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Official reprint from UpToDate www.uptodate.com ©2014 UpToDate

AuthorSheila E Crowe, MD,FRCPC, FACP, FACG,AGAF

Section EditorMark Feldman, MD, MACP,AGAF, FACG

Deputy EditorShilpa Grover, MD, MPH

Management of duodenal ulcers in patients infected with Helicobacter pylori

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Nov 2014. | This topic last updated: Nov 22, 2013.

INTRODUCTION — Peptic ulcer disease continues to be a common problem, although the incidence of duodenal

ulcers has declined in recent decades [1]. Different factors have been implicated as etiologies for DUs, including

diet, stress, smoking, and overproduction of gastric acid. However, the majority of patients with duodenal ulcers

(DU) are infected with Helicobacter pylori (H. pylori). (See "Association between Helicobacter pylori infection and

duodenal ulcer".)

The management of patients with H. pylori infection and DU disease will be reviewed here. Other aspects of H.

pylori infection are discussed separately.

ERADICATION OF H. PYLORI — All patients with duodenal ulcers (DUs) associated with H. pylori infection should

undergo therapy to eradicate the organism [2-4]. (See 'Treatment regimens for H. pylori' below.) This

recommendation is based upon overwhelming data showing that cure of H. pylori infection reduces ulcer recurrence

and complications such as bleeding [5-8]. In a study of 100 infected patients with DU, eradication of the infection

was associated with a higher rate of healing (92 versus 61 percent when H. pylori persisted after treatment) and a

lower rate of recurrence during a 12-month follow-up (21 versus 84 percent). (See 'Disease recurrence' below.)

Empiric treatment versus specific testing — In settings where the prevalence of H. pylori in DU is greater than

90 percent [9,10], empiric therapy for the infection is reasonable for uncomplicated cases [11].

In the United States, the prevalence of H. pylori in DU appears to be considerably less than 90 percent. (See

"Unusual causes of peptic ulcer disease".) The prevalence of H. pylori is also lower in patients with complicated

DUs (ie, those complicated by bleeding or perforation) compared with those with uncomplicated disease [12-14].

Patients with H. pylori negative ulcers appear to have a significantly worse outcome especially if treated empirically

for infection [15]. Thus, documenting infection in patients with DU (uncomplicated or complicated) is an appropriate

caution prior to initiating antimicrobial therapy. (See "Indications and diagnostic tests for Helicobacter pylori

infection".)

Uncomplicated duodenal ulcers — Patients with uncomplicated DUs should receive anti-H. pylori therapy if the

organism is present. Although, the eradication of H. pylori without concurrent acid suppression therapy is capable

of healing DUs [16], acid suppression has long been the mainstay of therapy. An intragastric pH >3 for 18 to 20

hours per day will heal nearly all duodenal ulcers within four weeks [17]; suppression of nocturnal acid secretion

appears to be the most important factor in ulcer healing [18]. Acid suppression can be discontinued in patients with

uncomplicated DUs after four weeks.

Complicated duodenal ulcers — Similar to patients with uncomplicated DUs, those with complicated DUs

should receive anti-H. pylori therapy if the organism is present [19-21].

Whether antisecretory medication should be continued after H. pylori eradication in patients with complicated

duodenal ulcers is controversial. While some studies have suggested that elimination of the infection alone is

sufficient [19-21], at least three consensus panels have addressed this issue, and recommended maintenance acid

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suppression following H. pylori eradication in patients with a complicated DU [2,22,23]. This is particularly important

if nonsteroidal antiinflammatory drugs (NSAIDs) were implicated as a possible cause, and if they are to be restarted

[24]. Most complicated ulcers occur in those using aspirin and NSAIDs and many patients continue to use these

medications despite physicians' best efforts at counseling against this. As a result, continuing acid suppression

indefinitely makes clinical if not economic sense.

