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A peptic ulcer

A peptic ulcer

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Published by: Munzir Munzir Khairuddin on Jan 18, 2011
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A peptic ulcer, also known as ulcus pepticum, PUD or peptic ulcer disease,[1] is an ulcer (defined as mucosal erosions equal

to or greater than 0.5 cm) of an area of thegastrointestinal tract that is usually acidic and thus extremely painful. As many as 70-90% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach, however only 40% of those cases go to a doctor. Ulcers can also be caused or worsened by drugs such as aspirin and otherNSAIDs. Contrary to general belief, more peptic ulcers arise in the duodenum (first part of the small intestine, just after the stomach) rather than in the stomach. About 4% of stomach ulcers are caused by a malignant tumor, so multiple biopsies are needed to exclude cancer. Duodenal ulcers are generally benign.

1 Classification 2 Signs and symptoms


2.1 Complications

3 Cause


3.1 Stress

4 Diagnosis

o o o

4.1 Macroscopic appearance 4.2 Microscopic appearance 4.3 Differential diagnosis of epigastric pain

5 Treatment 6 Epidemiology 7 History 8 Notes 9 References 10 External links



Stomach (called gastric ulcer) Duodenum (called duodenal ulcer) Oesophagus (called Oesophageal ulcer) Meckel's Diverticulum (called Meckel's Diverticulum ulcer)

Types of peptic ulcers: Type I: Ulcer along the lesser curve of stomach 

an ulcer can lead to a gastric or duodenal perforation. nausea. rarely. Symptoms of duodenal ulcers would manifest mostly before the meal²when acid (production stimulated by hunger) is passed into the duodenum. the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below). However. and most glucocorticoids (e. the symptoms of peptic ulcers may vary with the location of the ulcer and the patient's age. or after the meal. this is not a reliable sign in clinical practice. This is extremely painful and requires immediate surgery. while gastric ulcers are exacerbated by it). . Furthermore. after around 3 hours of taking a meal (duodenal ulcers are classically relieved by food. [2] Usually.g. which leads to acute peritonitis. loss of appetite and weight loss. or from damage to the esophagus from severe/continuing vomiting. as the alkaline duodenal contents reflux into thestomach. and copious vomiting. typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear.   Type II: Two ulcers present .one gastric. Medicines associated with peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase. dexamethasone and prednisolone). children and theelderly do not develop any symptoms unless complications have arisen. A history of heartburn. waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus). classically epigastric with severity relating to mealtimes. gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. as gastric acid is secreted. The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would giveepigastric pain during the meal. one duodenal Type III: Prepyloric ulcer Type IV: Proximal gastroesophageal ulcer  Type V: Anywhere [edit]Signs and symptoms Symptoms of a peptic ulcer can be abdominal pain. this can occur due to bleeding directly from a gastric ulcer.   melena (tarry.       bloating and abdominal fullness. In patients over 45 with more than two weeks of the above symptoms. Also. hematemesis (vomiting of blood). foul-smelling feces due to oxidized iron from hemoglobin).

it may last from few minutes to several hours and it may be worse when the stomach is empty.  Perforation (a hole in the wall) often leads to catastrophic consequences. Patient often presents with severe vomiting. initially chemical and later bacterial peritonitis. Gastrinstimulates the production of gastric acid by parietal cells and. pylori-caused ulceration declines in the Western world due to .[5] It occurs when the ulcer erodes one of the blood vessels. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawnrofecoxib) preferentially inhibit cox-2. The gastric mucosa protects itself from gastric acid with a layer of mucus. The first sign is often sudden intense abdominal pain.  Cancer is included in the differential diagnosis (elucidated by biopsy). The pain caused by peptic ulcers can be felt anywhere from the navel up to thebreastbone. the secretion of which is stimulated by certain prostaglandins. the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation. Perforation at the anterior surface of the stomach leads to acuteperitonitis. pylori colonization responses that increase gastrin. despite the appearance of antibodies. Also. which is essential for the production of these prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox1).Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers. Sudden large bleeding can be life-threatening.   Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas. and gastrin secretion can either be decreased (most cases) resulting in hypo. Thus. peptic ulcer disease symptoms may be different for every sufferer. Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer. Pain is usually caused by the ulcer but it may aggravated by the stomach acidwhen it comes into contact with the ulcerated area. [4] [edit]Complications  Gastrointestinal bleeding is the most common complication. indigestion or heartburn. pain in this situation often radiates to the back. Another major cause is the use of NSAIDs (see above). sometimes the pain may flare at night and it can commonly be temporarily relived by eating foods that buffer stomach acid or by taking anti-acid medication.[7] [edit]Cause A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori thatcolonizes the antral mucosa. [3] However. As the prevalence of H.[6] Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. and roughly halve the risk of NSAID-related gastric ulceration. Posterior wall perforation leads to pancreatitis.or achlorhydria or increased. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. resulting in a defect in the regulation of gastrin production by that part of the stomach. The immune system is unable to clear the infection. in H. thebacterium can cause a chronic active gastritis (type B gastritis). This pain can be misinterpreted as hunger. which is less essential in the gastric mucosa.

