Peptic ulcer

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Peptic ulcer
Classification and external resources

Deep gastric ulcer

ICD-10 K25.-K27.
ICD-9 531-534
DiseasesDB 9819
eMedicine med/1776 ped/2341
MeSH D010437

A peptic ulcer, also known as ulcus pepticum, PUD or peptic ulcer disease,[1] is an ulcer
(defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the
gastrointestinal tract that is usually acidic and thus extremely painful. As many as 70-
90% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that
lives in the acidic environment of the stomach, however only 40% of those cases go to a
doctor. Ulcers can also be caused or worsened by drugs such as aspirin and other
NSAIDs.

Contrary to general belief, more peptic ulcers arise in the duodenum (first part of the
small intestine, just after the stomach) rather than in the stomach. About 4% of stomach
ulcers are caused by a malignant tumor, so multiple biopsies are needed to exclude
cancer. Duodenal ulcers are generally benign.

Contents
[hide]

• 1 Classification
• 2 Signs and symptoms
o 2.1 Complications
• 3 Cause
o 3.1 Stress
• 4 Diagnosis
o 4.1 Macroscopic appearance
o 4.2 Microscopic appearance
o 4.3 Differential diagnosis of epigastric pain
• 5 Treatment
• 6 Epidemiology
• 7 History
• 8 Notes
• 9 References

• 10 External links

[edit] Classification
• Stomach (called gastric ulcer)
• Duodenum (called duodenal ulcer)
• Oesophagus (called Oesophageal ulcer)
• Meckel's Diverticulum (called Meckel's Diverticulum ulcer)

Types of peptic ulcers:

• Type I: Ulcer along the lesser curve of stomach

• Type II: Two ulcers present - one gastric, one duodenal
• Type III: Prepyloric ulcer
• Type IV: Proximal gastroesophageal ulcer
 • Type V: Anywhere

[edit] Signs and symptoms

Symptoms of a peptic ulcer can be

• abdominal pain, classically epigastric with severity relating to mealtimes, after

around 3 hours of taking a meal (duodenal ulcers are classically relieved by food,
while gastric ulcers are exacerbated by it);
• bloating and abdominal fullness;
• waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in
esophagus);
• nausea, and copious vomiting;
• loss of appetite and weight loss;
• hematemesis (vomiting of blood); this can occur due to bleeding directly from a
gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
• melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin);
• rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute
peritonitis. This is extremely painful and requires immediate surgery.

A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms
of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic
ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase,
and most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than two weeks of the above symptoms, the odds for peptic
ulceration are high enough to warrant rapid investigation by EGD (see below).

The timing of the symptoms in relation to the meal may differentiate between gastric and
duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric
acid is secreted, or after the meal, as the alkaline duodenal contents reflux into the
stomach. Symptoms of duodenal ulcers would manifest mostly before the meal—when
acid (production stimulated by hunger) is passed into the duodenum. However, this is not
a reliable sign in clinical practice.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the
patient's age. Furthermore, typical ulcers tend to heal and recur and as a result the pain
may occur for few days and weeks and then wane or disappear.[2] Usually, children and
the elderly do not develop any symptoms unless complications have arisen.

Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours
commonly accompanies ulcers. This pain can be misinterpreted as hunger, indigestion or
heartburn. Pain is usually caused by the ulcer but it may be aggravated by the stomach
acid when it comes into contact with the ulcerated area. The pain caused by peptic ulcers
can be felt anywhere from the navel up to the breastbone, it may last from few minutes to
several hours and it may be worse when the stomach is empty. Also, sometimes the pain
may flare at night and it can commonly be temporarily relived by eating foods that buffer
stomach acid or by taking anti-acid medication.[3] However, peptic ulcer disease
symptoms may be different for every sufferer.[4]

[edit] Complications

• Gastrointestinal bleeding is the most common complication. Sudden large

bleeding can be life-threatening.[5] It occurs when the ulcer erodes one of the
blood vessels.
• Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion
of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal
content into the abdominal cavity. Perforation at the anterior surface of the
stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis.
The first sign is often sudden intense abdominal pain. Posterior wall perforation
leads to pancreatitis; pain in this situation often radiates to the back.
• Penetration is when the ulcer continues into adjacent organs such as the liver and
pancreas.[6]
• Scarring and swelling due to ulcers causes narrowing in the duodenum and
gastric outlet obstruction. Patient often presents with severe vomiting.
• Cancer is included in the differential diagnosis (elucidated by biopsy),
Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to
develop stomach cancer from the ulcer.[7]

[edit] Cause
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 decreased (most cases) resulting in hypo- or achlorhydria or increased. Gastrin
stimulates the production of gastric acid by parietal cells and, in H. pylori colonization
responses that increase gastrin, the increase in acid can contribute to the erosion of the
mucosa and therefore ulcer formation.

Another major cause is the use of NSAIDs (see above). 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 withdrawn rofecoxib) preferentially inhibit cox-2, which is
less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric
ulceration. As the prevalence of H. pylori-caused ulceration declines in the Western
world due to increased medical treatment, a greater proportion of ulcers will be due to
increasing NSAID use among individuals with pain syndromes as well as the growth of
aging populations that develop arthritis.
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.[8]

Although some studies have found correlations between smoking and ulcer formation [9],
others have been more specific in exploring the risks involved and have found that
smoking by itself may not be much of a risk factor unless associated with H. pylori
infection [10][11][12] [nb 1]. Some suggested risk factors such as diet, spice, consumption and
blood type, were hypothesized as ulcerogens (helping cause ulcers) until late in the 20th
century, but have been shown to be of relatively minor importance in the development of
peptic ulcers.[13]. Similarly, while studies have found that alcohol consumption increases
risk when associated with H. pylori infection, it does not seem to independently increase
risk, and even when coupled with H. pylori infection, the increase is modest in
comparison to the primary risk factor [10][14][nb 2].

Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause

multiple and difficult to heal ulcers.