There is general agreement that these patients should undergo follow-up testing at least four weeks after the

completion of H. pylori therapy to assess eradication of the infection. Patients can be switched to H2 receptor

antagonists (H2RAs) for several weeks prior to noninvasive H. pylori testing, since maintenance PPIs can affect test

results. (See "Indications and diagnostic tests for Helicobacter pylori infection".)

Factors influencing treatment outcome — Patient compliance with treatment is critical to the successful

eradication of H. pylori. An illustrative study evaluated the efficacy of triple therapy for H. pylori [25]. Compliance

was the most important factor predicting success; successful eradication occurred in 96 percent of patients who

took more than 60 percent of the prescribed medications versus 69 percent in patients who took less. (See "Patient

information: Helicobacter pylori infection and treatment (Beyond the Basics)" and "Patient information: Peptic ulcer

disease (Beyond the Basics)".)

Factors other than compliance may also influence treatment outcome. As an example, tobacco smoking may slow

DU healing. However, once H. pylori is eradicated and the ulcer has healed, smoking does not increase the risk of

ulcer relapse [26].

It has been suggested that pretreatment with a proton pump inhibitor could decrease the efficacy of H. pylori

eradication. However, the data clearly show no change in eradication rates or ulcer recurrence at one year in

patients treated with proton pump inhibitors prior to anti-H. pylori therapy [27,28].

Disease recurrence — Multiple studies have evaluated the rate of disease recurrence following eradication of H.

pylori [5-7]. In one meta-analysis, recurrence of DU (as determined endoscopically) occurred in less than 10

percent of patients following H. pylori eradication versus 65 to 95 percent in those who remained infected [6]. A

higher rate of endoscopic recurrence (20 percent within six months of eradication of H. pylori in patients with no

evidence of NSAID use) was found in another meta-analysis but the outcome was still better than in patients who

remained infected (56 percent recurrence) [7]. Some studies have found lower relapse rates (as low as 2 percent

per year), particularly outside the United States, or when recurrence was defined symptomatically rather than

endoscopically [7,29].

Ulcer recurrence following eradication of H. pylori is not usually due to recurrent H. pylori infection [7,29]. Among

the factors that can contribute are NSAID use and continued acid hypersecretion (table 1) [29]. Maintenance

antisecretory treatment may be necessary to prevent relapse in this subset of patients.

Nonsteroidal antiinflammatory drugs — H. pylori infection and nonsteroidal antiinflammatory drugs (NSAIDs)

can act synergistically to cause ulcers. (See "NSAIDs (including aspirin): Pathogenesis of gastroduodenal

toxicity".) NSAID users with a history of DU disease should be tested and treated for H. pylori if they are infected.

There are also data suggesting that testing and treating (if positive) all patients for H. pylori prior to beginning NSAID

use may be warranted [30,31], although this is not currently the standard of care or of confirmed benefit [32].

Patients with a duodenal ulcer should avoid NSAIDs whenever possible. However, for those who require NSAIDs, we

recommended maintenance PPI treatment as long as the NSAID is continued to reduce recurrent ulcer risk. (See

"NSAIDs (including aspirin): Pathogenesis of gastroduodenal toxicity".)

Recently bleeding gastric or duodenal ulcers — The accuracy of various methods to detect H. pylori may be

affected in the presence of recent gastrointestinal bleeding. Recommendations for H. pylori testing in this setting

are presented separately. (See "Indications and diagnostic tests for Helicobacter pylori infection".)

TREATMENT REGIMENS FOR H. PYLORI — Multiple regimens have been evaluated for H. pylori therapy (table 2)

[33,34]. Eradication rates with the original bismuth triple regimens (bismuth, metronidazole, and either tetracycline

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or amoxicillin) are in the range of 75 to 90 percent [35,36]. The optimal therapeutic regimen has not yet been

defined. Treatment should be effective, but considerations such as cost, side effects, and ease of administration

must also be taken into account. (See "Treatment regimens for Helicobacter pylori".)

