Peptic ulcer disease case

CASE

 

A 37-year-old executive returns to your office for follow-up of recurrent

upper abdominal pain. He initially presented 6 weeks ago, complaining

of an increase in frequency and severity of burning epigastric pain,

which he has experienced occasionally for more than 2 years. Now the

pain occurs three or four times per week, usually when he has an empty

stomach, and it often awakens him at night. The pain usually is relieved

within minutes by food or over-the-counter antacids but then recurs

within 2 to 3 hours. He admitted that stress at work had recently

increased and that because of long working hours, he was drinking more

caffeine and eating a lot of take-out foods. His medical history and

review of systems were otherwise unremarkable, and, other than the

antacids, he takes no medications. His physical examination was normal,

including stool guaiac that was negative for occult blood. You

advised a change in diet and started him on an H 2 blocker. His symptoms

resolved completely with the diet changes and daily use of the

medication. Results of laboratory tests performed at his first visit show

no anemia, but his serum Helicobacter pylori antibody test was positive.

 

   # What is your diagnosis?

     

    #What is your next step?

Summary: A 37-year-old man presents with complaints of chronic and recurrent

upper abdominal pain with characteristics suggestive of duodenal ulcer: the

pain is burning, occurs when the stomach is empty, and is relieved within minutes

by food or antacids. He does not have evidence of gastrointestinal bleeding or

anemia. He does not take nonsteroidal anti-inflammatory drugs, which might

cause ulcer formation, but he does have serologic evidence of H pylori infection.

     Most likely diagnosis: Peptic ulcer disease (PUD)

    

     Next step: Antibiotic therapy for H pylori infection

CLINICAL APPROACH

Upper abdominal pain is one of the most common complaints encountered in

primary care practice. Many patients have benign functional disorders (ie, no

specific pathology can be identified after diagnostic testing), but others have

potentially more serious conditions such as PUD or gastric cancer. Historical

clues, knowledge of the epidemiology of diseases, and some simple laboratory

assessments can help to separate benign from serious causes of pain. However,

endoscopy is often necessary to confirm the diagnosis.

Dyspepsia refers to upper abdominal pain or discomfort that can be caused

by PUD, but it also can be produced by a number of other gastrointestinal disorders.

Gastroesophageal reflux typically produces “heartburn,” or burning

epigastric or mid chest pain, usually occurring after meals and worsening with

recumbency. Biliary colic caused by gallstones typically has acute onset of

severe pain located in the right upper quadrant or epigastrium, usually is precipitated

by meals, especially fatty foods, lasts 30 to 60 minutes with spontaneous

resolution, and is more common in women. Irritable bowel syndrome

is a diagnosis of exclusion but is suggested by chronic dysmotility symptoms,

(bloating, cramping) often relieved with defecation, without weight loss or

bleeding. If these causes are excluded by history or other investigations, it is

still difficult to clinically distinguish by symptoms the patients with PUD and

those without ulcers, termed nonulcer dyspepsia.

The classic symptoms of duodenal ulcers are caused by the presence of acid

without food or other buffers. Symptoms are typically produced after the

stomach is emptied but food-stimulated acid production still persists, typically

2 to 5 hours after a meal. They may awaken patients at night, when circadian

rhythms increase acid production. The pain is typically relieved within minutes

by neutralization of acid by food or antacids (eg, calcium carbonate,

aluminum-magnesium hydroxide). Gastric ulcers, by contrast, are more variable

in their presentation. Food may actually worsen symptoms in patients

with gastric ulcer, or pain might not be relieved by antacids. In fact, many

patients with PUD have no symptoms at all. Gastric cancers may present

with dysphagia if they are located in the cardiac region of the stomach, with

persistent vomiting if they block the pyloric channel, or with early satiety by

their mass effect or infiltration of the stomach wall. They may present with

pain symptoms as a result of ulcer formation.

Because the incidence of gastric cancer increases with age, patients older

than 45 years who present with new-onset dyspepsia should generally undergo

endoscopy. In addition, patients with alarm symptoms (eg, weight loss, recurrent

vomiting, dysphagia, evidence of bleeding, or anemia) should be referred

for prompt endoscopy. Finally, endoscopy should be recommended for patients

whose symptoms have failed to respond to empiric therapy. When endoscopy

is undertaken, besides visualization of the ulcer, biopsy samples can be taken

to exclude the possibility of malignancy as the cause of a gastric ulcer, and

biopsy specimens can be obtained for urease testing or microscopic examination

to prove current H pylori infection.