[edit] Stress

Researchers also continue to look at stress as a possible cause, or at least complication, in

the development of ulcers. There is debate as to whether psychological stress can
influence the development of peptic ulcers. Burns and head trauma, however, can lead to
physiologic stress ulcers, which are reported in many patients who are on mechanical
ventilation.

An expert panel convened by the Academy of Behavioral Medicine Research concluded

that ulcers are not purely an infectious disease and that psychological factors do play a
significant role.[1] Researchers are examining how stress might promote H. pylori
infection. For example, Helicobacter pylori thrives in an acidic environment, and stress
has been demonstrated to cause the production of excess stomach acid. This was
supported by a study on mice showing that both long-term water-immersion-restraint
stress and H. pylori infection were independently associated with the development of
peptic ulcers.[15]

A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly
associated with an increased risk of peptic ulcer, and a combination of chronic stress and
irregular mealtimes was a significant risk factor.[16]

[edit] Diagnosis
Endoscopic image of gastric ulcer, biopsy proven to be gastric cancer.

The diagnosis is mainly established based on the characteristic symptoms. The stomach
pain is usually the first to signal a peptic ulcer. In some cases, doctors may treat ulcers
without diagnosing them with specific tests and observe if the symptoms resolve,
meaning their primary diagnosis was accurate.

Confirming the diagnosis is made with the help of tests such as endoscopies or barium
contrast x-rays. The tests are typically ordered if the symptoms do not resolve after a few
weeks of treatment, or when they first appear in a person who is over age 45 or who has
other symptoms such as weight loss, because stomach cancer can cause similar
symptoms. Also, when severe ulcers resist treatment, particularly if a person has several
ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition
that causes the stomach to overproduce acid.[2]

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a

gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct
visual identification, the location and severity of an ulcer can be described. Moreover, if
no ulcer is present, EGD can often provide an alternative diagnosis.

One of the reasons why blood tests are not reliable on establishing an accurate peptic
ulcer diagnosis on their own is their inability to differentiate between past exposure to the
bacteria and current infection. Additionally, a false-negative is possible with a blood test
if the patient has recently been taking certain drugs, such as antibiotics or proton pump
inhibitors.[17]

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.[18] 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 carbon dioxide. This test provides the advantage of being able to monitor the
response to treatment used to kill the bacteria.

The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be
kept in mind. This is especially true in ulcers of the greater (large) curvature of the
stomach; most are also a consequence of chronic H. pylori infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract
(which always contains some air) to the peritoneal cavity (which normally never contains
air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as
when having a chest X-ray, the gas will float to a position underneath the diaphragm.
Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral
abdominal X-ray, is an omen of perforated peptic ulcer disease.

[edit] Macroscopic appearance

A benign gastric ulcer (from the antrum) of a gastrectomy specimen.

Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is
a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and
perpendicular borders. These borders are not elevated or irregular in the acute form of
peptic ulcer, regular but with elevated borders and inflammatory surrounding in the
chronic form. In the ulcerative form of gastric cancer the borders are irregular.
Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.

[edit] Microscopic appearance

A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and
muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular
and present chronic gastritis. During the active phase, the base of the ulcer shows 4
zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue.
The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.
[19]

[edit] Differential diagnosis of epigastric pain

• Peptic ulcer
• Gastritis
• Stomach cancer
• Gastroesophageal reflux disease
• Pancreatitis
• Hepatic congestion
• Cholecystitis
• Biliary colic
• Inferior myocardial infarction
• Referred pain (pleurisy, pericarditis)
• Superior mesenteric artery syndrome

[edit] Treatment
Younger patients with ulcer-like symptoms are often treated with antacids or H2
antagonists before EGD is undertaken. Bismuth compounds may actually reduce or even
clear organisms, though the warning labels of some bismuth subsalicylate products
indicate that the product should not be used by someone with an ulcer.[clarification needed]

Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be

prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers,
which may be a side-effect of the NSAIDs.

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.
Perforated peptic ulcer is a surgical emergency and requires surgical repair of the
perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with
cautery, injection, or clipping.

[edit] Epidemiology

Disability-adjusted life year for peptic ulcer disease per 100,000 inhabitants in 2004.[20]
no data less than 20 20-40 40-60 60-80 80-100 100-120 120-140
140-160 160-180 180-200 200-220 more than 220

The lifetime risk for developing a peptic ulcer is approximately 10%.[21]

In Western countries the prevalence of Helicobacter pylori infections roughly matches

age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc). Prevalence is higher in third
world countries. Transmission is by food, contaminated groundwater, and through human
saliva (such as from kissing or sharing food utensils.)[citation needed]

A minority of cases of Helicobacter infection will eventually lead to an ulcer and a larger
proportion of people will get non-specific discomfort, abdominal pain or gastritis.

Peptic ulcer disease had a tremendous effect on morbidity and mortality until the last
decades of the 20th century, when epidemiological trends started to point to an
impressive fall in its incidence.[22] The reason why the rates of peptic ulcer disease
decreased is thought to be the development of new effective medication and acid
suppressants and the discovery of the cause of the condition, H. pylori.

In the United States about 4 million people have active peptic ulcers and about 350,000
new cases are diagnosed each year. Four times as many duodenal ulcers as gastric ulcers
are diagnosed. Approximately 3,000 deaths per year in the United States are due to
duodenal ulcer and 3,000 to gastric ulcer.[23]

[edit] History
See also: Timeline of peptic ulcer disease and Helicobacter pylori

John Lykoudis, a general practitioner in Greece, treated patients for peptic ulcer disease
with antibiotics, beginning in 1958, long before it was commonly recognized that bacteria
were a dominant cause for the disease.[24]
Helicobacter pylori was rediscovered in 1982 by two Australian scientists, Robin Warren
and Barry J. Marshall as a causative factor for ulcers.[25] In their original paper, Warren
and Marshall contended that most stomach ulcers and gastritis were caused by
colonization with this bacterium, not by stress or spicy food as had been assumed before.
[26]

The H. pylori hypothesis was poorly received,[citation needed] so in an act of self-

experimentation Marshall drank a Petri dish containing a culture of organisms extracted
from a patient and soon developed gastritis. His symptoms disappeared after two weeks,
but he took antibiotics to kill the remaining bacteria at the urging of his wife, since
halitosis is one of the symptoms of infection.[27] This experiment was published in 1984 in
the Australian Medical Journal and is among the most cited articles from the journal.

