PUD lit review

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


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


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


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


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


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


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


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


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.


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.

Documents

PUD lit review