria Helicobacter pylori) | ||
| Localization of the defect | Multiple point lesions of the mucous membrane | The defect extends to the muscle layer of the gastric wall |
| Symptoms | Pain while eating | Pain before and after eating |
| Nausea | ||
| Stool instability | Nausea | |
| Loose stool | ||
| Exacerbation regardless of season | Heartburn | |
| Seasonal exacerbations | ||
| Consequences of the disease in case of recovery | The mucous layer completely regenerates without scarring | A scar forms |
The identity of the causes of occurrence, the mechanism of development and the clinical picture of the disease creates a problem in making the correct diagnosis. An ulcer can be considered a complication of erosion. The disease is more difficult to tolerate and leads to more serious complications and requires immediate medication or surgical intervention specialist when the first symptoms appear.
