1.0.

CASE STUDY
1.1 BIO DATA
Name: ST

Age: 45years

Sex: male

Address: 16 gambul street Makeni

Marital status: married

Occupation: farming

Next of kin: Son

Date of admission

1.2. PRESENTING COMPLAINT:

Abdominal pain for 2/52

1.3. HISTORY OF PRESENTING COMPLAINT:

A 45 years old with no background history of any underline chronic medical condition present
with the above symptom.

Abdominal pain at the epigastric region, that was gradual in onset and intermittent, burning in
nature, radiate to the back, associated with bleaching, vomiting and low grade fever, not
associated with vomiting of blood, loose stool neither weight loss. Tabs diclofenac, ibuprofen,
dragon extra and hunger aggravate the pain; sometimes relieved immediately after taking food
and syrup antacid, the severity is 6/10.

1.4. PAST MEDICAL HISTORY:

He has not been admitted, nor transfuse neither undergoes surgery, no history of any chronic
illness such as: hypertension, diabetic mellitus, sickle cell, asthma neither any
immunosuppression like HIV.

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 1.5. DRUG AND ALLERGIC HISTORY: Long time use of non-steroidal anti-
inflammatory drug (NSAID) no known allergy

1.6. FAMILY HISTORY: history of hypertension, no history of diabetic mellitus, sickle cell,
Epilepsy neither Asthma

1.7. SOCIAL HISTORY: He is a famer, married; smoked five stick of cigarette per day no
history of any alcohol neither intake nor chew cola nut, stays in an extended family including
the father, mother, brothers, sisters, the four children and the wife, no travel history.

1.8. SYSTEMIC REVIEW

General: No weight loss, not fatigue, no dizziness, and no body weakness

Gastrointestinal system: nausea, no hematemesis, no dysphagia, no constipation, no

Melina neither hematochezia

Respiratory System: chest pain, no cough, no difficulty in breathing

Cardiovascular system: no orthopnea, no proximal nocturnal dyspnea and no claudication

1.9. SUMMARY
A 45 years old man with a family history of hypertension has no underline medical condition,
present with abdominal pain for 2 weeks and it was associated with vomiting, nausea,
headache and low grade fever no hematemesis, no loose stool neither constipated. The pain
usually radiate to the back and aggravated by NSAID and hunger and sometimes relieved after
taken meal and syrup anti acid the severity is 6/10

1.10. PHYSICAL EXAMINATION

O/E: Acutely ill looking man, not warm to touch, in mild respiratory distress, not pale acyanose,
anicteric, no clubbing, hydrated, no lymphadenopathy and nil edema

AVPU=A GCS=15/15

Vitals: Temperature : 37.6oC ( mild febrile) blood pressure : 122/80mmHg ( Normotension)

respiratory rate: 24C/min (mild tachypnic) pulse: 98b/min ( normal) SPO 2: 98% on room air (
good saturation)

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Respiratory system: symmetrical chest wall, no scar, diaphragm moves with respiration, RR:
24C/min, normal tracheal centrality, normal chest wall expansion and relaxation and normal
tartar fremitus both the anterior and posterior lungs, resonant on percussion and adequate air
entering on both lung fills with vascular breath sounds

Cardiovascular system: Normal precordium, no scar apex beat at the fifth left intercostal
mid clavicle line, pulse is palpable, full volume, regular and rate is 98b/min, no heave and thrill,
S1 &S2 heard no added sound

Abdominal examination: Full, neither moves with respiration, no scar, soft and tender at
the epigastric region, no organomegaly or palpable mass nor ballotable kidney, tympanic and
normal bowel sounds

1.11. IMPRESSION:
Peptic ulcer

Gastritis

Stomach cancer

Gastro esophageal reflux disease

Acute pancreatitis

Cholecystitis

1.12. MANAGEMENT PLAN: admitted to the male medical ward

To do Abdominal ultra sound scan, Hemoglobin, malaria microscopy, wedal, and H. pylori, RVS,
upper GI endoscopy, barium test, urea breath test

- IV Omeprazole 20mg bd for 5/7

- IV Ceftriaxone 2g bd for 5/7
- IV Metronidazole 500mg bd
- Syrup Gastron 10mls Bd
- Tab Paracetamol 1g PRN
- Discourage cigarette smoking, and spicy food

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Day 2 ward rounds

A 45 years old man was admitted and been managed for PUD and GERD

C/O. NIL

O/E: Acutely ill looking man, not warm to touch, not in any respiratory distress, not pale
acyanose, anicteric, no clubbing, hydrated, no lymphadenopathy and nil edema

AVPU=A GCS=15/15

Vitals: Temperature : 36.0oC ( Normal) blood pressure : 120/80mmHg ( Normotension),

respiratory rate: 16C/min (normal) pulse: 88b/min ( normal) SPO2: 98% on room air ( good
saturation)

Abdomen: full, soft mild tender at the epigastric, nil palpable organ.

