1. Peptic Ulcer Disease
A Literature Review of Peptic Ulcer Disease
Hillary A. Sullivan
Ohio University
NUTR 4100: Medical Nutrition Therapy II
Professor Yoder
November 26, 2013

2. Peptic Ulcer Disease
Peptic Ulcer Disease (PUD) is a disorder of the upper gastrointestinal tract.
Ulcers occur when the mucosal lining of the GI tract breaks down, resulting in acute or
chronic inflammatory response.1 Ulcers can develop in the esophagus, stomach,
duodenum, or other regions of the GI tract.2 Based on hospitalization rates, the most
common form of PUD is gastric, or stomach ulcers.3 The rate of PUD hospitalizations
was found to be highest in adults > 65 years of age, Caucasians, and males.3 The
prevalence decreased with age.3 PUD was once thought to be a result of emotional stress
and diet.4 In 2005, Australian researchers Dr. Barry Marshall and Dr. Robin Warren
were awarded the Nobel Prize for their 1982 discovery of the Helicobacter pylori
bacteria (H. pylori) and its role in peptic ulcer disease.5 This revolutionary finding has
allowed researchers to determine H. pylori as being the primary culprit of PUD, along
with the use of non-steroidal anti-inflammatory drugs. Considering there are half a
million new cases reported each year in the United States, physicians have developed
many different was to assess, diagnose, and treat common symptoms of PUD.2 With
relatively recent discoveries regarding H. pylori, much is to be discovered about the
disease and its etiology.
The upper GI tract is dependent upon the equilibrium between hostile factors that
damage the mucous lining, like stomach acid, and protective factors, such as
prostaglandins and mucus.2 When the hostile factors outnumber the natural defenses of
the mucosa, ulcers form.2 Pepsin is an enzyme secreted by the mucosa in order to break
down protein and hydrochloric acid is produced by parietal cells and released in the
digestive process to help break down food.6 The corrosive actions of both pepsin and
hydrochloric acid are significant contributors to ulcer formation.6 Along with these

3. Peptic Ulcer Disease
causes there are 2 other major risk factors for Peptic ulcers. These factors are H. pylori
and the use of non-steroidal anti-inflammatory drugs (NSAIDs).
H. pylori is a gram-negative bacteria attached to gastric epithelial cells living
within the gastric mucous layer.7 Transmission of the organism is most likely from
person to person, either through oral or fecal contamination.7 Although the mechanism
by which H. pylori leads to ulcers is not fully understood, scientists believe an infection
may cause malfunction of acid secretion.8 They also believe the bacteria may cause
chronic inflammation of the GI tract, resulting in weakening mucosa and allowing acid to
form an ulcer in the mucosal lining.2 It is estimated that 92% of duodenal ulcers and
70% of gastric ulcers are caused by H. pylori.9 Even though H. pylori is a factor in a
considerable number of cases, only 15% to 20% of individuals infected with H. pylori
develop PUD in their lifetime.9 A study done from 1998 to 2005 showed a significant
decline of the overall rate for H. pylori diagnosis.3 This suggests that a decrease in H.
pylori infections may be partially responsible for the decrease in PUD hospitalizations.
Thanks to the scientific breakthrough by Dr. Marshall and Dr. Warren, PUD is no longer
a chronic, disabling condition, but a disease that can be cured by a short regimen of
antibiotics.5
NSAIDs, short for non-steroidal anti-inflammatory drugs, are medicines that
reduce pain, fever, and inflammation. NSAIDs offer many benefits, however, people
who regularly take these medicines are 5 times more likely to develop PUD than people
who do not take them.10 Cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) are
enzymes that produce prostaglandins, which promote pain, inflammation, and fever.11
NSAIDs work by inhibiting these two enzymes. These medications often cause ulcers

