Peptic ulcer

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Peptic ulcer disease is a defect in muscularis mucosa of gastrointestinal tract. Peptic ulcer is classified into 2 depending upon the location of ulcer, gastric ulcer and duodenal ulcer. The most common cause of peptic ulcer disease is H.pylori infection which is acquired in childhood but presents in adulthood. Other causes of peptic ulcer disease are chronic use of NSAID, family history of peptic ulcer disease. Persistant use of NSAIDS or chronic infection with H.Pylori results in inflammation of antral mucosa and ultimately causes the ulcer. The most common symptoms of peptic ulcer disease include episodic epigastric pain, heartburn, loss of appettite, gastroesophageal reflux, waterbrash, hematemesis and melena. Common physical examination findings of peptic ulcer disease include epigastric tenderness, tachycardia. Endoscopy is the gold standard test for the diagnosis of the peptic ulcer disease. Treatment of helicobacter pylori with antimicrobial agents is indicated for patients with gastric or duodenal ulceration. Pharmacologic therapies for peptic ulcer disease due to H. pylori is either triple or quadruple pharmacologic agents that include a Proton pump inhibitors plus a combination of antimicrobial agents.

Hundred years ago, Polish clinical researcher, professor W.Jaworski was the first to describe the spiral-shaped microorganism at Cracow Jagiellonian University but it was later confirmed in the animal by G.Bizzazero. Asklepios was the first to describe an association between GI bleeding and peptic ulcer disease. In 1982 Warren and B.J marshall cultured the organism and found a strong association between Helicobacter pylori and inflammation of gastric mucosa, not due to spicy food and stress and were awarded the noble prize.

Peptic ulcer disease may be classified into two types based on the location, gastric ulcer and duodenal ulcer. Gastric ulcers are present mostly at lesser curvature of the stomach. Duodenal ulcers are mostly present at the duodenal bulb.

A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonize 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. Excess Gastrin stimulates the production of gastric acid by parietal cells. The acid erodes the mucosa and causes the ulcer. Another major cause of PUD 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 activity of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins.

Common causes of peptic ulcer disease include Helicobacter pylori infection and NSAID use. Less common causes of peptic ulcer disease include Crohn’s disease, Zollinger-Ellison syndrome, Cushing and Curling ulcers, Carcinoid tumors, and carcinoid syndrome.

Peptic ulcer disease must be differentiated from other causes of acute upper gastrointestinal bleeding such as esophageal varices, Mallory-Weiss syndrome, gastrointestinal cancer, arteriovenous malformations, esophagitis, and esophageal ulcer. Peptic ulcer disease must also be differentiated from gastroesophageal reflux disease (GERD,pancreatitis, Zollinger-Ellison Syndrome, Cholelithiasis, gastric outlet syndrome, myocardial infarction ,pleural empyema and appendicitis.

The incidence and prevalence of Helicobacter pylori infection are generally higher among people born outside North America. Within North America, the prevalence of the infection is higher in certain racial and ethnic groups, and people who have immigrated to North America. Peptic ulcer disease is acquired during childhood.The incidence of Peptic ulcer disease increases with age; the median age at diagnosis is 18-30 years. Peptic ulcer disease affect equally in childhood. Men are more commonly affected by peptic ulcer disease than women in adulthood.

Common risk factors in the development of peptic ulcer disease include infection from Helicobacter pylori, chronic use of NSAIDs, cigarette smoking, alcohol intake, family history of peptic ulcer, and age >50 years. Less common risk factors in the development of peptic ulcer disease include psychological stress, nosocomial stress ulcers, and coagulopathy. Rare conditions associated with gastric acid hypersecretion, such as zollinger-ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy gastrinoma or multiple endocrine neoplasia types I (MEN-I), antral G cell hyperplasia, basophilic leukemias, short bowel syndrome.

According to the American Society of Gastroenterology, screening for the Peptic Ulcer Disease is not recommended.