TESTING FOR H. PYLORI FOLLOWING ERADICATION — The issue of testing for H. pylori following eradication

is discussed separately. (See "Indications and diagnostic tests for Helicobacter pylori infection".)

COST-EFFECTIVENESS OF ERADICATING H. PYLORI — As noted above, eradication of H. pylori at the time of

initial ulcer diagnosis facilitates healing. It is the most cost-effective long-term treatment of duodenal ulcer (DU)

disease [37-40]. One report, for example, estimated that the cost for DU management in an individual patient over

the course of 15 years is about $1000 for H. pylori eradication [39]. The estimated costs of intermittent acid-

suppression therapy ($10,350), maintenance acid suppression therapy ($11,186), and vagotomy ($17,661) were

much higher. A systematic review of 27 randomized controlled trials comparing H. pylori eradication to no treatment

in a total of 2509 patients after DU healing demonstrated an 80 percent decrease in the risk of relapse with H. pylori

eradication (RR 0.2, 95% CI 0.15-0.26) [41]. The number needed to treat to prevent one ulcer relapse was only two.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and

"Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5 to 6 grade

reading level, and they answer the four or five key questions a patient might have about a given condition. These

articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the

Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the

10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with

some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these

topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on

"patient info" and the keyword(s) of interest.)

Basics topics (see "Patient information: Peptic ulcers (The Basics)" and "Patient information: H. pylori

infection (The Basics)")

Beyond the Basics topics (see "Patient information: Peptic ulcer disease (Beyond the Basics)" and "Patient

information: Helicobacter pylori infection and treatment (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Patients with a duodenal ulcer (DU) should be tested for Helicobacter pylori (H. pylori).

We recommend patients who test positively should be treated with eradication therapy (Grade 1A). We also

suggest concomitant treatment with acid suppression for both patients with uncomplicated (Grade 2B) and

complicated (ie, those presenting with bleeding or perforation) ulcers (Grade 1B). (See "Treatment regimens

for Helicobacter pylori".)

Acid suppression can be discontinued in patients with uncomplicated DU after four weeks. However,

maintenance acid suppression (even after successful H. pylori eradication) may be appropriate in those with

complicated DU since cure of infection reduces but does not totally eliminate subsequent complications.

The most appropriate acid suppression is a once daily dose of a proton pump inhibitor (PPI) since PPIs are

more effective than H2 receptor antagonists (H2RAs) in maintaining pH >3, especially in H. pylori negative

individuals. Maintenance treatment should be continued indefinitely.

The accuracy of various methods to detect H. pylori may be affected in the presence of recent

gastrointestinal bleeding. Recommendations for H. pylori testing in this setting are presented separately.

(See "Indications and diagnostic tests for Helicobacter pylori infection".)

th th

th th

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The rate of successful treatment depends largely upon patient compliance. Thus, patients need to be

educated and involved in the decision making process. (See "Patient information: Helicobacter pylori

infection and treatment (Beyond the Basics)" and "Patient information: Peptic ulcer disease (Beyond the

Basics)".) Confirmation of eradication is reasonable because of the availability of accurate, relatively

inexpensive noninvasive tests (stool and breath tests). (See "Indications and diagnostic tests for

Helicobacter pylori infection".)

Patients with a duodenal ulcer should avoid NSAIDs whenever possible. However, for those who require

NSAIDs we recommended maintenance PPI treatment as long as the NSAID is continued to reduce

recurrent ulcer risk (Grade 1A). (See "NSAIDs (including aspirin): Secondary prevention of gastroduodenal

toxicity".)

Individuals who have frequent recurrence of ulcers or complications especially in the absence of H. pylori

infection or NSAID use should be evaluated for a condition associated with gastric acid hypersecretion such

as Zollinger-Ellison syndrome. (See "Unusual causes of peptic ulcer disease".)

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REFERENCES

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2. NIH Consensus Conference. Helicobacter pylori in peptic ulcer disease. NIH Consensus Development Panelon Helicobacter pylori in Peptic Ulcer Disease. JAMA 1994; 272:65.

