Synonyms in the broader sense

Medical: Ulcer

Gastroduodenal ulcer disease, gastric ulcer, duodenal ulcer, peptic ulcer, duodenal ulcer, ulcer disease, gastritis

Definition of gastric ulcer

An ulcer is a benign gastric ulcer or duodenal ulcer, which extends very deep into the mucosa, at least into the inner muscle layer of the mucous membrane ( lamina muscularis mucosae, see also stomach). A dangerous complication of peptic ulcer occurs when the ulcer reaches a larger vessel, causing life-threatening bleeding.
The predilection site for gastric ulcer is the small curvature of the stomach ( Curvatura minor ) in the area of ​​the gastric cavity (antrum) near the stomach outlet. The two major contributors to gastric ulcer are pain medications such as aspirin and NSAIDs and the bacterium Helicobacter pylori.

Gastric ulcer: A gastric clearing with gastric ulcer and B-section through the stomach wall

Defect of the gastric mucosa

  1. Gastric ulcer -
    Gastric ulcer
  2. Esophagus - Esophagus
  3. Stomach body -
    Corpus gastricum
  4. Small stomach curvature -
    Curvatura minor
  5. Duodenal -
  6. Magenpförtner - pylorus
  7. Gatekeeper Cave -
    Antrum pyloricum
  8. Mucus coating the
    stomach area
  9. surface tissue
    of the stomach
  10. Mouth of the
    stomach gland
  11. stomach gland
  12. Mucosal muscle layer

Frequency (epidemiology)

Occurrence in the population
About 10% of the population have had a stomach ulcer or duodenal ulcer at least once in their lifetime. The duodenal ulcer (duodenal ulcer) is about five times more common than the stomach ulcer (gastric ulcer).
Men are three times more likely to be affected by duodenal ulcer than women.
In the case of the gastric ulcer, the sex distribution is 1: 1.
The peak of the age of onset is between the 50th and 70th year of life.

Anatomy stomach

  1. Esophagus (esophagus)
  2. Kardia
  3. corpus
  4. small curvature
  5. fundus
  6. great curvature
  7. Duodenum (duodenum)
  8. pylorus
  9. antrum

Ulcus forms / classification

One distinguishes first an acute (sudden) from a chronic-recurring (recurrent) gastric ulcer (ulcer). The acute "stress ulcer" occurs as a result of superficially damaging (erosive) gastritis (gastritis). The cause of this ulcer formation are strong physical stressors that lead to the sudden collapse of the protective mucosal barrier. Such stressful situations are, for example, burns, major operations and many other medical conditions requiring intensive care.

Chronic recurrent ulcers occur more frequently and may have different causes (see below).

Furthermore, the ulcers are classified according to their location in gastric ulcers and duodenal ulcers. The gastric ulcer is most common in the area of ​​small gastric curvature (Curvatura minor).
The duodenal ulcer is almost exclusively at the beginning of the duodenum (duodenum) the bulbus duodeni.
If one finds ulcers in more distant intestinal sections than described (eg, jejunum section of the small intestine), this may be an indication of a rare Zöllinger-Ellison syndrome.

Causes of gastric ulcer

For the development of a gastrointestinal ulcer, the balance between the mucosal-aggressive and mucosal-protective (defensive) factors plays an essential role (see figure). If the aggressive factors outweigh or the defensive fail it can lead to an ulcer. One distinguishes among the causes, those which originate from the body itself (endogenous cause) and those which are caused from outside (exogenous cause).

1. Endogenous causes

As endogenous causes, ie causes that are caused by the body itself, are:

  • stomach acid
  • Gastrointestinal motility (peristalsis)
  • Zollinger-Ellison syndrome
  • hyperparathyroidism
  • Rare causes

a) stomach acid
A very important factor for the development of an ulcer is the stomach acid. This finding can be deduced from the fact that patients with autoimmune gastritis, who can no longer produce stomach acid, do not get ulcers. It should be noted, however, that gastric ulcer production is rarely elevated in gastric ulcer. Gastric ulcer is therefore not the triggering factor but an accompanying factor (permissive factor) for the maintenance / persistence of gastric ulcer.