rare gastrin-secreting tumors. it does not seem to independently increase risk. pylori infection. but have been shown to be of relatively minor importance in the development of peptic ulcers. and a combination of chronic stress and irregular mealtimes was a significant risk factor.[16] [edit]Diagnosis . mainly caused by the widespread use of NSAIDs. pylori infections. Gastrinomas (Zollinger Ellison syndrome). pyloriinfection. There is debate as to whether psychological stress can influence the development of peptic ulcers. consumption and blood type. pylori infection[10][11][12] [nb 1].increased medical treatment. pylori infection were independently associated with the development of peptic ulcers. and even when coupled with H. Burns and head trauma. and stress has been demonstrated to cause the production of excess stomach acid.[13]. or at least complication. Helicobacter pylori thrives in an acidic environment. in the development of ulcers.[15] A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer. [edit]Stress Researchers also continue to look at stress as a possible cause. also cause multiple and difficult to heal ulcers. the increase is modest in comparison to the primary risk factor [10][14][nb 2]. however. others have been more specific in exploring the risks involved and have found that smoking by itself may not be much of a risk factor unless associated with H. were hypothesized as ulcerogens (helping cause ulcers) until late in the 20th century. The drop in incidence is considered to be a cohort-phenomenon independent of the progress in treatment of the disease. while studies have found that alcohol consumption increases risk when associated with H. The cohort-phenomenon is probably explained by improved standards of living which has lowered the incidence of H. Some suggested risk factors such as diet. which are reported in many patients who are on mechanical ventilation. Similarly. The incidence of duodenal ulcers has dropped significantly during the last 30 years. spice. This was supported by a study on mice showing that both long-term water-immersion-restraint stress and H. An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role. a greater proportion of ulcers will be due to increasing NSAID use among individuals with pain syndromes as well as the growth of aging populations that develop arthritis. For example. can lead to physiologic stress ulcers. while the incidence of gastric ulcers has shown a small increase. pylori infection.[1] Researchers are examining how stress might promote H.[8] Although some studies have found correlations between smoking and ulcer formation [9].

particularly if a person has several ulcers or the ulcers are in unusual places. such as antibiotics or proton pump inhibitors.   . Confirming the diagnosis is made with the help of tests such as endoscopies or barium contrast x-rays. the location and severity of an ulcer can be described. The diagnosis is mainly established based on the characteristic symptoms. biopsy proven to be gastric cancer. if no ulcer is present. a doctor may suspect an underlying condition that causes the stomach to overproduce acid.[17] An esophagogastroduodenoscopy (EGD). when severe ulcers resist treatment. pylori cultures. a form of endoscopy. also known as agastroscopy. Additionally. By direct visual identification. Most labs are not set up to perform H. is carried out on patients in whom a peptic ulcer is suspected.Endoscopic image of gastric ulcer. or when they first appear in a person who is over age 45 or who has other symptoms such as weight loss. Direct culture from an EGD biopsy specimen. EGD can often provide an alternative diagnosis. One of the reasons why blood tests are not reliable on establishing an accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Also. Moreover. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment. this is difficult to do. a false-negative is possible with a blood test if the patient has recently been taking certain drugs. [18] The diagnosis of Helicobacter pylori can be made by: Urea breath test (noninvasive and does not require EGD). and can be expensive. because stomach cancer can cause similar symptoms. doctors may treat ulcers without diagnosing them with specific tests and observe if the symptoms resolve. In some cases. meaning their primary diagnosis was accurate. The stomach pain is usually the first to signal a peptic ulcer.

air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). . the patient will be asked to blow into a bag that is sealed. [edit]Macroscopic appearance A benign gastric ulcer (from the antrum) of a gastrectomy specimen. is an omen of perforated peptic ulcer disease. pylori. Therefore. If the patient stands erect. [19] To perform this exam the patient will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. gas in the peritoneal cavity. Histological examination and staining of an EGD biopsy. the breath sample will contain carbon dioxide. shown on an erect chest X-ray or supine lateral abdominal X-ray. The possibility of other causes of ulcers. This leads to "free gas" within the peritoneal cavity. notably malignancy (gastric cancer) needs to be kept in mind. most are also a consequence of chronic H. as when having a chest X-ray. pylori. pylori infection. the gas will float to a position underneath the diaphragm. If a peptic ulcer perforates. The breath test uses radioactive carbon atom to detect H.   Stool antigen test. Measurement of antibody levels in blood (does not require EGD). This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.  Direct detection of urease activity in a biopsy specimen by rapid urease test. If the patient is infected with H. This is especially true in ulcers of the greater (large) curvature of the stomach. It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy. After an hour.