The infection of Helicobacter pylori, a common cause of peptic ulcer disease is acquired usually during the childhood but presents in second to the fifth decade of life.Patient presents with episodic epigastric pain, indigestion, bloating, hematemesis and melena. Peptic ulcers tend to come back if untreated.

Peptic ulcer disease if not treated, the patient can develop complications like bleeding, perforation, obstruction, stricture.Chronic infection of Helicobacter pylori leads to gastric cancer, MALT lymphoma, Iron deficiency anemia, Idiopathic thrombocytopenic purpura.

Prognosis is good if the eradication therapy of Helicobacter pylori is taken.The recurrence rate of patients with peptic ulcer disease is less than 20%.

Endoscopy is the gold standard test for the diagnosis of the peptic ulcer disease.

The hallmark of peptic ulcer disease is an episodic epigastric pain which cause awakening at night.A positive history of epigastric pain, use of drugs like NSAIDs including aspirin which inhibit cyclooxygenase, use of antiplatelets, steroids and family history of peptic ulcer disease is suggestive of peptic ulcer disease. The most common symptoms of peptic ulcer disease include episodic epigastric pain, heartburn, loss of appettite, gastroesophageal reflux, waterbrash, hematemesis and melena. Less common symptoms of peptic ulcer disease include intolerance to fatty food.

Peptic ulcer disease patient appears in severe stress due to abdominal pain. Common physical examination findings of peptic ulcer disease include epigastric tenderness, tachycardia.Perforated peptic ulcer disease patient presents with classic triad of severe epigastric tenderness, tachycardia and abdominal rigidity. Clinical signs of perforated peptic ulcer comes in 3 stages: In the initial stage within first 2 hours, the patient presents with tachycardia, epigastric pain and cool extremities. In next 2 to 12 hours, the patient presents with lower right quadrant tenderness and abdominal rigidity. In more than 12 hours, the patient presents with abdominal distension, hypotension, and pyrexia with acute circulatory collapse.

There is no specific diagnostic laboratory test for peptic ulcer disease but in the patient with the history of peptic ulcer disease, the laboratory test is used to rule out bleeding and to document the status of eradication therapy and to test refractory ulcers.

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. 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.

Testing of H.pylori infection is very important for treating ulcers. H.pylori tested by 2 methods : invasive and non-invasive. Rapid urease testing is invasive test which is used as diagnostic study of choice. Stool monoclonal antigen test is one of the non-invasive test which is used to diagnose active infection.

Peptic ulcer disease is the cause of dyspepsia in about 10% of patients. 95% of duodenal and 70% of gastric ulcers are associated with Helicobacter pylori. Eradication of Helicobacter pylori with antimicrobial agents is indicated for patients with gastric or duodenal peptic ulceration, who are colonized with H. pylori, and patients with MALT lymphoma. Eradication therapy should also be considered in patients with immune thrombocytopenic purpura who are H. pylori-positive and patients who have undergone resection for early-stage gastric cancer. Pharmacologic therapies for peptic ulcer disease due to H. pylori is either triple or quadruple pharmacologic agents that include a Proton pump inhibitors plus a combination of antimicrobial agents. The use of antimicrobial therapy is discouraged among asymptomatic carriers.

Surgery for peptic ulcer is indicated for bleeding and perforated peptic ulcer.Bleeding ulcers are usually treated first with endoscopic therapy but if they bleed after endoscopic therapy, surgery is done to control bleeding. Perforated peptic ulcer is an emergency, immediate laparoscopic closure of ulcer is done.

Helicobacter pylori eradication has been proved as the most cost-effective strategy for primary prevention of NSAID-associated peptic ulcer, especially for patients above the age of 50 years.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Hundred years ago, polish clinical researcher professor W.Jaworski was the first to describe spiral-shaped microorganism at Cracow Jagiellonian University. Asklepios was the first to describe an association between GI bleeding and peptic ulcer disease. In 1982 Warren and B.J marshall cultured the organism and found a strong association between Helicobacter pylori and inflammation of gastric mucosa and were awarded the noble prize.

