Helicobacter pylori eradication protocols

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Helicobacter pylori eradication protocols is a standard name for all treatment protocols for peptic ulcers and gastritis in the presence of Helicobacter pylori infection. The primary goal of the treatment is not only temporary relief of symptoms but also total elimination of H. pylori infection. Patients with active duodenal or gastric ulcers and those with a prior ulcer history should be tested for H. pylori. Appropriate therapy should be given for eradication. Patients with MALT lymphoma should also be tested and treated for H. pylori since eradication of this infection can induce remission in many patients when the tumor is limited to the stomach. Several consensus conferences, including the Maastricht Consensus Report, recommend testing and treating several other groups of patients but there is limited evidence of benefit. This includes patients diagnosed with gastric adenocarcinoma (especially those with early-stage disease), patients found to have atrophic gastritis or intestinal metaplasia, as well as first-degree relatives of patients with gastric adenocarcinoma since the relatives themselves are at increased risk of gastric cancer partly due to the intrafamilial transmission of H. pylori. To date, it remains controversial whether to test and treat all patients with functional dyspepsia, gastroesophageal reflux disease, or other non-GI disorders as well as asymptomatic individuals. [1]

Contents

Antibiotic resistance

The success of H. pylori cure depends on the type and duration of therapy, patient compliance and bacterial factors such as antibiotic resistance. Patients most often fail to respond to initial H. pylori eradication therapy because of noncompliance or antibiotic resistance. Patients should be queried about any side effects, missed doses, and completion of therapy. As culture with antibiotic sensitivities is not routinely performed when a H. pylori infection is diagnosed, it is generally recommended that different antibiotics be given at higher doses for 14 days. [2]

Regimens for Helicobacter pylori therapy

Achieving optimal eradication of H. pylori has proven difficult. Combination regimens that use two or three antibiotics with a proton pump inhibitor and/or bismuth are required to achieve adequate rates of eradication and to reduce the number of failures due to antibiotic resistance. In the United States, up to 50% of strains are resistant to metronidazole and 13% are resistant to clarithromycin. At present, experts disagree on the optimal regimen. [3]

First-line therapy: triple therapy

In areas of low clarithromycin resistance, including the United States, a 14-day course of "triple therapy" with an oral proton pump inhibitor, clarithromycin 500 mg, and amoxicillin 1 g (or, if penicillin allergic, metronidazole 500 mg), all given twice daily for 14 days, is recommended for first-line therapy. This regimen can achieve rates of eradication in up to 70% of cases. [4]

Second-line therapy: quadruple therapy

A 14-day course of "quadruple therapy" with a proton pump inhibitor, bismuth, tetracycline, and metronidazole or tinidazole is a more complicated but also more effective regimen. In a 2011 randomized, controlled trial, the per protocol eradication rates were 93% with quadruple therapy and 70% with triple therapy. Bismuth-based quadruple therapy is recommended as first line therapy for patients in areas with high clarithromycin resistance (> 20%), in patients who have previously been treated with a macrolide antibiotic, or as second-line therapy for patients whose infection persists after an initial course of triple therapy. Several studies reported eradication rates of > 90% using a 10-day sequential regimen consisting of four drugs: a proton pump inhibitor and amoxicillin for 5 days, followed by a proton pump inhibitor, clarithromycin, and tinidazole for 5 days. However, subsequent studies confirmed equivalent or superior efficacy when all four drugs were given concomitantly for 10 days (non-bismuth quadruple therapy). [5] [6]

Sequential therapy

Sequential therapy is a newer approach that combines a 5-day course of a "dual therapy" using a proton pump inhibitor in combination with amoxicillin, with a sequential second 5-day course of the standard "triple therapy". [3] High-dose dual therapy has comparable efficacy with bismuth-containing quadruple therapy, with fewer adverse effects and higher compliance. [7] Although initial studies promisingly reported higher eradication rates, [3] there is no superiority compared to the other therapies except in the presence of clarithromycin resistant organisms. In regions of high clarithromycin resistance, there is a high rate of eradication with a 14-day quadruple therapy consisting of a proton pump inhibitor, amoxicillin, clarithromycin, and nitroimidazole; still, the latter not available in the United States. [4]

Other proposed regimes

A number of other eradication regimens have been proposed. In the Table below they are compared to with standard regimes.

