Symptomatic gastroduodenal ulcers

Symptomatic duodenal ulcers include:

• drug ulcers;
• "stress" ulcers;
• ulcers in Zollinger-Ellison syndrome;
• ulcers in hyperparathyroidism;
• ulcers in other diseases of internal organs.

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Drug-induced gastroduodenal ulcers

Gastroduodenal ulcers can be caused by various drugs: NSAIDs (most often in the treatment with acetylsalicylic acid, indomethacin, butadiene); rauwolfia preparations (reserpine, combined antihypertensive agents containing reserpine - adelfan, adelfan-ezidrex, cristepin-adelfan, etc.); glucocorticoids; drugs containing caffeine. Anticoagulants, potassium chloride, oral hypoglycemic agents - sulfonylurea derivatives, digitalis preparations, nitrofuran compounds can also have an ulcerogenic effect. The mechanism of the ulcerogenic effect of various drugs is different and varied. The main pathogenetic factors of drug ulcerogenesis are:

• inhibition of the formation of gastroprotective prostaglandins and protective mucus by the gastric mucosa (aspirin and other NSAIDs);
• direct damaging effect on the surface epithelium of the stomach with an increase in its permeability to hydrogen ions (other non-steroidal anti-inflammatory drugs, potassium chloride, sulfonamide drugs, etc.);
• stimulation of the secretion of hydrochloric acid by parietal cells and thus an increase in the aggressive properties of gastric juice (reserpine, caffeine, glucocorticoid drugs);
• hyperplasia of gastrin-producing cells of the gastric mucosa and increased secretion of gastrin, which in turn stimulates the secretion of gastrin and pepsin (glucocorticoid drugs);
• release of a number of biologically active compounds (histamine, serotonin, etc.), which promote increased secretion of hydrochloric acid (reserpine, etc.).

Drug-induced gastroduodenal ulcers are acute, usually more often they occur in the stomach than in the duodenum, can be multiple, often combined with erosions of the gastroduodenal region. The danger of drug-induced gastroduodenal ulcers is that they are often complicated or first manifested by gastrointestinal bleeding, sometimes perforation. Drug-induced gastric ulcers can be asymptomatic (this is typical primarily for glucocorticoid ulcers). The most important feature of drug-induced ulcers is their rapid healing after the withdrawal of the ulcerogenic drug.

Ulcerogenic drugs can cause an exacerbation of peptic ulcer disease.

"Stress" ulcers

"Stress" ulcers are gastroduodenal ulcers that occur during severe pathological processes that cause the development of a stressful state in the human body. "Stress" ulcers include:

• Cushing's ulcers in patients with severe CNS pathology;
• Curling's ulcers in extensive and deep burns;
• ulcers that develop after severe, traumatic operations;
• ulcers in myocardial infarction, various types of shock.

Cushing's ulcers and erosions of the gastroduodenal region are especially often observed in severe traumatic brain injuries.

Curling's ulcers develop with very extensive and deep burns during the first 2 weeks from the moment of the burn. They usually occur on the lesser curvature of the stomach and in the bulb of the duodenum and often manifest themselves with bleeding (hidden or obvious), accompanied by paresis of the stomach and intestines; perforation into the free abdominal cavity or hidden perforation is possible.

In some cases, "stress" ulcers develop after severe and traumatic surgical interventions, and they often proceed unnoticed and heal on their own. Gastroduodenal ulcers have also been described in patients in the acute period of myocardial infarction, with decompensated heart defects. They can also proceed latently or immediately manifest complications, most often gastrointestinal bleeding, which is generally characteristic of "stress" ulcers.

The main mechanisms of development of “stress” gastroduodenal ulcers are:

• activation of the hypothalamic-pituitary-adrenal system, increased secretion of glucocorticoids, which stimulate gastric secretion, reduce the production of protective mucus, reduce the regeneration of the gastric mucosa, increase the formation of histamine from histidine due to the activation of the enzyme histidine decarboxylase (which in turn leads to hyperproduction of hydrochloric acid);
• increased secretion of catecholamines, which contributes to the disruption of microcirculation in the gastric mucosa and the development of ischemia in it;
• disturbances of the motor function of the stomach, development of duodenogastric reflux, reflux of duodenal contents into the stomach and damage to the gastric mucosa;
• increased tone of the vagus nerve and increased activity of the acid-peptic factor of ulcerogenesis.