In a duodenal ulcer, however, the excessive secretion of the gastric juice plays an essential role. Particularly noteworthy is the still largely unexplained increased formation of stomach acid and pepsin (aggressive protein enzyme of the digestive chain) during the night.
In addition, inadequate binding of gastric acid by the basic bicarbonate, which is formed in the duodenum, as a partial cause of the development of the duodenal ulcer (lack of acid neutralization).

b) Gastrointestinal motility (peristalsis)
More and more frequently a disturbed coordination of the movement between the stomach cavity (antrum) and the duodenum is discussed. In some patients with gastric ulcer bile acid reflux (gallereflux) is observed in the stomach in addition to a longer gastric passage for food. Bile acids are among the mucosal-aggressive factors.

c) Zöllinger-Ellison syndrome
Behind this term is a rare tumor that is most frequently localized in the pancreas and produces the hormone gastrin.
The benign tumor is also referred to as gastrinoma. The gastrin excessively formed by the tumor leads to overstimulation of the acid-forming gastric cells (parietal cells). So too much gastric acid is produced. This excess of stomach acid leads to preponderance of the aggressive factors in the gastrointestinal tract and the formation of many simultaneous (multiple) gastric ulcer.
Zöllinger-Ellison syndrome often results in multiple ulcers in the duodenum and even later in the intestine (jejunum). These ulcers (ulcers) prove to be particularly persistent. A treatment is tedious and difficult.
This syndrome causes only 1% of all gastro-duodenal ulcer disease.

d) hyperparathyroidism
Hyperparathyroidism describes hyperparathyroidism (Parathyroidea). An overfunction of the hormone-producing cells (epithelial bodies) of the parathyroid gland leads to an excess of calcium (hypercalcemia) in the body.
This in turn leads to the stimulation of G cells in the stomach and duodenum, which produce the previously described hormone gastrin. This in turn leads to an overstimulation of acid-forming gastric cells.

e) Rare causes
Very rare causes are viral infections eg with the cytomegalovirus cytomegalovirus (CMV) or the herpes simplex virus (HSV) and chronic intestinal diseases, such as the Crohn's disease.

Further information can be found under our topic:

  • Crohn's disease and
  • Herpes simplex

Sometimes, an ulcer (ulcer) in the gastrointestinal area also arises as a result of therapeutic X-ray radiation (tumor therapy) or due to vascular disease.

2. Exogenous causes

Exogenous causes of gastric ulcer are causes which enter the stomach from the outside. Particularly suitable for this are:

  • Helicobacter pylori (Hp)
  • Non-steroidal anti-inflammatory drugs (NSAIDs)

a) Helicobacter pylori
The bacterium Helicobacter pylori (Hp) has been found since its discovery in the early 90s as one of the major causes of gastroduodenal ulcer disease (chronic ulcer).

The risk of developing a stomach ulcer increases in the presence of Helicobacter-related gastritis (gastritis) by 3-4 times.
This does not mean that every person whose gastric mucosa is colonized with the bacterium is a gastritis or ulcer imperatively developed. In almost all patients with a duodenal ulcer, the Helikobacter bacterium can be detected. Approximately 75% of patients with a gastric ulcer are infected with the Helicobacter bacterium.

Helicobacter pylori is also a permissive factor for the formation of ulcers, that is, the infection with the bacterium is not sufficient sole cause of the development of a gastrointestinal ulcer. Other aggressive factors (see above) must also be present.

b) Non-steroidal anti-inflammatory drugs
NSAIDs, such as acetylsalicylic acid (ASA), are also widely used as analgesics in joint disease and other pain conditions.

These drugs have a gastric mucus destroying effect. The machanism behind it is related to the inhibition of so-called prostaglandin formation.
Prostaglandins have a vasodilatory effect on the gastric mucosa and also promote the formation of protective gastric mucus. By reducing prostaglandin formation, the gastric mucosa thus loses important protective factors. The risk of developing a stomach ulcer increases. The risk of getting an ulcer multiplies in the case of NSAID medication and simultaneous Helicobacter pylori infestation.

Further information can be found under our topics:

  • NSAIDs
  • acetylsalicylic acid

Symptoms / complaints

The symptoms of a peptic ulcer are often very unspecific. This is shown by statistics, which show that 20% of Ulcuspatienten are completely symptom-free (unsymptomatic) and again 20% of patients with disease symptoms as in a peptic ulcer had no ulcer in the gastroscopy (endoscopy).
Typically, NSAID - related ulcers are those that produce no or very uncharacteristic signs of disease (symptoms).
Symptoms include:

  • Abdominal pain
  • nausea
  • bloating
  • Food intolerances.