Chest: clear

Laboratory results

Hemoglobin: 11.2g/dl (normal)

H. pylori: Reactive

Malaria thick film microscopy: not seen

Abdominal USS= normal findings

Wedal = ( O – reactive & H- none reactive) ( Acute infection)

1.13. WORKING DIAGNOSES:

PEPTIC ULCER DISEASE

PLAN:
Cont. with the current treatment.

Day 3 ward rounds

A 45 years old man was admitted and been managed for PUD

C/O = Nil
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O/E: Acutely ill looking man, not warm to touch, not in any respiratory distress, not pale
acyanose, anicteric, not club, hydrated, no lymphadenopathy and nil edema

AVPU=A GCS=15/15

Vitals: Temperature : 36.5oC ( Normal) blood pressure : 120/80mmHg ( Normo tension),

respiratory rate: 16C/min (normal) pulse: 86b/min ( normal) SPO2: 98% on room air ( good
saturation)

Abdomen: full, soft, not tender at the epigastric, nil palpable organ.

Chest: clear

IMPRESSION: IMPROVING ( responding to treatment)

Plan:

Cont. with current treatment

Possible discharge tomorrow

Encourage to continue stop smoking cigarette

Day 4 Ward Round

A 45 years old man was admitted and been mange for PUD

C/O: no complaint.

O/E: Acutely ill looking man, not warm to touch, not in any respiratory distress, not pale
acyanose, anicteric, not club, hydrated, no lymphadenopathy and nil edema

AVPU=A GCS=15/15

Vitals: Temperature : 36.6oC ( Normal) blood pressure : 120/80mmHg ( Normotension),

respiratory rate: 16C/min (normal) pulse: 88b/min ( normal) SPO2: 98% on room air ( good
saturation)

Abdomen: full, not tender at the epigastric, nil palpable organ.

Chest: clear

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Impression: improvement
Plan:

Discharge Home
Cap omeprazole 20mg bd for 2/52

Tab metronidazole 500mg bd 2/52

Tab cefixime 500mg bd for 2/52

Syrup Gastron 10mls bd for 2/52

To avoid late time eating, continue to avoid smoking and to avoid medication that has high
caffeine spicy food and regular meals

Follow up after 2 weeks .

1.14. FOLLOWED UP VISIT

A 45 years old man that was admitted and discharge 2 weeks back on account of peptic ulcer disease
come for a follow up visit.

C/O: no complain

Assessment: the 45 years old is doing well and ok

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2.0. LITERATURE REVIEW

2.1. INTRODUCTION
Peptic ulcer disease, resulting from inflammation caused by an imbalance between
cytoprotective and cytotoxic factors in the stomach and duodenum, manifests with varying
degrees of gastritis or frank ulceration. The pathogenesis of peptic ulcer disease is
multifactorial, but the final common pathway for the development of ulcers is the action of acid
and pepsin-laden contents of the stomach on the gastric and duodenal mucosa and the inability
of mucosal defense mechanisms to allay those effects. Abnormalities in the gastric and
duodenal mucosa can be visualized on endoscopy, with or without histologic changes. Deep
mucosal lesions that disrupt the muscularis mucosa of the gastric or duodenal wall define
peptic ulcers. Gastric ulcers are generally located on the lesser curvature of the stomach, and
90% of duodenal ulcers are found in the duodenal bulb. While there are no large population-
based pediatric studies, rates of peptic ulcer disease in childhood appear to be low.
Ulcers can be classified as primary peptic ulcers, which are chronic and more often duodenal,
or secondary, which are usually more acute in onset and are more often gastric. Primary ulcers
are most often associated with Helicobacter pylori infection. Secondary peptic ulcers can result
from stress caused by sepsis, shock, or an intracranial lesion (Cushing ulcer), or in response to a
severe burn injury (Curling ulcer). Secondary ulcers are often the result of using aspirin or
nosteroidal antiinflammatory drugs (NSAIDs); hypersecretory states like Zollinger-Ellison
syndrome, short bowel syndrome, and systemic mastocytosis are rare causes of peptic
ulceration.
2.2. DEFINITION:
Peptic ulcer are the areas of the degeneration and necrosis of gastrointestinal mucosa to acid
peptic secretion.