granulation tissue and fibrous tissue.Tetracycline. the most effective treatments are combinations of 2 antibiotics (e. as a consequence of the parietal scarring. with a smooth base and perpendicular borders. sometimes together with a bismuth compound. regular but with elevated borders and inflammatory surrounding in the chronic form. 2 to 4 cm diameter. Clarithromycin. These borders are not elevated or irregular in the acute form of peptic ulcer. In complicated. 3 antibiotics (e.[20] [edit]Differential diagnosis of epigastric pain           Peptic ulcer Gastritis Stomach cancer Gastroesophageal reflux disease Pancreatitis Hepatic congestion Cholecystitis Biliary colic Inferior myocardial infarction Referred pain (pleurisy.g.g. In the ulcerative form of gastric cancer the borders are irregular. When H. Bismuth compounds may actually reduce or even clear organisms. fibrinoid necrosis. Amoxicillin. pericarditis)  Superior mesenteric artery syndrome [edit]Treatment Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before EGD is undertaken. Surrounding mucosa may present radial folds. Ulcer margins are perpendicular and present chronic gastritis. though the warning labels of some bismuth subsalicylate products indicate that the product should not be used by someone with an ulcer.Gastric ulcers are most often localized on the lesser curvature of the stomach. produced by acid-pepsin aggression. The ulcer is a round to oval parietal defect ("hole"). pylori infection is present. the base of the ulcer shows 4 zones: inflammatory exudate. which may be a side-effect of the NSAIDs. Metronidazole) and 1 proton pump inhibitor (PPI). [edit]Microscopic appearance A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria. Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers. treatment-resistant cases. During the active phase. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis. amoxicillin + clarithromycin + metronidazole) .

injection. if necessary with other antibiotics. . An effective first-line therapy for uncomplicated cases would be Amoxicillin + Metronidazole +Pantoprazole (a PPI).[21] no data less than 20 20-40 40-60 60-80 80-100 100-120 120-140 140-160 160-180 180-200 200-220 more than 220 The lifetime risk for developing a peptic ulcer is approximately 10%. Prevalence is higher in third world countries. when epidemiological trends started to point to an impressive fall in its incidence. pylori.e. long-term higher dose PPIs are often used. Treatment of H. 80% at age 80 etc). 30% at age 30. H. surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete. [edit]Epidemiology Disability-adjusted life year for peptic ulcer disease per 100. contaminated groundwater. Transmission is by food. 20% at age 20.000 inhabitants in 2004.. abdominal pain or gastritis.may be used together with a PPI and sometimes with bismuth compound. pylori usually leads to clearing of infection. [23] The reason why the rates of peptic ulcer disease decreased is thought to be the development of new effective medication and acid suppressants and the discovery of the cause of the condition. In the absence of H. pylori.[22] In Western countries the prevalence of Helicobacter pylori infections roughly matches age (i. or clipping. and through human saliva (such as from kissing or sharing food utensils.)[citation needed] A minority of cases of Helicobacter infection will eventually lead to an ulcer and a larger proportion of people will get nonspecific discomfort. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery. Recurrence of infection can occur and retreatment may be required. relief of symptoms and eventual healing of ulcers. Since the widespread use of PPI's in the 1990s. Peptic ulcer disease had a tremendous effect on morbidity and mortality until the last decades of the 20th century. Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation.