3. Malfertheiner P, Megraud F, O'Morain C, et al. Current concepts in the management of Helicobacter pyloriinfection: the Maastricht III Consensus Report. Gut 2007; 56:772.

4. Chey WD, Wong BC, Practice Parameters Committee of the American College of Gastroenterology.American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am JGastroenterol 2007; 102:1808.

5. Marshall BJ, Goodwin CS, Warren JR, et al. Prospective double-blind trial of duodenal ulcer relapse aftereradication of Campylobacter pylori. Lancet 1988; 2:1437.

6. Hopkins RJ, Girardi LS, Turney EA. Relationship between Helicobacter pylori eradication and reducedduodenal and gastric ulcer recurrence: a review. Gastroenterology 1996; 110:1244.

7. Laine L, Hopkins RJ, Girardi LS. Has the impact of Helicobacter pylori therapy on ulcer recurrence in theUnited States been overstated? A meta-analysis of rigorously designed trials. Am J Gastroenterol 1998;93:1409.

8. Sonnenberg A, Olson CA, Zhang J. The effect of antibiotic therapy on bleeding from duodenal ulcer. Am JGastroenterol 1999; 94:950.

9. Borody TJ, George LL, Brandl S, et al. Helicobacter pylori-negative duodenal ulcer. Am J Gastroenterol 1991;86:1154.

10. Tytgat G, Langenberg W, Rauws E, Rietra P. Campylobacter-like organism (CLO) in the human stomach.Gastroenterology 1985; 88:1620.

11. Greenberg PD, Koch J, Cello JP. Clinical utility and cost effectiveness of Helicobacter pylori testing forpatients with duodenal and gastric ulcers. Am J Gastroenterol 1996; 91:228.

12. Reinbach DH, Cruickshank G, McColl KE. Acute perforated duodenal ulcer is not associated withHelicobacter pylori infection. Gut 1993; 34:1344.

13. Laine LA. Helicobacter pylori and complicated ulcer disease. Am J Med 1996; 100:52S.

14. Zelickson MS, Bronder CM, Johnson BL, et al. Helicobacter pylori is not the predominant etiology for pepticulcers requiring operation. Am Surg 2011; 77:1054.

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15. Bytzer P, Teglbjaerg PS, Danish Ulcer Study Group. Helicobacter pylori-negative duodenal ulcers:prevalence, clinical characteristics, and prognosis--results from a randomized trial with 2-year follow-up. Am JGastroenterol 2001; 96:1409.

16. Lam SK, Ching CK, Lai KC, et al. Does treatment of Helicobacter pylori with antibiotics alone heal duodenalulcer? A randomised double blind placebo controlled study. Gut 1997; 41:43.

17. Burget DW, Chiverton SG, Hunt RH. Is there an optimal degree of acid suppression for healing of duodenalulcers? A model of the relationship between ulcer healing and acid suppression. Gastroenterology 1990;99:345.

18. Jones DB, Howden CW, Burget DW, et al. Acid suppression in duodenal ulcer: a meta-analysis to defineoptimal dosing with antisecretory drugs. Gut 1987; 28:1120.

19. Graham DY, Hepps KS, Ramirez FC, et al. Treatment of Helicobacter pylori reduces the rate of rebleeding inpeptic ulcer disease. Scand J Gastroenterol 1993; 28:939.

20. Labenz J, Börsch G. Role of Helicobacter pylori eradication in the prevention of peptic ulcer bleeding relapse.Digestion 1994; 55:19.

21. Vergara M, Casellas F, Saperas E, et al. Helicobacter pylori eradication prevents recurrence from peptic ulcerhaemorrhage. Eur J Gastroenterol Hepatol 2000; 12:733.

22. Buckley M, Culhane A, Drumm B, et al. Guidelines for the management of Helicobacter pylori-related uppergastrointestinal diseases. Irish Helicobacter Pylori Study Group. Ir J Med Sci 1996; 165 Suppl 5:1.