• Hundred years ago, polish clinical researcher professor W.Jaworski was the first to describe the spiral-shaped microorganism at Cracow Jagiellonian University
• In pre-16th century:
  • Hippocrates gave a detailed describtion of symptoms of peptic ulcer
  • Avicenna described the relationship between abdominal pain and mealtimes in peptic ulcer patient^[1]
• In 1586, Marcellus Donatus of Mantua described gastric ulcers by performing autopsies
• In 1688, Johannes von Murault gave detailed description of duodenal ulcers
• In 1812, Broussais found that if acute gastritis is untreated, it can lead to chronic gastritis
• In 1821, Nepveu found a relationship between gastritis and gastric cancer
• In 1857, William Brintonin described ulcer of the stomach and gastric cancer in his book
• In 1875, G.Bottcher and M. Letulle hypothesize that ulcers are caused by bacteria
• In 1880, J.Cohnheim found that ulcers may be caused by chemical factors
• In 1889, Walery Jaworski found spiral organisms in sediment washings of humans and proposed that these organisms may be involved with gastric disease
• In 1910, Moynihan wrote a book on duodenal ulcer^[2]
• In 1971, Howard Steer found H. pylori from biopsies of a patient with ulcers^[3][4]
• In late 1970, J.R Warren, a pathologist in Perth, Australia found the appearance of spiral bacteria overlying gastric mucosa^[4][5]
• In 1982 , Warren and B.J marshall cultured the organism and found a strong association between Helicobacter pylori and inflammation of gastric mucosa^[4][5]
• 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.This experiment was published in 1984 in the Australian Medical Journal^[6]
• In 1994, Parsonnet et al found an association between H. pylori and lymphomas of the gastrointestinal tract^[7]
• In 1997 Tomb et al. completed sequencing of the entire 1,667,867 base pairs of the H. pylori genome. This helped in identifying new virulence factors for the infectivity of H. pylori at the molecular level^[8]
• In 2001, Chan et al. showed that eradication of H. pylori prevents bleeding from ulcers that is caused by aspirin and non-steroidal anti-inflammatory drugs^[9]
• In 2002, European Helicobacter Pylori Study Group published the Maastricht 2-2000 Consensus Report, found a “test-and-treat” strategy for H. pylori in young patients without atypical symptoms. It suggests the use of noninvasive testing to evaluate for H. pylori ^[10]
• In 2005 Warren and Marshall awarded the Nobel Prize in Physiology or Medicine by Karolinska Institute in Stockholm for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease^[11]

• In 1992,Covacci discovered CagA gene, which encodes for a cytotoxin-associated surface protein, related with strains of H. pylori that caused duodenal ulcers and was discovered by molecular techniques were first involved in the pathogenesis of peptic ulcer disease ^[12]

• In 1868, Kussmaul discovered that an antibacterial agent containing bismuth used to treat peptic ulcers
• In 1915, Antacids are first suggested for the treatment of Peptic ulcer disease^[13]
• In 1951, J. Allende wrote a book explaining the treatment of gastric ulcers with penicillin^[14]
• 1953, Dintzis and Hastings suggested a relationship between urease and a bacterial infection,by stopping urease production in mice with antibiotics^[15]
• 1957, Charles Lieber and Andre Lefèvre explained that antibiotics decreases the production of urea to ammonia in stomach^[16]
• In 1990
  • Borody’s triple therapy became commercialized under the product name Helidac in the United States^[17]
  • Rauws and Tytgat described treatment of duodenal ulcer by eradication of H. pylori using Borody’s triple therapy that is combination of proton pump inhibitor and two antibiotics, becomes first-line therapy for eradication^[18]
  • World Congress of Gastroenterology suggested eradicating H. pylori to treatment of duodenal ulcers
  • First report of resistance of H. pylori to the antibiotic metronidazole was found^[19]
  • The resistance of H. pylori to treatment leads to the development of new regimen which includes many different antibiotic and proton pump inhibitor regimens for eradication^[10]
• In 1996 first antibiotic was developed by the Food and Drug Administration to treat peptic ulcer disease^[20]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Peptic ulcer disease may be classified into two types based on the location within the gastrointestinal tract. gastric ulcer and duodenal ulcer. Gastric ulcers are present mostly at lesser curvature of the stomach while Duodenal ulcers are mostly present at the duodenal bulb.