in the recent past. actively eliminates the H. thus causing the development of the gastric ulcers. and that health can be greatly improved and money saved by disseminating information about H. but he took antibiotics to kill the remaining bacteria at the urging of his wife. the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Dr. multiple subsequent studies have found no effect of using mastic gum on reducing H.[27] The H. It was a previously widely accepted misunderstanding that the use of chewing gum resulted in gastric ulcers. and industry. [24] [edit]History See also: Timeline of peptic ulcer disease and Helicobacter pylori John Lykoudis. long before it was commonly recognized that bacteria were a dominant cause for the disease. since halitosis is one of the symptoms of infection. Marshall as a causative factor for ulcers. Marshall and his long-time collaborator Dr.000 deaths per year in the United States are due to duodenal ulcer and 3.[31] However. some believed that natural tree resin extract. treated patients for peptic ulcer disease with antibiotics. The medical profession believed that this was because the action of masticating on gum caused the over-stimulation of the production of hydrochloric acid in the stomach. pyloribacteria. This campaign reinforced the news that ulcers are a curable infection. Western Australia. or hyperchlorhydria was then believed to cause erosion of the stomach lining in the absence of food.[29] In 2005. Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease". pylori.[25] Helicobacter pylori was rediscovered in 1982 by two Australian scientists.In the United States about 4 million people have active peptic ulcers and about 350. a general practitioner in Greece. not by stress or spicy food as had been assumed before.[28] This experiment was published in 1984 in the Australian Medical Journal and is among the most cited articles from the journal. with other government agencies.[citation needed] so in an act of self-experimentation Marshall drank a Petri dish containing a culture of organisms extracted from a patient and soon developed gastritis. pylori and ulcers.[26] In their original paper. pylori levels. mastic gum.[30] On the other hand. pylori and runs a molecular biology lab at UWA in Perth.000 new cases are diagnosed each year. Robin Warren and Barry J. In 1997. the Centers for Disease Control and Prevention. Four times as many duodenal ulcers as gastric ulcers are diagnosed. Approximately 3. beginning in 1958.000 to gastric ulcer. Professor Marshall continues research related to H. The low (acidic) pH (pH 2). pylori hypothesis was poorly received. Warren and Marshall contended that most stomach ulcers and gastritis were caused by colonization with this bacterium. launched a national education campaign to inform health care providers and consumers about the link between H. His symptoms disappeared after two weeks. academic institutions.[32][33] .

Barik. researchers added stomach acid to the list of causes and began treating ulcers with antacids. PMID 1570818.S. "Meta-analysis of Risk Factors for Peptic Ulcer: Nonsteroidal Antiinflammatory Drugs.1989. Dobek. "Predictors of duodenal ulcer healing and relapse. Retrieved 2010/06/18. with cigarette smoking acting as a synergistic co-factor. (Major). ^ Sonnenberg in his study cautiously concludes that. Journal of Gastroenterology 81 (6): 1061±1067.D. Ersan Sander (June 2007). Strohmeyer G. 5. NSAIDS. ^ "Peptic ulcer". 9. .D. Peter P. M. Y. Schmid P. ^ Cullen DJ. PMID 2801677.M. and Smoking: Risk Factors for Peptic Ulcer Disease".[edit]Notes 1. Arthus S. Retrieved 2007-10-10.. 2..C. ^ http://www. PMID 7026344. Helicobacter pylori. ^ Martin. American Journal of Gastroenterology 84 (10): 1268±1272. M Fatih Abasiyanik. PMID 9013343. U. U. 4. Vogel E.PMID 17589905.tb06166. Ph. David F. Retrieved 2010-03-18. Blum AL (1981).... and alcohol. 3. 8. (28 Jun 2008). ^ "Ulcer Disease Facts and Myths".F. Aki N. et al. Retrieved 2010-03-18. U. M. PMC 1891536.S. PMID 1570818. Hawkey GM. Retrieved 2010-03-18. ^ For nearly 100 years.merck. Ikuko. Sonnenberg. pylori. ^ Kato. World Journal of Gastroenterology 13 (23): 3245± 3248. ^ a b Salih. Colonel David A. "Peptic ulcer disease".C. 10. 8 indicate that 89% of all serious upper GI disease can be accounted for by NSAIDs and H.x.1111/j. M. 7.. Retrieved 2010-03-18. ^ "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Nizamettin Bayyurt. Geoffrey A.H.". ^ a b "GI Consult: Perforated Peptic Ulcer". John H.P. American Journal of Epidemiology 135 (5): 521± 530.A. Later. (Jan 1997). National Digestive Diseases Information Clearinghouse 14. and Smoking".. Gut 41 (4): 459±62.A. 12. M. Nomura. Retrieved 2007-08-26.. Treatment involved bed rest and a bland diet. "Campylobacter pylori. and Diet". PMID 17589905.html ^ Johannessen T.PMID 9013343. Alcohol. PMID 9391242.S. ^ Kurata 1997 explains that "Data in Fig. ^ "Peptic Ulcer". Grant N. 1066) [edit]References 1. 13. among other potential factors that were found to correlate to ulcer healing. Gonvers JJ. Stemmermann and Po-Huang Chyou (1992). F. scientists and doctors thought that ulcers were caused by stress.C. "moderate alcohol intake might [also] favor ulcer healing" (p. ^ A.com/mmhe/sec09/ch121/ch121c.A. Abraham M. "Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs". Patrissi. Greenwood DC. (1997). "H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: A retrospective study". Nogawa.A.A.C. Captain Elizabeth Montgomery.15720241. Retrieved 2010/06/18.M. Retrieved 2010/06/18. Journal of Clinical Gastroenterology 24 (1): 2±17. Müller-Lissner SA. doi:10. Pasienthandboka. 11."(14) 2.G. "A Prospective Study of Gastric and Duodenal Ulcer and Its Relation to Smoking. 6. spicy food.S. ^ Kurata Ph. Peura.