In addition, pain may occur that is not uncommon in the chest, thorax, back or lower abdomen. This pain is often described as "hungry" and "nagging".

In some patients, a certain rhythm in the pain symptoms can be observed, which occasionally suggest the location of the ulcer / ulcer.
Nocturnal pain and relief of pain after eating seem to be typical of duodenal ulcer (duodenal ulcer). Deterioration after eating is more likely to occur in gastric ulcer (gastric ulcer).
However, the diagnosis can only be assured by a gastrointestinal examination.


If a gastric or duodenal ulcer breaks through the stomach or intestinal wall and the gastric juice is connected to the free abdominal cavity (peritoneal cavity), it is called ulcus perforation (gastric perforation).
In 10% of patients with a duodenal ulcer and in 2-5% with a gastric ulcer, such ulcer perforation occurs during the course of the disease. More often are breakthroughs in NSAID-related ulcers, because they are later recognized and treated because of the painless process. Breakthrough (perforation) of the stomach or intestinal wall can lead to life-threatening peritonitis (peritonitis), which must be treated as soon as possible.

In some cases, an ulcer may also "break" into an adjacent organ, which is called ulcer penetration ("covered perforation"). For example, due to the proximity to each other, for example, the pancreas may be affected when a duodenal ulcer exceeds the intestinal wall.
Rarely can a stomach ulcer break into the liver (hepar).

If an ulcer hits a blood vessel and damages it, bleeding of the ulcer / ulcer may occur. This complication is still associated with a mortality rate of 10%.
Bleeding may appear as a hidden (occult) blood in the stool, as a tarry stool (Mälena), or even as a hematemesis. The therapy is to inject the ulcer during a gastrointestinal examination with drugs such as epinephrine, which stops the bleeding, because adrenaline puts the bleeding vessel tight.
Even if the bleeding itself stops bleeding, the ulcer is still injected today to prevent recurrent (recurrent) bleeding.
Only if the haemostasis by endoscopy is in no way to accomplish, the bleeding during an open surgery must be breastfed. This complication is more common in gastric ulcers located on the posterior wall of the stomach, where anatomical proximity to a gastric artery (artery) tends to cause severe bleeding.

Complication of gastric bleeding

Caution: The complication of gastric bleeding is still associated with a mortality rate of 10%.
For more information on this topic, see: Stomach Bleeding

Figure gastric ulcer

The gastric ulcer is localized at the typical location at the exit of the stomach.

In the picture below, the stomach wall is shown in cross section and you can see how deep the gastric ulcer reaches.

Layers of the gastric mucosa

  1. Mucosa (mucous membrane)
  2. Ulcer (gastric ulcer)
  3. Submucosis (connective tissue layer)
  4. blood vessels

If the mucous membrane has a damage that extends into the underlying connective tissue, which can lead to gastric bleeding.

A rarer complication of a gastric ulcer is the gastric outlet or duodenal narrowing (stenosis). These arise mostly in the area of ​​the stomach outlet (pylorus) and the beginning of the small intestine (duodenal bulb), if it in this area to recurrent (recurrent) ulcers and thus to scarring and tissue shrinkage is coming. The typical first symptom of this complication is repeated vomiting, as the ingested food can no longer pass through the stomach or intestine in the area of ​​the narrowing.

Stress as the cause of a stomach ulcer?

Generally, a gastric ulcer results from an imbalance between the stomach protective factors and the attacking substances. Stress alone, however, can not lead to the development of a gastric ulcer. Nevertheless, it is possible that much and prolonged stress in combination with unhealthy diet, alcohol and smoking can lead to gastritis and thus trigger a gastric ulcer.

The reason for this is that these factors lead to increased acid production in the stomach. This attacks the gastric mucosa and can lead to inflammation of the mucous membrane. In addition, the sympathetic nervous system is activated during stress. This restores the body to flight and fight and stops the bowel activities. On the one hand stomach aches can be caused by stress, constipation or diarrhea, but also increased acid production.

However, the medically-cited stress ulcer (gastric ulcer triggered by stress) does not refer to everyday stress as the cause, but to previous major surgeries, massive burns, polytrauma, sepsis or shock. There is a reduced gastric blood flow and increased gastric acid production. Both lead to inflammation of the mucous membrane and can trigger a gastric ulcer. Since this complication is known and occur in the context of life-threatening diseases, the stress ulcer can be prevented by medication. For example, proton pump inhibitors or other drug-based acid blockers can be used. These prevent increased acid production and thus the development of a stress ulcer.