Peptic ulcer disease may be classified according to location into two subtypes: ^[1][2]

• Gastric ulcers
• Duodenal ulcers

*Adopted:American college of gasteroenterology^[3]

Gastric ulcer is further divided on the basis of location and endoscopic findings:

• Gastric ulcer is further classified into 3 subtypes depending upon their location:^[4][5][6]
  • Type 1: Ulcer present at the body of stomach without involving duodenum, pylorus or prepyloric region and not associated with hypersecretion of gastric acid
  • Type 2: Ulcer present at the body of stomach combined with duodenum and associated with gastric acid hypersecretion
  • Type 3: Ulcer close to pylorus and associated with gastric acid hypersecretion

• Gastric ulcer classification by using endoscopic staging system of Sakita into three stages:^[7]
  • Active
  • Healing
  • Scarring

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonize 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 known as type B gastritis. This results in a defect in gastrin production leading to increasedgastrin secretion. Gastrin stimulates the production of gastric acid by the parietal cells. The acid erodes the mucosa and causes the ulcer. Another major cause of peptic ulcer disease is the chronic 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.

Peptic ulcer occurs due to distruption of muscularis mucosa which is required in the maintenance of the integrity of the gastric mucosa

Defensive mechanism of gastric mucosa

Mucosal barrier consists of three protective components which include:^[1][2][3][4]

• Layer of epithelial cell lining which is bound by tight junctions that repel fluids
• Layer of mucus, secreted by surface epithelial cells and foveolar cells which forms a protective gel-like coating over the entire gastric mucosal surface
• Layer of bicarbonate ions, secreted by the surface epithelial cells which neutralize acids

The two most important etiological factors in the development of PUD are:^[6][7][8]

• Helicobacter pylori infection
• Nonsteroidal anti-inflammatory drugs (NSAIDs)

Penetration

Factors that help in penetration and growth of Helicobacter pylori are:^[9][10]

• Bicarbonate-mediated chemotactic motility of Helicobacter pylori which facilitates its penetration
• Neutral pH favors the growth of helicobacter pylori

Colonzation:

• The colonization of virulent CagA-positive Helicobacter pylori strains leads to the degeneration of surface epithelial cells
• This degeneration results in increased exfoliation of surface epithelial cells
• The exfoliation mediated compensatory cell proliferation leads to the movement of immature cells to the foveolae and surface

• Immature cells leads to impaired mucin and bicarbonate production and the integrity of the mucous barrier may be compromised
• All of above factors lead to activation of complement via the alternative pathway and the release of chemical mediators by mast cells and activated polymorphs may lead to microvascular disturbances and focal ischemic damage to the surface epithelium
• Helicobacter pylori infection down-regulates E-cadherin expression in gastric epithelial cells which affect the resistance of the mucosa to acid attack
• Decreased mucus production, release of chemical mediators and down-regulation of E- cadherin leads to mucosal damage leads to ulcer formation^[11][12][13]

Factors responsible for immunological response of Helicobacter pylori are :

• Helicobacter pylori infection triggers local production various proinflammatory mediators (cytokines, neutrophil infiltration, specific T- and B- cells)

• Of all the cytotoxins and virulence factors Cag A, VacA, and OipA play a key role in the pathogenesis of Helicobacter pylori infection
• Cag A, VacA, and OipA not only helps in the colonization of Helicobacter pylori but and also modulates host’s immune system
• Bacterial factors and complement activation leads to neutrophilic activation including reactive oxygen,release of leukocytes enzymes and leukotriens lead to mucosal injury ^{[14] [15][16][17][7]}
• Helicobacter pylori secretes various enzyme :Urease,Phospholipases,Alcohol dehydrogenase and Catalases- causes damage the host gastric muscosa by generating toxic metabolities^[18][19][20]