23. Professional Advisory Panel (CRAG) and Scottish Intercollegiate Guidelines Network (SIGN). Helicobacterpylori eradication therapy in dyspeptic disease: A clinical guideline. 1996.

24. Chan FK, Chung SC, Suen BY, et al. Preventing recurrent upper gastrointestinal bleeding in patients withHelicobacter pylori infection who are taking low-dose aspirin or naproxen. N Engl J Med 2001; 344:967.

25. Graham DY, Lew GM, Malaty HM, et al. Factors influencing the eradication of Helicobacter pylori with tripletherapy. Gastroenterology 1992; 102:493.

26. Chan FK, Sung JJ, Lee YT, et al. Does smoking predispose to peptic ulcer relapse after eradication ofHelicobacter pylori? Am J Gastroenterol 1997; 92:442.

27. Annibale B, D'Ambra G, Luzzi I, et al. Does pretreatment with omeprazole decrease the chance oferadication of Helicobacter pylori in peptic ulcer patients? Am J Gastroenterol 1997; 92:790.

28. Adamek RJ, Szymanski C, Pfaffenbach B. Pantoprazole suppresses Helicobacter pylori without affectingcure. Helicobacter 1999; 4:266.

29. Harris AW, Gummett PA, Phull PS, et al. Recurrence of duodenal ulcer after Helicobacter pylori eradicationis related to high acid output. Aliment Pharmacol Ther 1997; 11:331.

30. Chan FK, Sung JJ, Chung SC, et al. Randomised trial of eradication of Helicobacter pylori before non-steroidal anti-inflammatory drug therapy to prevent peptic ulcers. Lancet 1997; 350:975.

31. Chan FK, To KF, Wu JC, et al. Eradication of Helicobacter pylori and risk of peptic ulcers in patients startinglong-term treatment with non-steroidal anti-inflammatory drugs: a randomised trial. Lancet 2002; 359:9.

32. Hawkey CJ, Tulassay Z, Szczepanski L, et al. Randomised controlled trial of Helicobacter pylori eradicationin patients on non-steroidal anti-inflammatory drugs: HELP NSAIDs study. Helicobacter Eradication forLesion Prevention. Lancet 1998; 352:1016.

33. Laheij RJ, Rossum LG, Jansen JB, et al. Evaluation of treatment regimens to cure Helicobacter pyloriinfection--a meta-analysis. Aliment Pharmacol Ther 1999; 13:857.

34. Hojo M, Miwa H, Nagahara A, Sato N. Pooled analysis on the efficacy of the second-line treatment regimensfor Helicobacter pylori infection. Scand J Gastroenterol 2001; 36:690.

35. Soll AH. Consensus conference. Medical treatment of peptic ulcer disease. Practice guidelines. PracticeParameters Committee of the American College of Gastroenterology. JAMA 1996; 275:622.

36. Walsh JH, Peterson WL. The treatment of Helicobacter pylori infection in the management of peptic ulcerdisease. N Engl J Med 1995; 333:984.

37. Imperiale TF, Speroff T, Cebul RD, McCullough AJ. A cost analysis of alternative treatments for duodenal

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ulcer. Ann Intern Med 1995; 123:665.

38. O'Brien B, Goeree R, Mohamed AH, Hunt R. Cost-effectiveness of Helicobacter pylori eradication for the long-term management of duodenal ulcer in Canada. Arch Intern Med 1995; 155:1958.

39. Sonnenberg A, Townsend WF. Costs of duodenal ulcer therapy with antibiotics. Arch Intern Med 1995;155:922.

40. Sonnenberg A, Schwartz JS, Cutler AF, et al. Cost savings in duodenal ulcer therapy through Helicobacterpylori eradication compared with conventional therapies: results of a randomized, double-blind, multicentertrial. Gastrointestinal Utilization Trial Study Group. Arch Intern Med 1998; 158:852.