29. 1974) 31. PMID 16336147. PMID 18837773. Antimicrob. Retrieved 2010/06/18.doi:10. The general practitioner in Greece who in 1958 discovered the etiology of.ISBN 0-86793-035-7. (1984). (2003). (1983). doi:10. 20. "Emerging and reemerging diseases: a historical perspective". [edit]External links   Endoscopy Video of a deep gastric ulcer Gastric Ulcer Radiology and Endoscopy from MedPix . ^ Marshall B. ^ "Epidemiology of peptic ulcer disease". Gastroenterol. Retrieved 2010/06/18. ^ Medicine for Nurses (Toohey. Retrieved 2007-08-26. Gregory AT (2005). PMID 12562704.1600-065X. ^ "Peptic ulcer disease". Scand. "The 2005 Nobel Prize in physiology or medicine".. ^ Wachirawat W. 2009. Jenks PJ (February 2003). ^ Marshall B. Med. ^ Kim YH. 24. 339 (26): 1946.J. Cockayne A.x. ^ Loughlin MF. "Mastic gum kills Helicobacter pylori [Letter to the editor.00677. 19. Lancet 1(8390): 1311±5. World Health Organization. 183 (11±12): 612±4. Suriyawongpaisal P. N. 28. Ala'Aldeen DA. "Mastic gum has no effect on Helicobacter pylori load in vivo". Chemother. 11. Papavasassiliou. ^ Marshall B. J. "Helicobacter Pioneers: Firsthand accounts from the scientists who discovered helicobacters. ^ "Peptic Ulcer". Ala'Aldeen D. ^ Bebb JR. Immunol. Basil Rigas. (2002). PMID 9874617. PMID 12948263. "Long-term stress and Helicobacter pylori infection independently induce gastric mucosal lesions in C57BL/6 mice". 21.1080/003655202761020515. Diagnosis and Treatment . Retrieved 2010/06/18. "Unidentified curved bacillus on gastric epithelium in active chronic gastritis". "Unidentified curved bacilli in the stomach patients with gastritis and peptic ulceration". Aust. 225: 9± 26. doi:10. "Monotherapy with mastic does not eradicate Helicobacter pylori infection from mice". Atherton JC (September 2003). (2002). 22. J. Retrieved 2008-09-06. doi:10. Rev. ^ "Tests and diagnosis". Retrieved 2010/06/18. et al. Efstathios D. PMID 6145023. J. 32. 33.1016/S0140-6736(84)91816-6. peptic ulcer disease.1111/j. 17. 26. ^ "Peptic ulcer". Retrieved 2010/06/18. PMID 12888582. Hanucharurnkul S. 51 (2): 367±71. ^ "ATLAS OF PATHOLOGY".J. Engl.2008. Med. 1892± 1982". Retrieved Nov. but not Helicobacter pylori. 23. Lee SS. J. Bailey-Flitter N. ^ Huwez FU. 27.CDC Bacterial. "Stress.1093/jac/dkg366. doi:10. Chemother. Thirlwell D.. 2009.15. 52 (3): 522±3.1093/jac/dkg057. J Med Assoc Thai 86 (7): 672±85. Mycotic Diseases 30. ^ Van Der Weyden MB. John Lykoudis. ed. Armstrong RM. Lee JH. not a peer-reviewed scientific article"]. Antimicrob. 16. and a treatment for. 25. et al. 18. 37 (11): 1259± 64. ^ Snowden FM (October 2008). ^ "WHO Disease and injury country estimates". Lancet 1 (8336): 1273± 5. Warren J. PMID 12465722. is associated with peptic ulcer disease in a Thai population". See also their corrections in the next volume.J. ^ Ulcer.J. Ala'Aldeen DA (December 1998).PMID 6134060.R.

[show] v‡d‡e Infectious diseases · Bacterial diseases: Proteobacterial G. stomach and duodenum .(primarily A00±A79. 080±109) [show] v‡d‡e Digestive system · Digestive disease · Gastroenterology (primarily K20±K93. 530±579) Categories: Abdominal pain | Diseases of oesophagus. 001±041.

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