4. Peptic Ulcer Disease
because COX-1 produces an additional type of prostaglandin that protects the stomach
lining from stomach acid.11 By inhibiting COX-1, NSAIDs increase the risk of ulcers
and GI bleeding by making the mucosal cells more vulnerable to hydrochloric acid and
pepsin damage.11 The elderly population often suffers from musculoskeletal and joint
disorders, which are commonly treated with NSAIDs. This explains why peptic ulcer
bleeding is most common in adults > 65 years of age. Low-dose aspirin is also a cause of
drug-induced peptic ulcer bleeding.12 Aspirin is used for the prevention of
cardiovascular incidents.12 With the continuing rise of coronary and cerebrovascular
diseases, the number of low-dose aspirin users may also increase, leading to more cases
of PUD.
Lifestyle factors such as consumption of tobacco, alcohol, tea, coffee, and spicy
foods are believed to stimulate gastric acid secretion, however, findings of
epidemiological studies have been inconsistent.13 A Japanese study revealed that
smokers were at higher risk of gastric and duodenal ulcers, compared to non-smokers.
Yet, another study failed to confirm the association between PUD and use of tobacco.13
The inconsistent results from studies performed on the effect of lifestyle factors with
PUD leads the evidence to be inconclusive. Although emotional stress is no longer
though to be a cause of PUD, Physical stress may increase the risk of developing
complications.14 People with injuries such as severe burns, spinal injuries, brain damage
and people undergoing major surgery often require rigorous treatment to prevent ulcers
from developing as a secondary condition.14
When assessing a patient, typical symptoms of PUD to watch for include gnawing
or burning gastric pain, pain occurring 2-5 hours after meals or on an empty stomach, and

5. Peptic Ulcer Disease
nocturnal pain.15 Food intake or antacids may relieve these symptoms. Less common
features include indigestion, vomiting, loss of appetite, intolerance of fatty foods, and
heartburn.1 Emergency Symptoms consist of severe stomach pain, bloody or black
stools and bloody vomit.1 These deadly symptoms could be signs of bleeding,
hemorrhaging, perforation or obstruction.11 Anyone younger than 55 years old,
diagnosed with PUD, should be tested for H. pylori. They should also be advised to
discontinue the use of NSAIDs, tobacco, and alcohol.15 A food recall assessment should
focus on the patient’s consumption of food that could potentially increase gastric acidity
or foods that the patient cannot tolerate due to pain or gastric aggravation.1 Although
routine laboratory tests usually are not helpful in patients with PUD, lab values to be
cognizant of when assessing a patient are CBC (complete blood count), amylase,
hemoglobin and lipase.16 CBC and hemoglobin can help detect anemia, which mandates
early endoscopy to prevent GI blood loss. 16
According to the Academy of Nutrition and Dietetics’ Nutrition Care Manual,
common nutritional diagnoses are Food-and nutrition-related knowledge deficit (NB-1.1),
Inadequate oral intake (NI-2.1), Excessive oral intake (NI-2.2), and Undesirable food
choices (NB-1.7).1 Other diagnoses frequently accompanied with PUD are hypertension,
acute anemia, iron deficiency, diaphragmatic hernia, and H. pylori infection.3 Diagnostic
tests typically performed by a gastroenterologist to test for peptic ulcer include upper
gastrointestinal barium x-ray, and endoscopy.17 Tests to confirm H. pylori infection
include gastric biopsy, urea breath test, H. pylori culture, stool antigen test and a simple
blood test.7