Histologically is define as a breach in the mucosa of the alimentary tract that extends through
the muscularis mucosa into the sub mucosa or deep.

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2.3. TYPES:
1. Gastric ulcer
2. Duodenal ulcer

GASTRIC ULCER: it is the second most common, are found mainly along the lesser
curvature in the region of the pyloric antrum, more commonly in the posterior than the
anterior wall, they are more common to patient beyond the 6th decade of life

DUODENAL ULCER: (most common) are found in the first part of the duodenum, usually
immediate post pyloric, more common on the anterior than the posterior wall. Occur more
at 25 to 50 years of age.

It is more associated with H. pylori compared to gastric ulcer

2.4. CLASSIFICATION
By location :
1. Anterior wall of the Duodenum
2. Esophagus (called esophageal ulcer)
3. Stomach (called gastric ulcer)
4. Meckel's diverticulum (called Meckel's diverticulum ulcer; is very tender with palpation)
Modified Johnson :
Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura
angular is along the locus minor is resistantiae. Not associated with acid hypersecretion.
Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid over
secretion.
Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid over secretion.
Type IV: Proximal gastroesophageal ulcer.
Type V: Can occur throughout the stomach. Associated with the chronic use of NSAIDs (such as
ibuprofen).
Macroscopic appearance:

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

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

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Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is a
round to oval parietal defect ("hole"), 2–4 cm diameter, with a smooth base and perpendicular
borders. These borders are not elevated or irregular in the acute form of peptic ulcer, and
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.

Microscopic appearance

Micrograph sowing erosive gastric ulcer.

(H&E stain)

A gastric peptic ulcer is a mucosal perforation that penetrates the muscularis mucosae and
lamina propria, usually 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:
fibroid necrosis, inflammatory exudate, granulation tissue and fibrous tissue. The fibrous base
of the ulcer may contain vessels with thickened wall or with thrombosis.

2.5. Epidemiology
Peptic ulcer disease (PUD) is a global problem with a lifetime risk of development ranging from
5% to 10%. Overall, there is a decrease in the incidence of PUD worldwide due to improved
hygienic and sanitary conditions combined with effective treatment and judicious use of
NSAIDs. Duodenal ulcers are four times more common than gastric ulcers. Also, duodenal ulcers
are more common in men than in the women

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 2.6. Risk factors
1. Psychological stress
2. Physiological stress – they include
 Shock
 Severe trauma
 Septicemia
 Extensive burn ( Culling’s ulcers in the posterior aspect of the first part of the
duodenum)
 Intracranial lesion (Cushing ulcer which develop from hyperacidity following
excessive vagal stimulation)
 Drug intake (eg. Aspirin, steroids, buthazolidine, indomethacin)
 Local irritant ( eg. Alcohol, smoking, coffee etc)

2.7. Etiology
Peptic ulcer result from imbalance between mucosal defense mechanism and damaging factors
that cause chronic gastritis

Damaging factors Protective factors

1. H. pylori ( most common) 1. Mucus and bicarbonate
2. Gastric acid 2. Mucosal blood flow
3. Pepsin 3. Prostaglandin production
4. Smoking, Alcohol 4. Epithelial regeneration capacity
5. Drugs like NSAIDs
6. Ischemia and shock
7. Delayed gastric emptying
8. Duodenal gastric reflux or gastric
hyperacidity

2.8. PATHOGENESIS
Acid Secretion
By 3-4 yr of age, gastric acid secretion approximates adult values. Acid initially secreted by the
oxyntic cells of the stomach has a pH of approximately 0.8, whereas the pH of the stomach

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contents is 1-2. Excessive acid secretion is associated with a large parietal cell mass,
hypersecretion by antral G cells, and increased vagal tone, resulting in increased or sustained
acid secretion in response to meals and increased secretion during the night. The secretagogues
that promote gastric acid production include acetylcholine released by the vagus nerve,
histamine secreted by enterochromaffin cells, and gastrin released by the G cells of the antrum.
Mediators that decrease gastric acid secretion and enhance protective mucin production
include prostaglandins.