Comparison of Helicobacter pylori eradication regimens [8] [9]
RegimenDuration, daysDrugs usedNotes
Vonoprazan-amoxicillin dual therapy7-14 vonoprazan 20 mg bid and amoxicillin 750 mg bidAs successful as bismuth-containing quadruple therapy [10]
Triple therapy7–14PPI (standard dose) bid, amoxicillin 1 g bid and clarithromycin 0.5 g bidFirst line therapy in areas with low clarithromycin resistance
Sequential therapy101st 5 days: PPI (standard dose) bid and amoxicillin 1 g bid
2nd 5 days: metronidazole 0.5 g bid and clarithromycin 0.5 g bid		First line therapy
Concomitant therapy7–10PPI (standard dose bid), amoxicillin 1 g bid, metronidazole 0.5 g bid and clarithromycin 0.5 g bidFirst line therapy
Hybrid therapy141st week: PPI (standard dose) and amoxicillin 1 g bid
2nd week: PPI (standard dose), amoxicillin 1 g, metronidazole 0.5 g and clarithromycin 0.5 g bid		First line therapy
Bismuth-containing quadruple therapy10–14PPI (standard dose) bid, tetracycline 0.5 g qid, metronidazole 0.25 g qid and bismuth standard dose qidFirst line or second line therapy
Levofloxacin-based triple therapy10PPI (standard dose) bid, levofloxacin 0.5 g qid and amoxicillin 1 g bidSecond line therapy if there is no fluoroquinolone resistance
Culture-guided therapy10PPI (standard dose) bid, bismuth standard dose qid and two antibiotics selected by sensitivity testsThird line therapy if there is no fluoroquinolone resistance
Levofloxacin-based quadruple therapy10PPI (standard dose) bid, bismuth standard dose qid, levofloxacin 0.5 g qid and amoxicillin 1 g bidThird line therapy
High-dose dual PPI therapy14PPI (high dose) qid and amoxicillin 0.5 g qidThird line therapy
Rifabutin triple therapy14PPI (standard dose) bid, rifabutin 0.15 g bid and amoxicillin 1 g bidThird line therapy
Furazolidone-based quadruple therapy10-14PPI (standard dose) bid, bismuth standard dose qid, tetracycline 0.5 g bid and furazolidone 200 mg bidFirst line for penicillin-allergic patients

Note: bid – twice daily, qid – four times a day

Adjuvant therapies

Recent meta-analyses have proposed two adjuvant therapies which may help in the eradication of H. pylori. Periodontal therapy or what is known as scaling and root planing and probiotics both need further studies to confirm their adjuvant role.[ citation needed ]

Role of periodontal therapy

A 2016 systematic review has found that periodontal therapy may have a role as an added treatment for short- and long-term follow up. For these results to be confirmed with regards eradication and non-recurrence, larger studies need to be carried out. [11]

Role of probiotics

Some studies have recently evaluated the role of the yeast Saccharomyces boulardii as a coadjutant in the eradication of H. pylori and in the prevention of the secondary effects of antibiotic therapy such as antibiotic-associated diarrhea. A meta-analysis showed that supplementation with S. boulardii significantly increased the H. pylori eradication rate and reduced the risk of overall H. pylori therapy-related adverse effects. [12] In a cohort of patients in Korea who received S. boulardii for 4 weeks during and after a 1-week course of standard triple therapy, eradication rates were 10% higher than for those who did not receive the supplement.[ citation needed ]

Other studies in which Bifidobacterium spp. and Lactobacillus acidophilus have been administered revealed no significant difference in eradication rates in patients who were infected with strains susceptible to both antibiotics and who were treated with standard triple therapy. Further studies will be necessary to clarify the exact role of the probiotics in the eradication treatment. [13]