In younger patients with no alarm features, an acceptable strategy is to

perform a noninvasive H pylori antibody test to determine if the patient is

infected. Helicobacter pylori is more common in older patients, in lower socioeconomic

groups, in institutionalized patients, and in developing countries.

It has been established as the causative agent in the majority of duodenal and

gastric ulcers, and it is associated with the development of gastric carcinoma

and gastric mucosa–associated lymphoid tissue (MALT) lymphoma. The two

most common tests are the urea breath test, which provides evidence of current

active infection, and H pylori antibody tests, which provide evidence of

prior infection but will remain positive for life, even after successful treatment.

Because chronic infection with H pylori is found in 90% to 95% of duodenal

ulcers and in 80% of patients with gastric ulcers not related to NSAID

use, a suggested strategy is to test for infection and, if present, to treat it with

an antibiotic regimen such as clarithromycin and amoxicillin, as well as acid

suppression with a proton pump inhibitor. The reason for treating infection

with antibiotics is that eradication of the infection will largely prevent recurrence.

Whether treatment of H pylori infection reduces or eliminates dyspeptic

symptoms in the absence of ulcers (nonulcer dyspepsia) is uncertain.

Similarly, whether treatment of asymptomatic patients found to be H pylori

positive is beneficial is unclear. In H. pylori– positive patients with dyspepsia,

antibiotic treatment may be considered, but a follow-up visit is recommended

within 4 to 8 weeks. If symptoms persist or alarm features develop, then

prompt upper endoscopy is indicated.

In addition to H. pylori, the other major cause of duodenal and gastric

ulcers is the use of NSAIDs. They promote ulcer formation by inhibiting gastroduodenal

prostaglandin synthesis, resulting in reduced secretion of mucus

and bicarbonate and decreased mucosal blood flow. In other words, they

impair local defenses against acid damage. The risk of ulcer formation caused

by NSAID use is dose dependent and can occur within days after treatment is

initiated. If ulceration occurs, the NSAID should be discontinued if possible,

and acid-suppression therapy with an H 2-receptor antagonist or proton pump

inhibitor should be initiated.

A rare cause of ulcer is the Zollinger-Ellison syndrome, a condition in

which a gastrin-producing tumor (usually pancreatic) causes acid hypersecretion,

peptic ulceration, and often diarrhea. This condition should be suspected

if ulcer disease occurs and the patient is H pylori negative and does not

use NSAIDs. To diagnose this condition, one should measure serum gastrin

levels, which are markedly elevated (>1000 pg/mL), and then try to localize

the tumor with an imaging study.

Hemorrhage is the most common severe complication of PUD and can present

with hematemesis or melena. Free perforation into the abdominal cavity

may occur in association with hemorrhage, with sudden onset of pain and development

of peritonitis. If the perforation occurs adjacent to the pancreas, it may

induce pancreatitis. Some patients with chronic ulcers later develop gastric outlet

obstruction, with persistent vomiting and weight loss but no abdominal distention.

Perforation and obstruction are indications for surgical intervention.

DEFINITIONS

DYSPEPSIA: Pain or discomfort centered in the upper abdomen (mainly in or

around the midline), which can be associated with fullness, early satiety, bloating,

or nausea. Dyspepsia can be intermittent or continuous, and it may or may not

be related to meals.

FUNCTIONAL (NONULCER) DYSPEPSIA: Symptoms as described for dyspepsia,

persisting for at least 12 weeks but without evidence of ulcer on endoscopy.

HELICOBACTER PYLORI: A gram-negative microaerophilic bacillus that

resides within the mucus layer of the gastric mucosa and causes persistent gastric

infection and chronic inflammation. It produces a urease enzyme that splits

urea, raising local pH and allowing it to survive in the acidic environment.

PEPTIC ULCER DISEASE (PUD): Presence of gastric or duodenal ulcers as

demonstrated by endoscopy or by upper gastrointestinal barium study.