6. Peptic Ulcer Disease
PUD is primarily treated using medication intervention.1 Medical treatment for
an H. pylori infection includes 1-2 weeks of antibiotics with an antacid. Other
medications such as Proton Pump Inhibitors, H2 blockers and mucosal protectants are
used to treat PUD. A Swedish study conducted from 1974 to 2002 reported that the
increase of proton pump inhibitors (PPI) has reduced the incidence of peptic ulcer
complications.12 Administration of a H2 blocker or PPI for 4 weeks induces healing in
most ulcers.1 PPIs are recommended as initial therapy for most PUD patients because
they suppress acid, increase healing rates and relieve most symptoms. A research trial
comparing PPIs with H2 blockers revealed that after 4 weeks PPIs provided earlier pain
control and better healing rates.18 Another study revealed that PPIs healed duodenal
ulcers in more than 95% of patients in 4 weeks and gastric ulcers in 80- 90% of patients
in 8 weeks.19 Based on these results, there is little reason to prescribe PPIs for longer
than 4 weeks for duodenal ulcers or longer than 8 weeks for gastric ulcers, unless ulcers
are unresponsive to initial treatment. Maintenance therapy with H2 blockers or PPIs
prevents PUD recurrence in high-risk patients but is not generally recommended for
patients in which H. pylori has been eliminated or who are taking short-term NSAIDs.15
Surgery is rarely performed to treat PUD, due to the effectiveness of anti-ulcer
medications like PPIs, H2 blockers and mucosal protectants. However, some patients do
not respond to medication and may require surgery to treat serious complications such as
GI hemorrhage, perforation, or gastric obstruction.14 When patients with duodenal ulcers
require surgery, it is usually a vagotomy, vagotomy with antrectomy, or subtotal
gastrectomy.2

7. Peptic Ulcer Disease
Even though the evidence of lifestyle factors on PUD remains inconclusive, it is
recommended to avoid certain habits such as smoking, alcohol use, and the consumption
of high caffeine and spicy foods, in order to achieve optimal health. People who need the
benefits of NSAIDs, and continue taking them may take steps to reduce the risk of ulcer
occurrence. They can do this by taking the NSAID with a meal, using the lowest
effective dose possible, and avoid smoking and alcohol.11 Patients suffering from painful
PUD symptoms may consider eating smaller, more frequent meals and avoid eating
before bedtime.1 A study of Traditional Iranian Medicine claims there are several edible
fruits and spices used for the management of PUD. They found these remedies were
effective in reducing inflammation, discouraging H. pylori growth and healing wounds.20
Nevertheless, this holistic approach of managing PUD needs pharmaceutical and clinical
verification of conclusive results. Goals for patients with PUD are to optimize nutritional
intake to meet nutrient needs and implement dietary and lifestyle factors that will reduce
symptoms, decrease pain, and promote healing.1
The identification of H. pylori as the causative agent in the majority of PUD cases
has revolutionized the understanding and management of the GI disease.4 The overall
incidence of peptic ulcers is declining, perhaps as a result of the increasing use of PPIs
and decreasing rates of H. pylori infection.21 This disease causing bacteria was identified
as a major culprit only 20 years ago, which leads much to be discovered about the
development of PUD. The use of surgery to treat PUD has also declined thanks to the
widespread use of H2 blockers and PPIs.2 These highly effective anti-ulcer medications
have been some of the most significant advances in the field of gastroenterology in the
past 15 years.22 Researchers are searching for ways to give people the benefits of

8. Peptic Ulcer Disease
NSAIDs without the risk of gastrointestinal bleeding. 11 Current research includes
studies that; Compare the effectiveness of current medicines used to treat PUD and its
complications, Develop new drugs to prevent ulcer development and complications,
Identify GI-friendly alternatives to NSAIDs, and Improve understanding of how the
mucosal lining can protect itself from stomach-acid erosion.11 Although PUD is
primarily treated using medication intervention, it is important to assess patients
thoroughly and treat using proper medical nutrition therapy. Goals for patients with PUD
are to optimize nutritional intake to meet nutrient needs and implement dietary and
lifestyle factors that will reduce symptoms, decrease pain, and promote healing.1