In 1997, the Centers for Disease Control and Prevention, with other government
agencies, academic institutions, and industry, launched a national education campaign to
inform health care providers and consumers about the link between H. pylori and ulcers.
This campaign reinforced the news that ulcers are a curable infection, and that health can
be greatly improved and money saved by disseminating information about H. pylori.[28]

In 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or
Medicine to Dr. Marshall and his long-time collaborator Dr. Warren "for their discovery
of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease".
Professor Marshall continues research related to H. pylori and runs a molecular biology
lab at UWA in Perth, Western Australia.

It was a previously widely accepted misunderstanding that the use of chewing gum
resulted in gastric ulcers. The medical profession believed that this was because the
action of masticating on gum caused the over-stimulation of the production of
hydrochloric acid in the stomach. The low (acidic) pH (pH 2), or hyperchlorhydria was
then believed to cause erosion of the stomach lining in the absence of food, thus causing
the development of the gastric ulcers.[29]

On the other hand, in the recent past, some believed that natural tree resin extract, mastic
gum, actively eliminates the H. pylori bacteria.[30] However, multiple subsequent studies
have found no effect of using mastic gum on reducing H. pylori levels.[31][32]

Signs & Symptoms of Bleeding Stomach

Ulcer
Contributor
By George N Root III, eHow Contributing Writer
Article Rating:

(2 Ratings)

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A bleeding stomach ulcer can give sometimes give the same symptoms as an upset
stomach or the stomach flu. If you find that some of your common stomach symptoms
are mixed in with feelings of abdominal pain, then it is possible that you have a bleeding
stomach ulcer. It is important to get to a doctor before the ulcer gets worse and develops
into a more serious medical condition such as a complete penetration of the stomach
lining.

Burning Sensation
1. One of the more common symptoms of a bleeding stomach ulcer is also one of the
symptoms that gets misdiagnosed a great deal. A bleeding stomach ulcer will
cause you to have an extremely uncomfortable burning feeling in your stomach
that can last as long as three hours. It can feel as though something is gnawing at
your stomach from the inside, and it can become extremely painful. In many
cases, people will misinterpret this as heartburn, or they may even mistake it as a
sign that the patient is hungry. The pain can sometimes be so severe that it will
wake the patient up at night. This is usually a sign that it is something a doctor
needs to look at.

Weight Changes
2. People who disregard the symptoms of a bleeding stomach ulcer as being
heartburn or some other common ailment will sometimes find comfort in treating
the condition by eating each time it occurs. This will result in excessive eating
 because the person can only find relief from filling his stomach with food. As a
result of this practice, the patient gains weight. There is also the opposite effect
when a person is experiencing a bleeding ulcer in that it is too painful for the
person to allow her stomach to digest food. Inexplicable weight changes
accompanied by continued feelings of heartburn are signs of a bleeding ulcer.

Abdominal Pain
3. In the more severe cases of a bleeding stomach ulcer, it is possible that the
perforation in the stomach lining has gone completely through the stomach and is
allowing undigested food and stomach acids to enter into the abdominal cavity.
This is signified by extreme abdominal pain that seems to be made worse by any
kind of movement. Once the ulcer has penetrated the stomach lining, the episodes
of abdominal pain can become frequent and severe.

Bloating
4. In some cases, the bleeding ulcer may occur closer to the base of the stomach near
the duodenum. If this happens, then scar tissue may occur in the connection
between the stomach and the duodenum, and this will block the path that food
uses to leave the stomach. The patient will begin to feel bloated and nauseous,
which could lead to vomiting.

Belching
5. One symptom of a bleeding stomach ulcer that is commonly ignored is continued
belching. When it is the symptom of a bleeding stomach ulcer, the belching can
be accompanied by abdominal pain and acid reflux.

Read more: Signs & Symptoms of Bleeding Stomach Ulcer | eHow.com

http://www.ehow.com/about_5341141_signs-symptoms-bleeding-stomach-
ulcer.html#ixzz0wHAUP8Os

What is Peptic Ulcer?

Peptic Ulcer, as the second part of the name suggests, is a "wound, an open sore," an
excoriated area in the mucosa (inner wall) that penetrates the muscle layer of the stomach
or of the duodenum (the first part of the small intestine attached to the stomach). The
symptom is typically burning, gnawing or hunger pains in the epigastric (stomach pit)
area, often relieved by food or antacids.

How large are these ulcers?

These ulcers in the stomach (gastric ulcer) or in the duodenum (duodenal ulcer) could
range from a few millimeters to several centimeters. When the ulcer erodes deeper into
the wall of the stomach or duodenum, it could cut into the blood vessels and cause
bleeding, which could be fatal.

What causes peptic ulcer disease?

There was a time when stomach acid hypersecretion (due to stress, spicy food, alcohol,
tobacco, etc.) was universally accepted in the medical community as the cause of peptic
ulcer disease. A brilliant physician, Marshall, who was ridiculed by his colleagues in the
scientific world for postulating that peptic ulcer disease was caused by a bacterial
infection (Helicobacter pylori organism), ingested the organism himself and produced
acute peptic ulcer disease, proving to the medical community that his postulate was
correct. Multicenter studies following his treatise proved that he was right. Marshall has
radically revolutionized the understanding of the disease, its diagnosis, and most
importantly, its treatment.

How did this change the treatment?

Before Marshall's discovery, gastrectomy (cutting part or whole of the stomach out) was
very common as a treatment for peptic ulcer disease. Today, with appropriate triple
antibiotic therapy, peptic ulcer disease is effectively managed, transforming a former
surgical disease to a medical disease. Occasionally, however, surgery may still be needed
for severe bleeding peptic ulcer disease but this is not as common today, with proper
antibiotic treatment.