Role of Helicobacter pylori in causing gastric ulcer

• Factors responsible for ulcer formation:^[21]
• There is decrease in acid and decrease in parietal cell volume which further predisposes to development to ulcer formation.^[13]

Role of Helicobacter pylori in causing duodenal ulcer

• Factors responsible for ulcer formation:
  • Hypergastrenemia which leads to low pH
  • Decreased in bicarbonate secretion
  • Both of these factors leads to gastric metaplasia induced duodenitis ^{[22][23][24][25][26]}

• NSAID’s are more commonly responsible for gastric ulcers than duodenal ulcers
• NSAID’s cause ulcers by following mechanism:^[27][28][29]
  • Inhibit systemic prostaglandins production
    • Decreases blood flow
    • Decreases mucus production
    • Inhibits leucocyte adhesion

Other factors responsible for peptic ulcer disease:

• Chronic smoking leads to mucosal damage or deals healing of ulcer by following mechanism:^[30]

• Decreases the production of prostaglandins
• Triggers reflux of bile acids into the duodenum which results in alteration of blood flow leading to ischaemia

• Severe stress eg: brain injury, burns causes increase in production of gastric acid and increases the risk of ulcer formation

• Genes involved in the pathogenesis of peptic ulcer disease include:^[31][32]
  • cagA
  • vacA

• The conditions associated with infection caused by helicobacter pylori include:^{[33][34][35][36][37]}
  • Gastric cancer
  • Gastric mucosa-associated lymphoid tissue lymphoma (MALT)
  • Idiopathic thrombocytopenic purpura

• Gastric ulcers are most often localized on the lesser curvature of the stomach
• Duodenal ulcers are more located at bulb of duodenum
• Characteristic findings of a peptic ulcer on gross pathology include:
  • Round to oval
  • Two to four cm diameter
  • Smooth base with perpendicular borders.
  • Parietal scarring with radial folds may be evident in the surrounding mucosa

• 
  A benign gastric ulcer (from the antrum) of a gastrectomy Source:https://commons.wikimedia.org/wiki/File:Benign_gastric_ulcer_1.jpg#/media/File:Benign_gastric_ulcer_1.jpg
• 
  Duodenal ulcer specimen. Source: https://commons.wikimedia.org/wiki/File:Duodenal_ulcer01.jpg#/media/File:Duodenal_ulcer01.jpg
• 
  Gastric ulcer specimen Source:https://commons.wikimedia.org/wiki/File:Gastric_ulcer_3.jpg#/media/File:Gastric_ulcer_3.jpg

• A peptic ulcer is a mucosal defect produced by acid-pepsin aggression which penetrates the muscularis mucosae and muscularis propria
• There is increased plasma cells, neutrophilic infiltrate, villous blunting
• The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
• During the active phase, the base of the ulcer shows 4 zones:
  • Inflammatory exudate: polymorphonuclear infiltration which along with bacterial products stimulate the production of IL-8 and tumor necrosis factor alpha (TNF-α) and IL-1 released by macrophages in response to bacterial lipopolysaccharide
  • Fibrinoid necrosis
  • Granulation tissue
  • Fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis^[38]

• 
  Erosive gastric ulcer source: https://commons.wikimedia.org/wiki/File:Erosive_gastric_ulcer.jpg#/media/File:Erosive_gastric_ulcer.jpg

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Common causes of peptic ulcer disease include Helicobacter pylori infection and NSAID use. Less common causes of peptic ulcer disease include Crohn’s disease, Zollinger-Ellison syndrome, Cushing and Curling ulcers, Carcinoid tumors, and carcinoid syndrome.