Mucosal Defense
A continuous layer of mucous gel that serves as a diffusion barrier to hydrogen ions and other
chemicals covers the gastrointestinal (GI) mucosa. Mucus production and secretion are
stimulated by prostaglandin E2 . Underlying the mucous coat, the epithelium forms a second-
line barrier, the characteristics of which are determined by the biology of the epithelial cells
and their tight junctions. Another important function of epithelial cells is to secrete chemokines
when threatened by microbial attack. Secretion of bicarbonate into the mucous coat, which is
regulated by prostaglandins, is important for neutralization of hydrogen ions. If mucosal injury
occurs, active proliferation and migration of mucosal cells occurs rapidly, driven by epithelial
growth factor, transforming growth factor-α, insulin-like growth factor, gastrin, and bombesin,
and covers the area of epithelial damage

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 2.9. Clinical manifestation
FEATURES DUODENAL ULCER GASTRIC ULCER
Age 25 yrs – 50yrs >50yrs
Periodicity Attack are classically worsened Attacks last for 2-6 weeks, with
by ‘’ work, worry and weather) intervals of freedom foe 1-6
month
Pain Pain is severe, occur late at night Epigastric pain occurs
(hunger pain) and usually immediately or within 2 hours
recover by food intake after food and never occur at
night
Vomiting Rare have vomiting but get heart The pain is sometime relive
burn ( retrosternal pain) after vomiting and is a
conspicuous feature
Hematemesis and melaena They occur in a ration 40:60 They occur in a ratio 60:40
Appetite They have good appetite Though have good appetite but
are afraid to eat because it can
aggravate the pain
Weight loss They tend to gain weight do to Weight loss is a common
the frequent ingestion of milk to finding in patient with gastric
relived the pain ulcer
Deep tenderness More ate the right At the epigastric region
hypochondriac region

2.10. DIAGNOSIS
Radiologic and/or endoscopic procedures are usually required to document the presence of
ulcers. Because endoscopic testing is invasive and expensive, it is only indicated in patients 60
years of age or older with new-onset dyspepsia. Patients with dyspepsia who are younger than
60 years may forego endoscopy but should be tested for H. pylori using noninvasive testing and
treated if positive. Those who test negative for H. pylori should be offered a trial (4–8 weeks) of
acid suppression therapy or proceed to endoscopy. Persistent dyspepsia despite a trial of acid
suppressive therapy warrants upper endoscopy evaluation.
Routine laboratory tests are not helpful in establishing a diagnosis of PUD. Hematocrit,
hemoglobin, and stool guaiac tests are used to detect bleeding.
Diagnostic tests to detect H. pylori presence can be either endoscopic or nonendoscopic.

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Endoscopic diagnosis involves extraction of gastric tissue samples that are subsequently
tested for H. pylori.
Nonendoscopic testing methods for H. pylori include the urea breath test, serologic testing,
and stool antigen assay. These tests are less invasive and less expensive than endoscopy.
The urea breath test is usually first line because of its high sensitivity and specificity and
short turnaround time. Concomitant acid suppressive or antibiotic therapy may give false-
negative results. The urea breath test can also be used to confirm eradication of H. pylori
infection.
Serologic testing provides a quick (within 15 minutes) office-based assessment of
exposure to H. pylori, but it cannot differentiate active infection from previously treated
infection; patients can remain seropositive for years after eradication. Serologic testing is
recommended in patients with recent or current antibiotic or acid-suppressive therapy.
Stool antigen assays can be useful for initial diagnosis or to confirm H. pylori eradication.
They have high sensitivity and specificity and are affected less by concomitant medication use.

2.11. Differential diagnosis

 Conditions that may appear similar include:
 Gastritis
 Stomach cancer
 Gastroesophageal reflux disease
 Pancreatitis
 Hepatic congestion
 Cholecystitis
 Biliary colic
 Inferior myocardial infarction
 Referred pain (pleurisy, pericarditis)
 Superior mesenteric artery syndrome

2.12. Management
The management of peptic ulcer disease is been divided in pharmacological and none
pharmacological therapy.

