Duodenal Ulcer

Definition of Duodenal Ulcer

A duodenal ulcer is a type of peptic ulcer that occurs in the duodenum. Four times as many peptic ulcers arise in the duodenum—the first part of the small intestine, just after the stomach—as in the stomach itself. Peptic ulcers are eroded areas in the lining of stomach and duodenum, which result in abdominal pain, possible bleeding, and other gastrointestinal symptoms. The most common cause of duodenal ulcer is a stomach infection associated with the Helicobacter pylori (H pylori) bacteria.

Cause of Duodenal Ulcer

The stomach normally produces acid to help with the digestion of food and to kill bacteria. This acid is corrosive so some cells on the inside lining of the stomach and duodenum produce a natural mucous barrier which protects the lining of the stomach and duodenum. There is normally a balance between the amount of acid. An ulcer may develop if there is an alteration in this balance, allowing the acid to damage the lining of the stomach or duodenum. Causes of this include the following:

Infection with Helicobacter pylori

A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion can either be increased, or as in most cases, decreased, resulting in hypo- or achlorhydria. Gastrin stimulates the production of gastric acid by parietal cells. In H. pylori colonization responses to increased gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation. Studies in the varying occurrence of ulcers in third world countries despite high H. pylori colonization rates suggest dietary factors play a role in the pathogenesis of the disease

Anti-inflammatory medicines – including aspirin

Another major cause is the use of NSAIDs. Anti-inflammatory medicines are sometimes called non-steroidal anti inflammatory drugs (NSAIDs). There are various types and brands. For example: aspirin, ibuprofen, diclofenac, etc. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawnrofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.

The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs. The drop in incidence is considered to be a cohort-phenomenon independent of the progress in treatment of the disease. The cohort-phenomenon is probably explained by improved standards of living which has lowered the incidence of H. pylori infections.

Other causes and factors

Other causes are rare. For example, the Zollinger-Ellison syndrome. In this rare condition, much more acid than usual is made by the stomach. Other factors such as smoking, stress, and drinking heavily may possibly increase the risk of having a duodenal ulcer. However, these are not usually the underlying cause of duodenal ulcers.

Signs and Symptoms of Duodenal Ulcer

Duodenal ulcer causes inflammation and damage to the stomach lining that may result in a number of symptoms. The symptoms can vary in intensity among individuals.

Common symptoms of a duodenal ulcer

Duodenal ulcer symptoms may be experienced daily or just once in a while. At times any of these abdominal symptoms can be severe:

Abdominal pain classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal;
Belching
Burning stomach or upper abdominal pain that may be severe
Loss of appetite
Nausea with or without vomiting
Unexplained weight loss
Bloating and abdominal fullness
rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This is extremely painful and requires immediate surgery.

Serious symptoms that might indicate a life-threatening condition

In some cases, duodenal ulcers can be life threatening. Seek immediate medical care if you, or someone you are with, have any of these life-threatening symptoms including:

Bloody stool (blood may be red, black, or tarry in texture)
Severe abdominal pain
Vomiting blood

Risk Factors for Duodenal Ulcer

Risk factors for duodenal ulcer include:

Alcohol abuse
H pylori infection
History of radiation therapy
Regularly taking nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Advil, Motrin), naproxen (Aleve), or aspirin
Stress or severe illness
Tobacco use

Not all people with risk factors will get duodenal ulcer.

Diagnosis of Duodenal Ulcer

Endoscopy is the test that can confirm a duodenal ulcer. In this test a doctor or nurse looks inside the patient’s stomach and duodenum by passing a thin, flexible telescope down your oesophagus. They can see any inflammation or ulcers.

A test to detect the H. pylori bacterium is usually done if the patient has a duodenal ulcer. If H. pylori is found then it is likely to be the cause of the ulcer. Briefly, it can be detected in a sample of faeces (bowel motions), or in a breath test, or from a blood test, or from a biopsy sample taken during an endoscopy.

The diagnosis of Helicobacter pylori can be made by:

Urea breath test (noninvasive and does not require EGD);
Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform H. pylori cultures;
Direct detection of urease activity in a biopsy specimen by rapid urease test;
Measurement of antibody levels in blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;
Stool antigen test;
Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon atom to detect H. pylori. To perform this exam the patient will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. After an hour, the patient will be asked to blow into a bag that is sealed. If the patient is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.

Prevention from Duodenal Ulcer

Protectection from infections, such as H. pylori, is important. It’s not clear just how H. pylori spreads, but there’s some evidence that it could be transmitted from person to person or through food and water. frequently wash your hands with soap and water and eat foods that have been cooked completely.

Treatment of Duodenal Ulcer

Acid suppressing medication

A 4-8 week course of a medicine that greatly reduces the amount of acid that your stomach makes is usually advised. The most commonly used medicine is a proton pump inhibitor (PPI). These are a class (group) of medicines that work on the cells that line the stomach, reducing the production of acid. They include: esomeprazole, lansoprazole, omeprazole, pantoprazole and rabeprazole, and come in various brand names. Sometimes another class of medicines called H2 blockers is used. They are also called histamine H2-receptor antagonists but are commonly called H2 blockers. H2 blockers work in a different way on the cells that line the stomach, reducing the production of acid. They include: cimetidine, famotidine, nizatidine and ranitidine, and come in various brand names. As the amount of acid is greatly reduced, the ulcer usually heals.

If the ulcer was caused by H. pylori

When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Clarithromycin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI), sometimes together with a bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used together with a PPI and sometimes with bismuth compound. An effective first-line therapy for uncomplicated cases would be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.

Treatment of H. pylori usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI’s in the 1990s, surgical procedures (like “highly selective vagotomy“) for uncomplicated peptic ulcers became obsolete.

If the ulcer was caused by an anti-inflammatory medicine

If possible, patient should stop the anti-inflammatory medicine. Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers, which are a side-effect of the NSAIDs.

However, in many cases the anti-inflammatory medicine is needed to ease symptoms of arthritis or other painful conditions, or aspirin is needed to protect against blood clots. In these situations, one option is to take an acid-suppressing medicine each day indefinitely. This reduces the amount of acid made by the stomach, and greatly reduces the chance of an ulcer forming again.

Surgery

A duodenal ulcer was treated by surgery before it was discovered that H. pylori was the cause of most duodenal ulcers, and before modern acid-suppressing medicines became available. Surgery is now usually only needed if a complication of a duodenal ulcer develops such as severe bleeding or a perforation.