Common Causes^[1][2][3]

• Helicobacter pylori
• NSAIDs

Less common causes

• Hormonal or mediator-induced including secondary acid hypersecretory states
  • Gastrinomas
  • Systemic mastocytosis
  • Carcinoid syndrome
  • Myeloproliferative disorder
• Antral G-cell hyperfunction
• Post-surgical antral exclusion and post gastric bypass surgery
• Cancers and lymphomas
• Cameron ulcer (gastric ulcer where a hiatus hernia passes through the diaphragmatic hiatus)
• True idiopathic ulcer

Rare causes of peptic ulcer disease

• Crohn’s disease of the stomach or duodenum
• Eosinophilic gastroduodenitis
• Systemic mastocytosis
• Radiation damage
• Viral infections (eg cytomegalovirus or herpes simplex infection, in particular in immunocompromised patients)
• Colonization of stomach with H heilmanii
• Severe systemic disease

Genetic causes^[4]

• Peptic ulcer disease caused by gastrinomas (Zollinger-Ellison syndrome) caused by a mutation in MEN gene present on chromosome 11q13

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Guillermo Rodriguez Nava, M.D. [2] Manpreet Kaur, MD [3]

Peptic ulcer disease must be differentiated from other causes of acute upper gastrointestinal bleeding such as esophageal varices, Mallory-Weiss syndrome, gastrointestinal cancer, arteriovenous malformations, esophagitis, and esophageal ulcer. Peptic ulcer disease must also be differentiated from gastroesophageal reflux disease (GERD,pancreatitis, Zollinger-Ellison Syndrome,cholelithiasis,gastric outlet syndrome,myocardial infaraction ,pleural empyema and appendicitis

Peptic ulcer disease must be differentiated from other diseases that presents with epigastric pain such as gastritis, gastroesophageal reflux disease,acute pancreatitis,prmary biliary cirrhosis,cholelithiasis,gastric outlet syndrome,myocardial infaraction ,pleural empyema,acute appendicitis ^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]}

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

The incidence and prevalence of Helicobacter pylori infection are generally higher among people born outside North America. Within North America, the prevalence of the infection is higher in certain racial and ethnic groups, and people who have immigrated to North America. Peptic ulcer disease is acquired during childhood. The incidence of Peptic ulcer disease increases with age; the median age at diagnosis is 18-30 years. Peptic ulcer disease affects both sexes equally in childhood. Men are more commonly affected by peptic ulcer disease than women in adulthood.

• The incidence of peptic ulcer disease is approximately 10-19 per 100,000 individuals worldwide^[1]
• In 2011, the incidence rate of peptic ulcer disease was estimated to be one case per 1000 individuals and its complications was 0.7 per 1000 individuals^[2]
• The incidence and prevalence of Helicobacter pylori infection are generally higher among people born outside North America. Within North America, the prevalence of the infection is higher in certain racial and ethnic groups, and people who have immigrated to North America^[3]

• The prevalence of peptic ulcer disease is approximately 23.1 per 100,000 individuals but higher in men 29.4 per 100,000 than women 14.9 per 100,000
• The prevalence of peptic ulcer disease is estimated to be 4.5 million cases annually
• Lifetime prevalence is 11-14% in men and 8-11% in women^{[4][5][1][6][7][8][9][10]}

• The mortality rate of peptic ulcer disease is approximately 1 per 100,000 individuals

• Peptic ulcer disease is acquired during childhood
• The incidence of Peptic ulcer disease increases with age; the median age at diagnosis is 18-30 years

• Peptic ulcer disease usually affects individuals of the African Americans with a higher proportion of African ancestry race and Mexican Americans^[11][12]
• Non-Hispanic whites individuals are less likely to develop the peptic ulcer disease

• Peptic ulcer disease affect equally in childhood^[13]
• Men are more commonly affected by peptic ulcer disease than women in adulthood^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: :Manpreet Kaur, MD [2]

Common risk factors in the development of peptic ulcer disease include infection from Helicobacter pylori, chronic use of NSAIDs, cigarette smoking, alcolhol intake, family history of peptic ulcer, and age >50 years. Less common risk factors in the development of peptic ulcer disease include psychological stress, nosocomial stress ulcers, and coagulopathy. Rare conditions associated with gastric acid hypersecretion, such as zollinger-ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy, gastrinoma or multiple endocrine neoplasia types I (MEN-I), antral G cell hyperplasia, basophilic leukemias or short bowel syndrome.