How does the H. pylori bacteria cause ulcers?

There are theories as to how this organism causes peptic ulcers. H. pylori produces
urease, an enzyme that catalyzes urea to ammonia. The ammonia, which enables the
bacteria to survive the acidic environment in the stomach or duodenum, also causes
erosions into the mucosal lining and causes epithelial damage. Cytotoxins from the
bacteria also damages the epithelium. The organism also produces mucolytic enzymes
(protease and lipase) that lead to the degradation of the mucosa, making the epithelium
more vulnerable to acid damages. Also, cytokines produced in response to the
inflammation may damage the mucosa and lead to ulcer formation.

Do aspirin and arthritis medications cause peptic ulcers?

Yes, aspirin and NSAIDs (non-steroidal arthritis medications) are known to cause peptic
ulcers and severe bleeding. The irritation is both local (on the mucosa of the stomach)
and systemic (inhibiting prostaglandin production adversely affecting mucosal defenses,
and thinning the blood), leading to ulcerations and hemorrhage.

Is alcohol bad for those with peptic ulcer?

Yes, most definitely. The same thing is true with cigarette smoking, chocolate, tea,
coffee, spicy foods, which are also irritants for the stomach. They increase hydrochloric
acid production in the stomach, which bathes and damages the stomach mucosal lining,
making it more susceptible to the H. pylori bacteria. Milk, which used to be prescribed
decades ago as a part of peptic ulcer therapy is now avoided since it also causes
"rebound" acid production and retards ulcer healing.

Do children develop peptic ulcers?

Yes, but it is relatively uncommon among children compared to among adults. About
15% to 20% of abdominal pains in children is due to peptic ulcer. Most primary peptic
ulcer disease in children are seen in the ages between 8 and 17. The pains usually wakes
the child from sleep, and are sometimes aggravated by eating. About 25% of these
pediatric patients have bleeding ulcers. Peptic Ulcer due to H. pylori infection is not very
common in children. Any persistent abdominal pains in children warrants prompt medical
consultation.

How is the diagnosis made?

After a good history-taking and physical examination, the physician can already make a
strong presumptive diagnosis of peptic ulcer disease. Fiberoptic gastroscopy (a lighted
magnifying flexible scope passed through the mouth down to the stomach used to view
its inside) is today a part of the state-of-the-art investigative tool in the diagnosis of
peptic ulcer disease or malignant tumor (cancer) of the stomach. Bacterial cultures may
likewise be taken to check the presence of Helicobacter pylori organism. Through the
scope, cytology (microscopic examination for cancer cells), cultures for bacteria and tiny
biopsies may be done to make a diagnosis.

What are the possible complications of peptic ulcer disease?

Hemorrhage is the most common complication, leading to vomiting of blood or blood in

the stools, coloring them black, anemia, weakness or even dizziness and syncope (passing
out spells). Perforation of the wall when the ulcer "eats" the entire thickness of the
stomach wall, creating a hole, allowing stomach contents to spill into the abdominal
cavity causing peritonitis (severe inflammation and infection). Inflammation from peptic
ulcer involving the stomach outlet into the duodenum can cause spasm and scar that
blocks this outlet, causing vomiting. Stomach cancer has been reported 3 to 6 times more
common in peptic ulcer due to H. pylori infection. Gastric lymphomas have also been
linked to this bacteria.

Are TUMS and ROLAIDS safe for ulcer pains?

Tums, Rolaids and other over-the-counter self-proclaimed "treatment" for peptic ulcers or
hyperacidity are quite popular among lay people. These will not cure hyperacidity or
peptic ulcers. If the symptoms persist, it is most prudent to seek medical consultation.
Remember, peptic ulcers can have life-threatening complications if not properly treated,
and cancer of the stomach must be ruled out as the cause of the symptoms.

What is the treatment?

For Peptic Ulcer due to H. pylori infection, the combination of bismuth, metronidazole
and tetracycline cures about 80% of this infection, leading to ulcer healing. Proton pump
inhibitors capsules, H2 Blocker pills, and antacids are other adjunctive modalities of the
comprehensive regimen many physicians use in conjunction with the triple antibiotic
therapy above.

How about surgery?

Surgery used to be very common for peptic ulcer disease. With the discovery of H. pylori
infection as the major cause of peptic ulcer disease, surgery has declined precipitously.
Today, surgery is relegated to the complications, like uncontrollable bleeding,
perforation, gastric outlet obstruction, suspected cancerous peptic ulcer, and symptoms
refractory to medical treatment. With this new triple antibiotic therapy, even the
complications of peptic ulcer disease have been reduced significantly.

http://www.cebudoctorsuniversity.edu/hospital/cardio/chua129.html

pathophysiology

Gastric mucosal damage occurs in critically ill patients in intensive care units and
develops in the setting of severe physiologic stress. Within 24 hrs of admission to the
intensive care unit, 75% to 100% of critically ill patients demonstrate evidence of stress-
related mucosal disease. Stress ulcers present a risk of clinically important bleeding,
which is associated with alterations in physiology, such as hypotension or tachycardia, or
results in anemia or the need for transfusion. Clinically important bleeding occurs in
approximately 1% to 4% of critically ill patients. The pathophysiology of stress-related
mucosal disease is complex. Major factors responsible for stress ulcer are decreased
blood flow, mucosal ischemia, and hypoperfusion and reperfusion injury. Acid-
suppressive regimens that elevate the intragastric pH and maintain the pH over time have
the potential to prevent stress-related mucosal disease. Intragastric pH studies have
demonstrated that, whereas a pH of >4 may be adequate to prevent stress ulceration, a pH
of >6 may be necessary to maintain clotting in patients at risk of rebleeding from peptic
ulcer. Studies comparing the ability of intravenous administrations of histamine-2-
receptor antagonists and proton pump inhibitors to raise and maintain intragastric pH
suggest that, although both can raise the pH to >4, proton pump inhibitors are much more
likely to maintain this pH. Unlike histamine-2-receptor antagonists, proton pump
inhibitors can elevate and maintain the intragastric pH at >6. This is relevant for patients
in the intensive care unit at risk for rebleeding from peptic ulcers after hemostasis.