NONPHARMACOLOGIC TREATMENT
Any Patients with PUD should eliminate or reduce psychological stress, cigarette smoking, and
use of NSAIDs.
Although there is no need for a special diet, patients should avoid foods and beverages that
cause dyspepsia or exacerbate ulcer symptoms (eg, spicy foods, caffeine, and alcohol).

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Emergency surgery may be required for bleeding, perforation, or obstruction.

PHARMACOLOGIC TREATMENT
INITIAL MANAGEMENT
Treat the underlying etiology.
Eradication of Helicobacter pylori (H. pylori) — Patients with peptic ulcers should be tested for
infection with H. pylori and treated accordingly. Eradication of H. pylori in patients with peptic
ulcer disease is associated with higher healing rates in patients with duodenal and gastric
ulcers. In addition, eradication of H. pylori infection is associated with lower ulcer recurrence
rates in patients with gastric and duodenal ulcers who are not placed on maintenance anti-
secretory therapy.
Discontinue nonsteroidal anti-inflammatory drugs (NSAIDs) — Patients with peptic
ulcers should be advised to avoid NSAIDs. NSAIDs, including aspirin, increase the risk of peptic
ulcer disease and are associated with an increased risk of complications from a peptic ulcer.

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 Rare or unclear cause — Rare causes of ulcer disease (eg, infections, Crohn disease, and
ischemia) should be addressed and treated. In patients with peptic ulcer disease of unclear
etiology, additional evaluation is needed to exclude other rare causes of peptic ulcer.
Initial anti-secretory therapy
Choice of therapy — All patients with peptic ulcers should receive anti-secretory therapy with a
proton pump inhibitor (PPI) (eg, omeprazole 20 to 40 mg daily or equivalent) to facilitate ulcer
healing. PPI use results in faster control of peptic ulcer disease symptoms and higher ulcer
healing rates as compared with H2RA as a consequence of stronger acid suppression. PPIs also
heal NSAID-related ulcers more effectively as compared with H2RAs.

Duration
The duration of initial anti-secretory therapy varies based on the ulcer characteristics, the
underlying etiology (H. pylori, NSAID use) and the presence of ulcer complications (eg,
bleeding, perforation, penetration, or gastric outlet obstruction).

a) Treatment of H. Pylori-Associated Ulcers

All patients with evidence of active infection with H. pylori should be offered treatment.
Goal of H. pylori therapy: complete eradication.
Anti-secretory therapy in H. pylori-positive ulcer
● Uncomplicated ulcer – In patients with uncomplicated ulcers, PPI (eg, omeprazole 20 mg
twice daily) given for 14 days, along with the antibiotic regimen to treat H. pylori, is usually
adequate to induce healing.

● Complicated ulcer – All patients with complicated peptic ulcers (ulcers with bleeding,
perforation, penetration, or gastric outlet obstruction) should initially receive acid suppressive
therapy with an intravenous PPI. Once patients are tolerating oral medications, they should be
switched to an oral PPI at high-dose twice daily to enhance healing (eg, omeprazole 40 mg
twice daily). Dosing should generally be reduced to once daily after four weeks. However, in
patients with bleeding, the intravenous PPI can be switched to a lower oral dose (eg, 20 mg
omeprazole once daily) 72 hours after endoscopy, provided there is no evidence of recurrent
bleeding.

The duration of treatment depends on the location and cause of the ulcer, but is typically
between 4 and 12 weeks in total.
In patients with complicated duodenal ulcers, we suggest anti-secretory treatment for four to
eight weeks.

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In patients with complicated gastric ulcers, we suggest anti-secretory therapy for a total
duration of 8 to 12 weeks.
The choice of initial antibiotic regimen to treat H. pylori should be guided by the presence of
risk factors for macrolide resistance and the presence of a penicillin allergy.

b) NSAID-related peptic ulcers

● Any Patients with PUD should eliminate or reduce use of NSAIDs (including aspirin). If
possible, alternative agents such as acetaminophen or a nonacetylated salicylate (eg, salsalate)
should be used for pain relief.
● Patients with NSAID-associated ulcers should be treated with a PPI (eg, omeprazole 20 to 40
mg daily) for four to eight to weeks based on the size of the ulcer. In patients with peptic ulcers
who need to remain on NSAIDs or aspirin, maintenance antisecretory therapy with a PPI (eg,
omeprazole 20 mg daily) can reduce the risk of ulcer complications or recurrence