The most potent risk factor leading to the development of peptic ulcer disease is an infection of Helicobacter pylori. Other risk factors include chronic use of NSAIDs, family history of peptic ulcer, tobacco smoking, and psychological and nosocomial stress.^{[1][2][3][4][5][6][7][8]}

Common risk factors in the development of peptic ulcer disease include:

• Helicobacter pylori infection
• Chronic use of NSAIDs
• Family history of peptic ulcer

Less common risk factors in the development of peptic ulcer disease include:

• Tobacco
• Alcohol
• Psychological stress
• Nosocomial stress ulcers due the to the use of mechanical ventilation for more than 48 hours, and coagulopathy
• Rare conditions associated with gastric acid hypersecretion such as:
  • Zollinger-Ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy
  • gastrinoma or multiple endocrine neoplasia types I (MEN-I), antral G cell hyperplasia, basophilic leukemias, short bowel syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

According to the American Society of Gastroenterology, screening for PUD is not recommended.

According to the American Society of Gastroenterology, screening for PUD is not recommended.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Helicobacter pylori infection is a common cause of peptic ulcer disease which is acquired usually during childhood but presents in second to fifth decade of life. Patient presents with episodic epigastric pain, indigestion, bloating,hematemesis and melena. If not treated, patients can develop complications like bleeding, perforation, obstruction or stricture. Chronic infection of helicobacter pylori leads to gastric cancer, MALT lymphoma, iron deficiency anemia, Idiopathic thrombocytopenic purpura. Peptic ulcers tend to recur if left untreated. Prognosis is good if the eradication therapy of Helicobacter pylori is taken.The recurrence rate of patients with peptic ulcer disease is less than 20%.

• The infection of Helicobacter pylori , common cause of peptic ulcer disease is acquired usually during the childhood, mainly in those who have low socioeconomic status, increased number of siblings and similar infection in the mother.^[1][2][3]
• The duodenal ulcer occurs in second to fifth decade of life. where as gastric ulcer occurs in the 4th decade of life.
• Peptic ulcer disease starts with symptoms such as episodic epigastric pain, indigestion, bloating.
• Without treatment, the patient will develop symptoms of perforation like severe abdominal pain. Chronic infection leads to gastric atrophy, gastric metaplasia and ultimately leads to gastric cancer and MALT lymphoma.^[4]

• Bleeding is the commonest complication.
  • Sudden large bleeding can be life threatening.
  • Bleeding occurs when the ulcer erodes one of the blood vessels around the stomach.^[5][6]
• Perforation
  • Perforation is most common occur at the duodenal bulb (62%), followed by the pyloric region (20%), and the gastric body (18%).
  • Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into abdominal cavity leading to fatal consequences.
  • Perforation at the anterior surface of stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis.
  • Often, the first symptom is a sudden intense abdominal pain.
  • Posterior wall perforation leads to pancreatitis, pain in this situation often radiates to back.
  • Penetration is also a form of perforation, when the ulcer continues into adjacent organs such as liver and pancreas.^[7][8]
• Obstruction
  • Occurs as a result of stricture and scarring narrowing in the duodenum leading to gastric outlet obstruction.

Chronic Helicobacter pylori infection leads to:

• Gastric cancer
• MALT lymphoma
• Iron deficiency anemia
• Idiopathic thrombocytopenic purpura

• Prognosis is good if the eradication therapy of Helicobacter pylori is taken.
• The recurrence rate of patients with peptic ulcer disease is less than 20%.

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