INTODUCTION
BACKGROUND AND AIMS: The declining global prevalence of peptic ulcer disease
(PUD) might be because of the decreasing prevalence of Helicobacter pylori (Hp)
infection. The aims of the present study were to determine the prevalence of PUD during
a 7-year period and to investigate its relationship with the prevalence of Hp infection
during the same period. METHODS: All upper gastrointestinal endoscopies carried out at
Santo Tomas Hospital in Manila from January 1996 to December 2002 were evaluated.
Endoscopies reporting gastric ulcers (GU) and duodenal ulcers (DU) with Hp status were
analyzed. RESULTS: A total of 15 341 endoscopies were evaluated. Overall, 2600
(16.95%) GU and 1575 (10.27%) DU were identified. There was a decreasing trend in
the prevalence of GU (P < 0.0001) and DU (P < 0.0001) during the study period. Overall
PUD prevalence declined from 35.87% in 1996 to 18.80% in 2002. This decline was seen
for both GU and DU (20.05 vs 14.34%, and 15.83 vs 7.02%, respectively). The
prevalence of Hp infection decreased significantly from 1996 to 2002 for both GU and
DU (68.13 vs 33.48%, P < 0.0001; and 76.67 vs 36.50%, P < 0.0001, respectively). The
decrease in Hp prevalence was significantly related to the decrease in ulcer prevalence (r
= 0.97, P = 0.0004 for GU; r = 0.89, P = 0.0079 for DU; and r = 0.92, P = 0.0035 for all
PUD). The prevalence of bleeding secondary to PUD remained stable during the 7-year
period (P = 0.87). CONCLUSIONS: During the 7-year period, there was a significant
decline in the prevalence of PUD. This decline in PUD prevalence was associated with a
corresponding decrease in Hp prevalence.

Patients with upper

gastrointestinal (GI) complaints visit their general practitioner (GP) more often than
patients with other conditions. Scientists writing in the open access journal BMC Family
Practice observed that people with dyspepsia, heartburn, epigastric discomfort and other
upper-abdominal complaints had almost twice as a number of GP contacts, which were
ultimately linked to problems in all organ systems. These patients were twice as
frequently referred to specialist care and received twice as a number of prescriptions.
Henk van Weert led a team of scientists from the University of Amsterdam who set out to
investigate the correlation between psychological conditions and upper-GI symptoms. He
said, "Traditionally, psychological factors were held responsible for upper-GI symptoms.
With the identification of Helicobacter pylori the etiological paradigm changed
dramatically, but eradication treatment has proved to be of only limited value in
functional dyspepsia. We aimed to investigate whether psychological and social problems
are more frequent in patients with upper GI symptoms".

The scientists observed that the prevalence of upper-GI symptoms was actually linked to
a broader pattern of illness-related health care use GI patients' increased health care
demands were not restricted to psychosocial problems, but comprised all organ systems.
As per van Weert, "Patients with upper-GI symptoms visited their GP twice as often and
received up to double the number of prescriptions as control patients. We demonstrated
that not psychological and social co-morbidity, but high contact frequency in general is
most strongly linked to upper-GI symptoms".

Speculating as to the reason for the increased care-seeking among people with upper-GI
symptoms, van Weert said, "Patients who consult their GP frequently because of their
coping style and attentiveness to physical symptoms may just have a high chance to be
diagnosed in any health domain, including the psychosocial. In other words, upper GI
symptoms and psychosocial complaints may both be manifestations of increased health
care demands and not etiologically related".

An ulcer is damage to the inner lining (the mucosa) of the stomach or the upper part of
the intestine (duodenum). A bacterium, Helicobacter pylori, is the main cause of ulcers in
this area.

A peptic ulcer, also known as ulcus pepticum, PUD or peptic ulcer disease, is an ulcer
(defined as mucosal erosions equal to or greater than 0.5 cm) of an area of
the gastrointestinal tract that is usually acidic and thus extremely painful. As many as
80% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that
lives in the acidic environment of the stomach, however only 40% of those cases go to a
doctor. Ulcers can also be caused or worsened by drugs such as aspirin and
other NSAIDs (Nonsteroidal anti-inflammatory drugs)

Contrary to general belief, more peptic ulcers arise in the duodenum (first part of
the small intestine, just after the stomach) than in the stomach itself. About 4% of
stomach ulcers are caused by a malignant tumor, so multiple biopsies are needed to
exclude cancer.

Why do people get ulcers?

Helicobacter

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 gastrinproduction by that part of the stomach, and gastrin
secretion can either be decreased (most cases) resulting in hypo- or achlorhydria or
increased. Gastrin stimulates the production ofgastric acid by parietal cells and, in H.
pylori colonization responses that increase gastrin, the increase in acid can contribute to
the erosion of the mucosa and therefore ulcer formation.

NSAIDs

Another major cause is the use of NSAIDs . 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 ascelecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is
less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric
ulceration. As the prevalence of H. pylori-caused ulceration declines in the Western
world due to increased medical treatment, a greater proportion of ulcers will be due to
increasing NSAID use among individuals with pain syndromes as well as the growth of
aging populations that develop arthritis.

Severe disease

Ulcers can also occur in people weakened by severe disease (such as chronic respiratory
disease or major trauma). This is thought to result from poor oxygenation to the lining of
the stomach.

Occasionally (in Europeans), a stomach ulcer is caused by cancer and rarely, some other
specific illness is found to be responsible. Such conditions include: excessive production
of hydrochloric acid in the stomach (Zollinger-Ellison syndrome) & Crohn's disease (an
inflammatory condition affecting any part of the gut).
Smoking

Tobacco smoking leads to atherosclerosis and vascular spasms, causing vascular

insufficiency and promoting the development of ulcers through ischemia. Nicotine
contained in cigarettescan increase parasympathetic nerve activity to the gastrointestinal
tract by acting on the nicotinic receptors at synapses - increased stimulation to
the enterochromaffin-like cells and G cells increases the amount of histamine and gastrin
secreted and therefore increases the acidity of the gastric juice.