9. Peptic Ulcer Disease
Citations
1. Academy of Nutrition and Dietetics (AND). Peptic Ulcers: Nutrition Care
Manual. 2013.
2. Johns Hopkins Medicine. Peptic Ulcer: U.S. News Health. 2009
3. Feinstein L, Holman R, Yorita Christensen K, Steiner C, Swerdlow D. Trends in
Hospitalizations for Peptic Ulcer Disease, United States, 1998–2005. Emerging
Infectious Diseases.2010;16(9).
4. Bashinskaya B, Nahed B, Redjal N, Kahle K, Walcott B. Trends in Peptic Ulcer
Disease anf the Identification of Heliobacter Pylori as a Causative Organism:
Population-based Estimates from the US Nationwide Impatient Sample. Journal
of Global Infections Disease. 2011. Oct-Dec; 3(4): 366-370.
5. Adams P, Marshall B. Helicobacter pylori: A Nobel pursuit? Canadian Journal of
Gastroenterology, 2008. 22(11): 895–896.
6. Bradford N, Davies R. The site of hydrochloric acid production in the stomach as
determined by indicators. Biochem J. 1950 April; 46(4): 414–420.
7. Kenneth E, McColl M. Helicobacter pylori Infection. New England Journal of
Medicine 2010; 362:1597-1604 DOI: 10.1056/NEJMcp1001110
8. Elsevier. Peptic Ulcer Disease. Clinical Key. 2012
9. Makola D, Peura D, Crowe S. Helicobacter pylori infection and related
gastrointestinal disease. Journal of Clinical Gastroenterology 2007;41(6):548-
558.
10. Huang J, Sridhar S, Hunt R. Role of Helicobacter pylori infection and non-
steroidal antiinflammatory drugs in peptic ulcer disease: a metaanalysis. Lancet.
2002;359:14–22.
11. National Digestive Diseases Information Clearinghouse (NDDIC). NSAIDs and
Peptic Ulcers. U.S. Department of Health and Human Services. 2010.
12. Fujinami H, Kudo T, Hosokawsa A. A Study of the Changes in the cause of
Peptic Ulcer bleeding. World Journal of Gastrointestinal Endoscopy. 2012.
16;4(7): 323-327.
13. Wang F, Tu M, Mar G. Prevalence and risk factors of asymptomatic peptic ulcer
disease in Taiwan. World Journal of Gastroenterology. 2011 March 7;17(9):
1199-1203.

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14. Stanford University School of Medicine. Stomach and Duedenal Ulcers (Peptic
Ulcers). Lucile Packard Children’s Hospital. 2013.
15. Ramakrishnam K, Salinas R, Peptic Ulcer Disease. American Family Physician,
2007; 1;76(7):1005-1012.
16. Anand B. Peptic Ulcer Disease Workup. Medscape. 2012.
17. Laws H, McKernan J. Endoscopic management of peptic ulcer disease. Annals of
Surgery, 1993 May; 217(5): 548–556.
18. Poynard T, Lemaire M, Agostini H. Meta-analysis of randomized clinical trials
comparing lansoprazole with ranitidine or famotidine in the treatment of acute
duodenal ulcer. Eur J Gastroenterol Hepatol. 1995;7:661–5.
19. Vakil N, Fennerty MB. Direct comparative trials of the efficacy of proton pump
inhibitors in the management of gastro-oesophageal reflux disease and peptic
ulcer disease. Aliment Pharmacol Ther. 2003;18:559–68.
20. Farzeli M, Shams-Ardekani M, Abbasabadi Z, Rahimi R. Scientific Evaluation of
Edible Fruits and Spices Used for the Treatment of Peptic Ulcer in Traditional
Iranian Medicine. ISRN Gastroenterology. 2013;12.
21. Kang JY, Tinto A, Higham J, Majeed A. Peptic ulceration in general practice in
England and Wales 1994–98: period prevalence and drug management. Aliment
Pharmacol Ther. 2002;16:1067–74.
22. Richardson P, Hawkey C, Stack W. Proton Pump Inhibitors. September 1998;
56(3):307-335.