Diagnosis of gastric ulcer

The diagnosis of gastric ulcer is made by various diagnostic tools:

  • patient consultation
  • X-Breischluck
  • Gastroscopy (gastroscopy)
  • Urease test
  • 13 C urea breath test

1. Patient talk

First indications of the underlying disease of the gastric ulcer results in the patient interview ( anamnesis ) in which after typical complaints, medication (NSAIDs, aspirin? Etc) is asked. During physical examination, a painful upper abdomen may be noticed. In the laboratory, a low hemoglobin level may indicate anemia ( anemia ) and thus ulcer bleeding.
Invisible "occult" blood can be detected in the stool examination (hemocult test).
False positive results of the hemocult test due to certain medications (eg iron supplements) or foods are possible. However, the final diagnosis gastric ulcer is made only in the gastrointestinal tract.

2. X-ray Breischluck

In this gastric ulcer diagnosis, the stomach area is X-rayed while the patient swallows an X-ray contrast agent. The contrast agent fills the stomach, so that one can then judge the surface condition (the relief) of the gastric mucosa. This study is mainly performed in patients who refuse gastric mirroring or in whom the gastric mirroring can not be performed. The ulcers typically present as niches in the stomach wall relief in which contrast agents are collected.

However, this method of examination is not the drug of choice in gastric ulcer diagnosis, because not all ulcers / gastric ulcer are discovered and also ulcer / gastric ulcer can not be distinguished from gastric cancer (gastric carcinoma).
Particularly valuable is the investigation in suspected gastric outlet obstruction. One typically recognizes a constriction on the X-ray images which impresses like an hourglass silhouette. Therefore, this narrowing is also called "hourglass stomach".

3. gastroscopy (gastroscopy)

The "mirroring" ( endoscopy ) of the stomach and duodenum is the means of choosing a "diagnosis gastric ulcer" for direct assessment and classification of mucous membrane damage and should be performed in suspected stomach or duodenal ulcer. During this examination, images are transferred to a monitor via a tube camera (endoscope).
During endoscopy, tissue samples (biopsy) can also be taken from suspicious mucosal areas. From a ulcer / ulcer at least six tissue samples should be taken to a tumor (carcinoma) of the stomach, which is sometimes not distinguishable during ulceration from a ulcer / gastric ulcer during the reflection.
The tissue assessment under the microscope (histological findings) is far more meaningful than the (macroscopic) findings detected with the naked eye. In addition, one can use a piece of tissue to perform the urease test. The urease test is used to detect the bacterium Helicobacter pylori.

4. urease test

In this gastric ulcer diagnosis, the removed piece of tissue is placed in a special medium for 3 hours. In this medium, only Helicobacter pylori can produce ammonia from the bacterial enzyme urease, and the medium becomes discolored. The evidence of Helicobacter pylori infection in the gastric mucosa is obtained so quickly and cheaply.

5. 13C urea breath test

By this test one can also prove the bacterium Helicobacter pylori. The patient is orally administered a 13 C-labeled urea (radioactively labeled) via a beverage.
The patient must then exhale vigorously through a straw into a special glass tube. By cleaving this urea into CO 2 and ammonia by the bacterium, the proportion of labeled 13 C in the exhaled CO 2 can be measured. This not-so-cheap procedure can be used to test the success of antibiotic therapy against Helicobacter pylori (eradication therapy). The advantage of this examination is that it is non-invasive, meaning that it does not interfere with the patient's body and is therefore almost free of complications.

Further diagnosis of gastric ulcer

In treatment-resistant ulcers (ulcers) should always induce additional diagnostics to safely exclude gastric carcinoma (gastric cancer) or more rare ulcer disease. In case of uncertainties regarding gastric cancer (gastric carcinoma), a second gastroscopy with additional tissue collection and examination may provide additional assurance.

To rule out rare causes of ulcer, gastrin levels in the blood are measured to exclude Zöllinger-Ellisson syndrome or calcium in the blood is examined to detect hyperparatyroidism (parathyroid dysfunction).
Reasons for a treatment resistance may also be rare Helicobacter strains, in which the usual antibiotic therapy does not work or an inflammatory bowel disease, such as Crohn's disease or a herpes simplex virus infection.

Further information is also available under our topic: Crohn's disease

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