History

One of the first "eradication protocols", if not the first, was used by J. Robin Warren and Barry Marshall. Barry Marshall treated his own gastritis, which developed following intentional ingestion of H. pylori culture. He used bismuth salt and metronidazole. This treatment effectively cured his gastritis and eliminated the H. pylori infection. This is not the current eradication protocol.[ citation needed ]

One of the first "modern" eradication protocols was a one-week triple therapy, which the Sydney gastroenterologist Thomas Borody formulated in 1987. [14] As of 2006, a standard triple therapy is amoxicillin, clarithromycin, and a proton pump inhibitor such as omeprazole, [15] lansoprazole, pantoprazole, or esomeprazole. Protocols with metronidazole were also in use. [15] An example of a fixed-dose combination is PantoPac, containing pantoprazole, clarithromycin, and amoxicillin.[ citation needed ]

Research

Giving acetylcysteine before antibiotic treatment was effective in overcoming H. pylori antibiotic resistance in a study with 40 patients who had at least four eradication failures in their history. The researchers believe it works by inhibiting the formation of biofilm. [16]

Whereas the conventional proton pump inhibitor-based triple therapy is effective, there is research in using longer acid suppression therapies, in particular, using potassium competitive acid blocker triple and dual therapy. In particular, vonoprazan is approved by the US Food and Drug Administration (FDA) for H. pylori eradication. [17]

Related Research Articles

Peptic ulcer disease is a break in the inner lining of the stomach, the first part of the small intestine, or sometimes the lower esophagus. An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people with peptic ulcers have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

<i>Helicobacter pylori</i> Species of bacteria

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape, and these are less effective. Its helical body is thought to have evolved in order to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. The bacterium was first identified as the causal agent of gastric ulcers in 1983 by the Australian doctors Barry Marshall and Robin Warren.

<span class="mw-page-title-main">Pantoprazole</span> Stomach acid suppressing medication

Pantoprazole, sold under the brand name Protonix, among others, is a proton pump inhibitor used for the treatment of stomach ulcers, short-term treatment of erosive esophagitis due to gastroesophageal reflux disease (GERD), maintenance of healing of erosive esophagitis, and pathological hypersecretory conditions including Zollinger–Ellison syndrome. It may also be used along with other medications to eliminate Helicobacter pylori. Effectiveness is similar to other proton pump inhibitors (PPIs). It is available by mouth and by injection into a vein.

<span class="mw-page-title-main">Esomeprazole</span> Medication which reduces stomach acid

Esomeprazole, sold under the brand name Nexium [or Neksium] among others, is a medication which reduces stomach acid. It is used to treat gastroesophageal reflux disease, peptic ulcer disease, and Zollinger–Ellison syndrome. Its effectiveness is similar to that of other proton pump inhibitors (PPIs). It is taken by mouth or injection into a vein.

<span class="mw-page-title-main">Gastritis</span> Stomach disease

Gastritis is inflammation of the lining of the stomach. It may occur as a short episode or may be of a long duration. There may be no symptoms but, when symptoms are present, the most common is upper abdominal pain. Other possible symptoms include nausea and vomiting, bloating, loss of appetite and heartburn. Complications may include stomach bleeding, stomach ulcers, and stomach tumors. When due to autoimmune problems, low red blood cells due to not enough vitamin B12 may occur, a condition known as pernicious anemia.

<span class="mw-page-title-main">Achlorhydria</span> Medical condition

Achlorhydria and hypochlorhydria refer to states where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, respectively. It is associated with various other medical problems.

Timeline of peptic ulcer disease and <i>Helicobacter pylori</i>

This is a timeline of the events relating to the discovery that peptic ulcer disease and some cancers are caused by H. pylori. In 2005, Barry Marshall and Robin Warren were awarded the Nobel Prize in Physiology or Medicine for their discovery that peptic ulcer disease (PUD) was primarily caused by Helicobacter pylori, a bacterium with affinity for acidic environments, such as the stomach. As a result, PUD that is associated with H. pylori is currently treated with antibiotics used to eradicate the infection. For decades prior to their discovery, it was widely believed that PUD was caused by excess acid in the stomach. During this time, acid control was the primary method of treatment for PUD, to only partial success. Among other effects, it is now known that acid suppression alters the stomach milieu to make it less amenable to H. pylori infection.