Zollinger-Ellison syndrome

Described by Zollinger and Ellison in 1955. It has now been established that this syndrome is caused by a gastrin-producing tumor. In 85-90% of cases, it is located in the head or tail of the pancreas, originating from the cells of the islets of Langerhans, but not from the a-cells that produce glucagon, and not from the beta-cells that produce insulin, but from the cells that produce gastrin. In 10-15% of cases, the tumor is localized in the stomach, duodenum, liver, and adrenal glands. There is a point of view that gastrinomas of extrapancreatic localization are even more common than pancreatic ones. Sometimes Zollinger-Ellison syndrome is a manifestation of multiple endocrine adenomatosis (multiple endocrine neoplasia) type I.

In 60-90% of cases, gastrinomas are malignant tumors with slow growth rates.

The leading feature of Zollinger-Ellison syndrome is the formation of peptic ulcers that are resistant to treatment, caused by hyperproduction of gastrin and, accordingly, hyperproduction of hydrochloric acid and pepsin.

In the vast majority of patients, the ulcer is localized in the duodenum, less often in the stomach, and also in the jejunum. Multiple ulcers of the stomach, duodenum and jejunum are quite common.

Clinical manifestations of the disease:

• epigastric pain has the same patterns in relation to food intake as with a common ulcer of the duodenum and stomach, but unlike them, it is very persistent, intense and does not respond to antiulcer therapy;
• persistent heartburn and sour belching are extremely characteristic;
• an important symptom of the disease is diarrhea, caused by the entry of a large amount of hydrochloric acid into the small intestine and, as a result, increased motility of the small intestine and a slowdown in absorption; the stool is abundant, watery, with a large amount of fat;
• a significant decrease in body weight is possible, which is most typical for malignant gastrinoma;
• gastric and duodenal ulcers in Zollinger-Ellison syndrome do not heal even with prolonged adequate therapy;
• many patients experience pronounced symptoms of esophagitis, sometimes even with the formation of ulcers and strictures of the esophagus;
• when palpating the abdomen, severe pain is detected in the epigastrium or pyloroduodenal zone, Mendel's symptom may be positive (local palpation pain in the ulcer projection), there is local protective muscle tension;
• in cases of malignant nature, metastases to the liver are possible and, accordingly, its significant enlargement;
• X-ray and endoscopic examination of the stomach and duodenum reveals an ulcer, the signs of which do not differ from those described above for common gastric ulcer and duodenal ulcer.

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Laboratory criteria for Zodlinger-Ellison syndrome

Relatively reliable laboratory signs of Zollinger-Ellison syndrome are the following:

• hypergastrinemia (the content of gastrin in the blood is up to 1000 pg/ml or more, while in peptic ulcer disease it does not exceed the upper limit of the norm of 100 pg/ml);
• secretin test - the patient is given intravenous secretin at a dose of 1-2 U per 1 kg of body weight. In Zollinger-Ellison syndrome, the gastrin content in the blood increases significantly compared to the initial level, while gastric secretion increases. In peptic ulcer disease, the gastrin content in the blood after the use of secretin, on the contrary, decreases, and gastric secretion is inhibited;
• calcium gluconate test - calcium gluconate is administered intravenously at a dose of 4-5 mg per 1 kg of body weight. In Zollinger-Ellison syndrome, an increase in the level of gastrin in the blood is observed by more than 50% compared to the initial level (almost to a level of 500 pg/ml and higher), while in peptic ulcer disease, the increase in gastrinemia is much less pronounced;
• gastric secretion indices (A. A. Fisher, 1980):
  • basal acid production over 15 and especially 20 mmol/h;
  • the ratio of basal acid production to maximum is 0.6 or more;
  • basal secretion volume over 350 ml/h;
  • acidity of basal secretion (basal secretion flow rate) more than 100 mmol/h;
  • maximum acid production over 60 mmol/h.

Instrumental methods for detecting gastrinoma

The tumor itself (gastrinoma) is detected using ultrasound, computed tomography, and selective abdominal angiography.

Ultrasound of the pancreas and computed tomography reveal a tumor in only 50-60% of patients due to the small size of the tumor.

The most informative method is selective abdominal angiography with blood sampling from the pancreatic veins and determination of gastrin in it. With this method, the correct diagnosis is established in 80% of patients.

CT scans usually do not detect tumors less than 1 cm in diameter.

Ulcers in hyperparathyroidism

Hyperparathyroidism is a disease caused by pathological overproduction of parathyroid hormone by the parathyroid glands.