Glucocorticoids

Similarly, glucocorticoids lead to atrophy of all epithelial tissues. However, these factors,
along with diet or spices, blood type, and other factors suspected to cause ulcers until late
in the 20th century, are actually of relatively minor importance in the development of
peptic ulcers.[5]

Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause

multiple and difficult to heal ulcers.

Stress

Researchers also continue to look at stress as a possible cause, or at least complication, in

the development of ulcers. There is debate as to whether psychological stress can
influence the development of peptic ulcers. Burns and head trauma, however, can lead to
physiologic stress ulcers, which are reported in many patients who are on mechanical
ventilation.

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-
phenomena independent of the progress in treatment of the disease. The cohort-
phenomena is probably explained by improved standards of living which has lowered the
incidence of H. pylori infections.

An expert panel convened by the Academy of Behavioral Medicine Research concluded

that ulcers are not purely an infectious disease and that psychological factors do play a
significant role. Researchers are examining how stress might promote H. pylori infection.
For example, Helicobacter pylori thrives in an acidic environment, and stress has been
demonstrated to cause the production of excess stomach acid. This was supported by a
study on mice showing that both long-term water-immersion-restraint stress and H.
pylori infection were independently associated with the development of peptic ulcers.

A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly
associated with an increased risk of peptic ulcer, and a combination of chronic stress and
irregular mealtimes was a significant risk factor.
Signs & Symptoms

Symptoms of a peptic ulcer can be

• abdominal pain, classically epigastric with severity relating to mealtimes, after

around 3 hours of taking a meal (duodenal ulcers are classically relieved by food,
while gastric ulcers are exacerbated by it);
• bloating and abdominal fullness;
• waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in
esophagus);
• nausea, and copious vomiting;
• loss of appetite and weight loss;
• hematemesis (vomiting of blood); this can occur due to bleeding directly from a
gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
• melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin);
• rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely
painful and requires immediate surgery.

A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms
of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic
ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase,
and most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than two weeks of the above symptoms, the odds for peptic
ulceration are high enough to warrant rapid investigation by EGD (see below).

The timing of the symptoms in relation to the meal may differentiate

between gastric and duodenal ulcers: A gastric ulcer would give epigastric
pain during the meal, as gastric acid is secreted, or after the meal, as the alkaline
duodenal contents reflux into the stomach. Symptoms of duodenal ulcers would manifest
mostly before the meal-when acid (production stimulated by hunger) is passed into
the duodenum. However, this is not a reliable sign in clinical practice.

Complications
Gastrointestinal bleeding is the most common complication. Sudden large bleeding can
be life-threatening. It occurs when the ulcer erodes one of the blood vessels.
Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the
gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into
the abdominal cavity. Perforation at the anterior surface of the stomach leads to
acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often
sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in
this situation often radiates to the back.

Penetration is when the ulcer continues into adjacent organs such as the liver
and pancreas.

Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet
obstruction. Patient often presents with severe vomiting.

What does an ulcer feel like?

This varies greatly from person to person. Many people never realise that they have an
ulcer. Others feel pain or a burning sensation in their upper abdomen. The symptoms are
often described as indigestion, heartburn, hunger pangs or dyspepsia. Some sufferers find
that eating actually helps settle their discomfort for a while, others find it makes them
worse. Citrus drinks, spicy and smoked foods can make the pain worse.

Finally, it is important to stress that most people with a stomach ache do not have ulcers.
An ulcer is potentially dangerous - the warning signs are:

• difficulty swallowing or regurgitation

• persistent nausea and vomiting
• vomiting blood or vomit with the appearance of coffee grounds
• black or tar-like stools
• unintended weight loss
• anaemia (paleness and fatigue)
• sudden, severe and incapacitating abdominal pains.

How does the doctor make a diagnosis?

The diagnosis can only be definitely confirmed or excluded by a gastroscopy. A
gastroscopy (or upper GI endoscopy) involves the visualisation of the lining of your
gullet (oesophagus), stomach and duodenum with a small fibre-optic camera that can be
swallowed.

The gastroscopy is more helpful in diagnosis if it is performed before you take anyacid-
reducing medication.

An X-ray examination (involving a Barium meal) can also be used, but it is not quite as
reliable or helpful a diagnostic tool as a gastroscopy. It does not offer any opportunity to
take tissue samples (biopsies) for microscopic diagnosis of tissue abnormalities and
infection.

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as

a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct
visual identification, the location and severity of an ulcer can be described. Moreover, if
no ulcer is present, EGD can often provide an alternative diagnosis.

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 possibility of other causes of ulcers, notably malignancy (gastric cancer)
needs to be kept in mind. This is especially true in ulcers of thegreater (large)
curvature of the stomach; most are also a consequence of chronic H. pylori
infection.
• If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal
tract (which always contains some air) to the peritoneal cavity (which normally
never contains air). This leads to "free gas" within the peritoneal cavity. If the
patient stands erect, as when having a chest X-ray, the gas will float to a position
underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an
erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated
peptic ulcer disease.

Macroscopic appearance
Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is
a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and
perpendicular borders.

These borders are not elevated or irregular in the acute form of peptic ulcer, regular but
with elevated borders and inflammatory surrounding in the chronic form. In the
ulcerative form of gastric cancer the borders are irregular. Surrounding mucosa may
present radial folds, as a consequence of the parietal scarring.

A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and
muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular
and present chronic gastritis. During the active phase, the base of the ulcer shows 4
zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue.
The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.

Differential diagnosis of epigastric pain

• Peptic ulcer
• Gastritis
• Stomach cancer
• Gastroesophageal reflux disease
• Pancreatitis
• Hepatic congestion
• Cholecystitis
• Biliary colic
• Inferior myocardial infarction
• Referred pain (pleurisy, pericarditis)
• Superior mesenteric artery syndrome

What is Helicobacter pylori?