41. Ford A, Delaney B, Forman D, Moayyedi P. Eradication therapy for peptic ulcer disease in Helicobacterpylori positive patients. Cochrane Database Syst Rev 2004; :CD003840.

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GRAPHICS

Causes of refractory or recurrent peptic ulcer disease

Persisting H. pylori infection

Poor compliance with treatment

Resistant organism

Inadequate H. pylori regimen

Unrecognized H. pylori infection:

False negative H. pylori testing

Skipped or inadequate testing

Ulcers related to nonsteroidal antiinflammatory drugs (NSAIDs)

Continued NSAID use

Undiscovered NSAID use

Poor response to PPI co-therapy

Other mechanisms

Impaired healing:

Dense fibrosis

C igarette smoking, especially heavy

Giant ulcer

Inadequate inhibition of acid secretion:

Non-compliance

Pharmacologic resistance to histamine type 2 receptor antagonists (H2RAs) or PPIs

Rapid PPI metabolizers

Tolerance to H2RAs

Hypersecretory states:

Gastrinoma

Antral G cell hyperfunction

Idiopathic hypersecretory duodenal ulcer

Comorbid conditions:

Uremia

Cirrhosis

Catabolic state

Pulmonary or multisystem failure

Co-therapies:

Glucocorticoids

Cytotoxic drugs

Other drugs, such as methamphetamine or cocaine use

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Uncommon causes:

Cancer

Crohn disease

Infections other than H. pylori

Eosinophilic and other inflammatory conditions

H. pylori: Helicobacter pylori; PPI: proton pump inhibitor.

Graphic 76314 Version 6.0

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American College of Gastroenterology first-line H. pylori regimens

(adult dosing, oral administration)

Patients who are not allergic to penicillin and

have not previously received a macrolide

Standard dose PPI* twice daily (or

esomeprazole 40 mg once daily) plus

clarithromycin 500 mg twice daily, and

amoxicillin 1000 mg twice daily for 10-14

days

Patients who are allergic to penicillin, and

who have not previously received a macrolide

or metronidazole or are unable to tolerate

bismuth quadruple therapy

Standard dose PPI twice daily, clarithromycin

500 mg twice daily, metronidazole 500 mg

twice daily for 10-14 days

Patients who are allergic to penicillin or failed

one course (above) of H. pylori treatment

Bismuth subsalicylate 525 mg four times

daily, metronidazole 250 mg four times daily,

tetracycline 500 mg four times daily, standard

dose PPI* twice daily for 10-14 days

OR

Bismuth subcitrate 420 mg four times daily,

metronidazole 375 mg four times daily,

tetracycline 375 mg four times daily ,

standard dose PPI* twice daily for 10-14

days

H. pylori: Helicobacter pylori; PPI: proton pump inhibitor.

* Lansoprazole 30 mg twice daily, omeprazole 20 mg twice daily, pantoprazole 40 mg twice daily,

or rabeprazole 20 mg twice daily.

• Eradication rates of 70 to 85 percent.

Δ Eradication rates of 75 to 90 percent.

◊ A combination preparation of bismuth subcitrate-metronidazole-tetracycline is available in the

United States (trade name Pylera).

Table adapted from data published in: Chey WD, Wong BCY. American College of Gastroenterology

Guideline on the Management of Helicobacter pylori Infection. Am J Gastroenterol 2007; 102:1808.

Graphic 65237 Version 5.0

•

•

Δ

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Δ

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Disclosures: Sheila E Crowe, MD, FRCPC, FACP, FACG, AGAF Nothing to disclose. Mark Feldman,MD, MACP, AGAF, FACG Nothing to disclose. Shilpa Grover, MD, MPH Employee of UpToDate, Inc.

Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, theseare addressed by vetting through a multi-level review process, and through requirements for referencesto be provided to support the content. Appropriately referenced content is required of all authors andmust conform to UpToDate standards of evidence.

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