Other therapy
1. Misoprostol: Synthetic PG E1 analog that exogenously replaces PG stores.
Limited use, because of high frequency of bothersome GI effects such as abdominal pain,
flatulence, and diarrhea.
Not Use in pregnancy; Abortifacient effects.
2. H2-Receptor Antagonists: Standard doses of H2RAs (e.g., famotidine 40 mg/day) are
effective in preventing NSAID-related duodenal ulceration but not gastric ulceration (the most
frequent type of ulcer-associated with NSAIDs).
3. Proton Pump Inhibitors: is more effective than H2RAs in reducing the risk of nonselective
NSAID-related gastric and duodenal ulceration. PPIs are also as effective as misoprostol but
better tolerated. All PPIs are effective when used in standard doses
4. COX-2 Selective Inhibitors: Selective COX-2 inhibitors are no more effective than the
combination of a PPI and a nonselective NSAID in reducing the incidence of ulcers and are
associated with a greater incidence of CV events (e.g., ischemic stroke).
Celecoxib is the only agent in this class that remains on the market; its postulated improved GI
safety when compared to nonselective NSAIDs.
Longer-term studies evaluating the CV risks associated with the use of COX-2 inhibitors have
found a higher incidence of CV mortality with these agents compared to traditional NSAIDs
5. Sucralfate: Is a negative charged, nonabsorbable agent that forms a complex by binding with
positively-charged proteins in exudates, forming a viscous, paste-like, adhesive substance.
Limited use, need for multiple daily dosing, large tablet size, and interaction with a number of
other medications (e.g., digoxin and fluoroquinolones).

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Side effects: constipation, nausea, metallic taste, and the possibility for aluminum toxicity in
patients with renal failure.

2.13. Complications
Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-
threatening. It is associated with 5% to 10% death rate.

Perforation (a hole in the wall of the gastrointestinal tract) following a gastric ulcer often leads
to catastrophic consequences if left untreated. Erosion of the gastrointestinal wall by the ulcer
leads to spillage of the stomach or intestinal contents into the abdominal cavity, leading to an
acute chemical peritonitis. The first sign is often sudden intense abdominal pain, as seen in
Valentino's syndrome. Posterior gastric wall perforation may lead to bleeding due to the
involvement of gastroduodenal artery that lies posterior to the first part of the duodenum. The
death rate in this case is 20%.

Penetration is a form of perforation in which the hole leads to and the ulcer continues into
adjacent organs such as the liver and pancreas.

Gastric outlet obstruction is a narrowing of the pyloric canal by scarring and swelling of the
gastric antrum and duodenum due to peptic ulcers. The person 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.

2.14. Prevention
Prevention of peptic ulcer disease for those who are taking NSAIDs (with low cardiovascular
risk) can be achieved by adding a proton pump inhibitor (PPI), an H2 antagonist, or misoprostol.
NSAIDs of the COX-2 inhibitors type may reduce the rate of ulcers when compared to non-
selective NSAIDs. PPI is the most popular agent in peptic ulcer prevention. However, there is no
evidence that H2 antagonists can prevent stomach bleeding for those taking NSAIDs. Although
misoprostol is effective in preventing peptic ulcer, its properties of promoting abortion and
causing gastrointestinal distress limit its use. For those with high cardiovascular risk, naproxen
with PPI can be a useful choice. Otherwise, low-dose aspirin, celecoxib, and PPI can also be
used.

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2.15. Zollinger-Ellison Syndrome
Zollinger-Ellison syndrome is a rare syndrome characterized by refractory, severe peptic ulcer
disease caused by gastric hypersecretion due to the autonomous secretion of gastrin by a
neuroendocrine tumor, a gastrinoma. Clinical presentations are similar to those of peptic ulcer
disease with the addition of diarrhea. The diagnosis is suspected by the presence of recurrent,
multiple, or atypically located ulcers. More than 98% of patients have elevated fasting gastrin
levels. Zollinger-Ellison syndrome is common in patients with multiple endocrine neoplasia 1
and rare with neurofibromatosis and tuberous sclerosis. Prompt and effective management of
increased gastric acid secretion is essential in the management. PPIs are the drug of choice due
to their long duration of action and potency. H2 -receptor antagonists are also effective, but
higher doses are required than those used in peptic ulcer disease.

3.0. References:
 Harrison’s principle of internal medicine 20th edition
 Home health handbook for patients and caregivers
 World Health Organization (WHO) 2009

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