Gastroduodenal ulcers in hyperparathyroidism occur with a frequency of 8-11.5%. The mechanism of ulcer formation is as follows:

• excess parathyroid hormone has a damaging effect on the mucous membrane of the gastroduodenal zone and stimulates gastric secretion and the formation of hydrochloric acid;
• hypercalcemia stimulates the secretion of hydrochloric acid and gastrin;
• In hyperparathyroidism, the trophism of the mucous membrane of the gastroduodenal zone is sharply reduced.

Clinical features of the course of gastroduodenal ulcers in hyperparathyroidism:

• ulcers are most often localized in the duodenum;
• ulcers have a long atypical course;
• clinically manifest forms are characterized by severe pain syndrome, persistent course, resistance to antiulcer therapy, and a tendency to complications (bleeding, perforation);
• ulcers often recur.

During FGDS and X-ray examination of the stomach, an ulcer is detected, characterized by the same endoscopic and radiological manifestations as a common peptic ulcer.

The clinical picture and diagnosis of hyperparathyroidism are described in the corresponding chapter of the manual “Diagnostics of diseases of internal organs”.

Gastroduodenal ulcers in other diseases of internal organs

Gastroduodenal ulcers in atherosclerosis of the abdominal aorta and arteries of the abdominal cavity

In severe atherosclerosis of the abdominal aorta, the incidence of gastroduodenal ulcers is 20-30%. The main factors in the origin of such ulcers are the deterioration of the blood supply to the stomach and a sharp decrease in the trophism of the mucous membrane of the gastroduodenal zone.

The clinical features of gastroduodenal ulcers developing as a result of atherosclerosis of the abdominal aorta are the following:

• ulcers develop not only in asthenics (which is more typical for peptic ulcer sui generis), but also in hypersthenics;
• Quite often ulcers are multiple;
• characterized by a tendency to complications, most often there are bleedings that have a tendency to relapse;
• ulcers heal very slowly;
• the course of ulcers is often latent;
• mediogastric localization of ulcers is often observed;
• Patients exhibit clinical and biochemical symptoms of atherosclerosis.

Ulcers in liver cirrhosis

Ulcers of the gastroduodenal region are observed in 10-18% of patients with liver cirrhosis. The mechanism of ulcer formation is as follows:

• decreased inactivation of histamine and gastrin in the liver, increased levels of them in the blood, which leads to hyperproduction of hydrochloric acid;
• disruption of blood flow in the portal system and the development of hypoxia and ischemia of the mucous membrane of the gastroduodenal region;
• decreased secretion of protective gastric mucus;

Clinical features of ulcers in liver cirrhosis are:

• predominantly localized in the stomach;
• quite often the clinical picture is blurred;
• frequent complication of ulcers - gastroduodenal bleeding;
• low efficiency of antiulcer therapy.

Ulcers in chronic pancreatitis

Pancreatogenic ulcers develop in 10-20% of patients with chronic pancreatitis. Their pathogenesis is influenced by decreased secretion of bicarbonates by the pancreas, alcohol abuse, duodenogastric reflux, and increased production of kinins.

Pancreatogenic ulcers have the following features:

• most often localized in the duodenum;
• have a persistent course;
• less likely to occur acutely compared to other symptomatic ulcers;
• rarely complicated by bleeding.

Gastroduodenitis ulcers in chronic non-specific lung diseases

In chronic non-specific lung diseases, gastroduodenal ulcers develop in 10-30% of patients. The main reason for their development is hypoxemia and decreased resistance of the gastroduodenal mucosa to aggressive factors of gastric juice.

The clinical features of these ulcers are:

• predominantly gastric localization;
• weak expression of pain syndrome; lack of a clear connection between pain and food intake;
• moderate dyspeptic disorders;
• tendency to bleeding.

Gastroduodenal ulcers in chronic renal failure

In chronic renal failure, gastroduodenal ulcers are observed in 11% of patients. The development of ulcers is especially characteristic in patients undergoing programmed hemodialysis. In the pathogenesis of these ulcers, a decrease in the destruction of gastrin in the kidneys and the damaging effect of uremic toxic substances on the gastric mucosa are important.

Ulcers in chronic renal failure are most often localized in the duodenum and are prone to severe bleeding.

Gastroduodenal ulcers in diabetes mellitus

In the origin of gastroduodenal ulcers in diabetes mellitus, the most important role is played by damage to the vessels of the submucosal layer ("diabetic microangiopathy"). These ulcers are usually localized in the stomach, occur with erased symptoms, and are often complicated by gastroduodenal bleeding.