Helicobacter pylori is a minute bacteria living inside and under the lining of the stomach.
The groups most often affected are: elderly people & people in developing countries.

Those who carry this bacteria today have most probably been infected during childhood.
The risk of acquiring infection for an adult is modest - less than 1 per cent every year.
Helicobacter pylori in itself does not usually cause any ulcer symptoms. Nevertheless,
this bacteria is the most common cause of ulcers in the stomach and the duodenum.

The bacteria may also have a role in the development of cancer of the stomach.
Helicobacter pylori infection can be eliminated by taking antibiotics. There is about an 80
per cent chance of successful treatment of the infection and a cure for the ulcer. If the
bacteria is not eliminated, most people get a recurrence of their ulcer after a short period
of time.

Who should be screened and treated for Helicobacter

pylori?
These questions continue to be debated.

• All patients with a proven ulcer of the stomach or duodenum should be tested, and
treated if the bacteria is found.
• People under the age of 45 with ulcer-like symptoms can avoid gastroscopy by
choosing the breath test. If it is positive for Helicobacter pylori infection the
patient should be treated with antibiotics.
• People with diagnosed lymphatic cancer of the stomach (very rare) should be
examined and, if the bacteria are present, treated.
• People with diagnosed early stages of cancer of the stomach should be examined
and treated if the bacteria are present.
• Almost everyone with a past history of proven ulcers in the duodenum has
Helicobacter pylori and, therefore, it has been proposed that these people could be
treated without testing.
• Anyone with ulcer-like symptoms, but a normal gastroscopy, will not benefit
from testing or treatment.
Which types of medicine can cause ulcers and ulcer
complications?

Aspirin (eg Disprin) and non-steroidal anti-inflammatory drugs (NSAIDs such as

diclofenac or naproxen) can cause ulcers, but only a small proportion of the people taking
these drugs develop an ulcer. However, because they are so widely used, hundreds of
people in the UK die each year as a result of ulcer complications associated with these
drugs.

Some people have a very high sensitivity to aspirin and NSAIDs and such people should
not take this sort of medication.

If you have previously had a bleeding ulcer, you must not take medicine that includes
aspirin (acetylsalicylic acid) or NSAIDs.

Who is at risk from treatment with aspirin

(acetylsalicylic acid) and NSAIDs?
• People older than 60 - the risk increases with age.
• If you have had a previous ulcer, the risk is high.
• If you are taking anticoagulants (blood-thinning treatment) at the same time,
bleeding is more likely and more serious when it occurs.
• Oral corticosteriods (such as prednisolone (eg Precortisyl)) increase the chances
of gastric irritation and ulcers.
• The larger the dose of aspirin or NSAIDs the greater the risk.
• The longer duration of the treatment, the greater the risk.

Can I reduce the risk from aspirin or NSAIDs?

 • If you are predisposed to this problem, the risk is not diminished by taking the
medication:
• on a full stomach
• as a dissolved or glazed tablet ('enteric coated')
• through other routes, such as suppositories or injections.
• However, acid-reducing medication (H2 inhibitors, such as ranitidine (eg Zantac)
ornizatidine (Axid)) does diminish the ulcer risk associated with aspirin and
NSAIDs.
• Treatment with another medicine called misoprostol (eg Cytotec) offers
protection for the mucosa and is also potentially beneficial. Misoprostol can cause
diarrhoea but this tendency varies from person to person.

Can you avoid treatment with NSAIDs?

Pain can often be alleviated by medication that does not predispose to peptic
ulceration. Paracetamol (eg Panadol) may be worth trying in this respect, as it is not
associated with peptic ulceration.

Headaches, migraine and chronic abdominal pain are conditions for which NSAIDs can
easily be substituted by other painkillers.

In the case of gout, acute attacks can be treated with other drugs such as colchicineinstead
of NSAIDs.

For arthritis, traditional NSAIDs can be replaced with a new sub-group of NSAIDS
called cox-2 selective inhibitors, eg celecoxib (Celebrex) or etoricoxib (Arcoxia). These
have a lower risk of serious gastrointestinal side effects and can be used for people at
high risk, eg people over 65 years of age or those taking other medicines that increase the
risk of ulcers. However, as these medicines can still cause ulcers, they should not be used
in people with an active ulcer, and only after careful consideration in people with a
history of ulcers.

Can you avoid treatment with aspirin?

In many cases, aspirin can be substituted with other medication, such as paracetamol,
which will not predispose to peptic ulcers and yet offer the same therapeutic effect. In the
case of aspirin, paracetamol is equally effective with no ulcer risk. When low dose aspirin
(eg Caprin 75mg) is prescribed for the reduction of cardiovascular risk (complications
arising from 'hardening of the arteries' -atherosclerosis), a balance needs to be struck
between the risk of heart/arterial disease and the risk of peptic ulceration.

If you have a history of peptic ulcers, your cardiovascular risk can be reduced with
alternatives to aspirin, such as dipyridamole (Persantin) or Clopidogrel (Plavix).
The relative risk of each of these conditions and their management varies from person to
person, so it is always worth talking it over with your doctor.

Treatment

The treatment is targeted at eradicating the bacterial infection; the ulcer then heals and
relapses are prevented. Generally, three different medicines are taken two to three times
daily for a short course - usually seven days.

Younger patients with ulcer-like symptoms are often treated with antacids or H2
antagonists before EGD is undertaken. Bismuth compounds may actually reduce or even
clear organisms, though it should be noted that the warning labels of some bismuth
subsalicylate products indicate that the product should not be used by someone with an
ulcer.

Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be

prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers,
which may be aside-effect of the NSAIDs.

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.

Perforated peptic ulcer is a surgical emergency and requires surgical repair of the
perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with
cautery, injection, orclipping.

The lifetime risk for developing a peptic ulcer is approximately 10%.

In Western countries the prevalence of Helicobacter pylori infections roughly matches

age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc). Prevalence is higher in third
world countries. Transmission is by food, contaminated groundwater, and through human
saliva (such as from kissing or sharing food utensils.)

A minority of cases of Helicobacter infection will eventually lead to an ulcer and a larger
proportion of people will get non-specific discomfort, abdominal pain or gastritis.

They are a combination of:

one proton pump inhibitor (omeprazole (eg Losec), lansoprazole (Zoton),pantoprazole

(Protium), rabeprazole (Pariet) or esomeprazole (Nexium)).

two antibiotics (amoxicillin (eg Amoxil), clarithromycin (Klaricid) ormetronidazole (eg

Flagyl)).

Possible combinations could be:

omeprazole + amoxicillin + clarithromycin.

omeprazole + metronidazole + clarithromycin (if penicillin allergic).

HeliClear (lansoprazole, amoxicillin, clarithromycin) - a one-pack treatment now

available on prescription that contains all the necessary treatments in a one-week course.

A less common type of treatment is three to four different types of medicine four times
daily for a total of 14 days (proton pump inhibitor + bismuth subcitrate + amoxicillin +
metronidazole). This treatment form is only used under special circumstances.

The treatment types listed above are both effective and not too difficult to take.

Can Helicobacter pylori be resistant to the treatment?

Yes, but it is uncommon, and a check-up after treatment to see if the bacteria have been
eliminated is generally not recommended because:

you cannot feel if the bacteria has been eliminated, and the physician cannot find out by
taking a blood test because Helicobacter antibiotics persist even after the infection is
cured.

to check effectively would involve another gastroscopy for more samples from the
stomach's lining, or a 'breath-test'.

Will the ulcer heal after one week of treatment?

In many cases, one week of treatment is sufficient. It is enough time to remove all the
ulcer bacteria.

In some cases, the wound is not fully healed and it is necessary to continue for a few
weeks with further acid-inhibiting treatment.

Does the ulcer treatment have to be monitored?

If the ulcer is located in the stomach, there is a slight possibility that it is stomach cancer.

It is therefore necessary to perform another gastroscopy after four to six weeks of

treatment. It is then possible to confirm that the ulcer is healing and, at the same time,
take repeat biopsies from the area affected.

If the ulcer is located in the duodenum (the outlet from the stomach), then it is not
necessary to monitor the healing of the ulcer because ulcers in this area are virtually
never cancerous. Only if the symptoms reappear should an examination be considered.

How are ulcers treated when aspirin or NSAIDs have

caused them?
First of all, it is necessary to stop taking these medicines.

Under special circumstances, the physician may find it necessary for the patient to
continue with NSAIDs (see next section).

If Helicobacter pylori are present in the stomach, the bacteria are treated as described
earlier.

If there are no signs of Helicobacter pylori, the ulcer is treated with a histamine H2
antagonist or a proton pump inhibitor.
Stomach ulcers are examined again with gastroscopy after six weeks.

Is it necessary to discontinue the medication that has caused an ulcer?

If there are complications (bleeding ulcers or perforated ulcers), then treatment with this
medication should be stopped and never resumed.

There are often good alternatives to NSAIDs or aspirin.

Substantial medical reasons should be present to justify resuming such medication. Under
these circumstances, the ulcer should be treated as mentioned earlier. The medication that
triggered the ulcer should be changed as follows:

NSAID: a low-risk preparation at lowest possible dose should be used.Selective cox-2

inhibitors are a recently introduced type of NSAID that have a lower likelihood of
causing ulcers.

aspirin: the lowest possible dose should be used (75mg daily).

This medication can be combined with a proton pump inhibitor. Alternatively, it is

possible to combine the NSAID with misoprostol (Cytotec), which counters the harmful
effect that NSAIDs and aspirin have on the stomach's lining (mucosa). There may be a
positive effect when combining a proton pump inhibitor and misoprostol with NSAIDs,
but this has not yet been established.

How are bleeding ulcers treated?

A bleeding ulcer is a serious condition and requires emergency attention in hospital; a
blood transfusion is often required. Treatment with NSAIDs and aspirin should be
discontinued immediately. A gastroscopy is performed urgently to:

• find the cause of bleeding, and make the diagnosis.

• estimate the risk of new bleeds.
• inject a substance into the mucosa adjacent to the ulcer to minimise the chance of
a significant recurrence of bleeding.
• stop fresh arterial bleeding if possible.

In such circumstances, the patient remains hospitalised for some days after an episode of
bleeding. In rare cases, when heavy bleeding occurs that cannot be stopped at
gastroscopy, emergency surgery is then required.

During surgery, any small bleeding vessel is tied up and the ulcer is 'oversewn'. This
procedure is very effective in treating serious loss of blood that cannot be staunched with
less invasive techniques.
How is a perforated ulcer treated?
A perforated ulcer is a serious condition that requires emergency attention. To make a
diagnosis, an X-ray of the stomach area is required (seeking air under the diaphragm). A
perforated ulcer requires emergency surgery.

How is scarring of the duodenum treated?

A chronic ulcer can cause scarring of the stomach outlet (the pylorus and the duodenum),
causing restricted emptying of the stomach. The symptoms may include vomiting and
weight loss. This condition is often treated surgically by creating a shortcut around the
scarred or narrowed duodenum to facilitate gastric emptying ('gastro-enteric-
anastomosis').

When is a chronic ulcer treated surgically?

Treating a chronic ulcer with surgery is rarely seen today. An exception is surgery for
bleeding or perforated ulcers and in cases where the stomach outlet or the duodenum has
become deformed and restricted by scar tissue.

It was quite common some years ago to treat chronic ulcers surgically (because effective
acid-suppressing medicine did not exist, and Helicobacter pylori had not yet been
discovered). The surgical procedure depended on the ulcer's position.

Generally, three different types of surgery were used.

• The nerves to the stomach were cut (vagotomy).

• A part of the stomach was removed (partial gastrectomy).
• Combinations with adjustment to the duodenum's attachment to the stomach.

Side effects were frequent and included stomach upsets, reflux and abdominal pain,
fatigue, diarrhoea, and weight loss. The operations used at the time must be seen from the
perspective that no other treatment options were available.

In rare cases, it is possible today to require one of these surgical procedures - but only
when medication has failed.