<i>Saccharomyces boulardii</i> Species of fungus

Saccharomyces boulardii is a tropical yeast first isolated from lychee and mangosteen fruit peel in 1923 by French scientist Henri Boulard. Although early reports claimed distinct taxonomic, metabolic, and genetic properties, S. boulardii is genetically a grouping of S. cerevisiae strains, sharing >99% genomic relatedness, giving the synonym S. cerevisiae var. boulardii.

Helicobacter felis is a bacterial species in the Helicobacteraceae family, Campylobacterales order, Helicobacter genus. This bacterium is Gram-negative, microaerophilic, urease-positive, and spiral-shaped. Its type strain is CS1T. It can be pathogenic.

Helicobacter salomonis is a species within the Helicobacter genus of Gram-negative bacteria. Helicobacter pylori is by far the best known Helicobacter species primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the nonlymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases, although its role in the development of many of these other diseases requires further study. Humans infected with H. salomonis may develop some of the same gastrointestinal diseases viz., stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter bizzozeronii, Helicobacter suis, Helicobacter felis, and Helicobacter heilmannii s.s. Because of their disease associations, these four Helicobacter species plus H. salomonis are often group together and termed Helicobacter heilmannii sensu lato.

The drug combination bismuth subcitrate/metronidazole/tetracycline is used for the treatment of peptic ulcer with an infection by the bacterium Helicobacter pylori. It is taken by mouth.

<span class="mw-page-title-main">Vonoprazan</span> Chemical compound

Vonoprazan, sold under the brand name Voquezna among others, is a first-in-class potassium-competitive acid blocker medication. Vonoprazan is used in form of the fumarate for the treatment of gastroduodenal ulcer and reflux esophagitis, and can be combined with antibiotics for the eradication of Helicobacter pylori. It is a potassium-competitive acid blocker.

Bismuth subcitrate potassium is a bismuth salt used in combination with antibiotics and a proton pump inhibitor for the treatment of Helicobacter pylori infections.

Helicobacter heilmannii sensu lato refers to a group of bacterial species within the Helicobacter genus. The Helicobacter genus consists of at least 40 species of spiral-shaped flagellated, Gram-negative bacteria of which the by far most prominent and well-known species is Helicobacter pylori. H. pylori is associated with the development of gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and various subtypes of extranodal marginal zone lymphomas, e.g. those of the stomach, small intestines, large intestines, and rectum. H. pylori has also been associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study.

Helicobacter bizzozeronii is a species within the Helicobacter genus of Gram-negative bacteria. Helicobacter pylori is by far the best known Helicobacter species, primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the nonlymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study. Humans infected with H. bizzozeronii are prone to develop some of the same gastrointestinal diseases viz., stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter felis, Helicobacter salomonis, Helicobacter suis, and Helicobacter heilmannii s.s. Because of their disease associations, these four Helicobacter species plus H. bizzozeronii are often grouped together and termed Helicobacter heilmannii sensu lato.

Helicobacter suis is a species within the Helicobacter genus of Gram-negative bacteria. Helicobacter pylori is by far the best known Helicobacter species, primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the nonlymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectumn. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study. Humans infected with H. suis may develop some of the same gastrointestinal diseases - stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter bizzozeronii, Helicobacter salomonis, Helicobacter felis, and Helicobacter heilmannii s.s. Because of their disease associations, these four Helicobacter species plus H. suis are often group together and termed Helicobacter heilmannii sensu lato.

Helicobacter heilmannii s.s. is a species within the Helicobacter genus of Gram negative bacteria. Helicobacter pylori is by far the best known Helicobacter species primarily because humans infected with it may develop gastrointestinal tract diseases such as stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers of the non-lymphoma type, and various subtypes of extranodal marginal zone lymphomass, e.g. those of the stomach, small intestines, large intestines, and rectum. H. pylori is also associated with the development of bile duct cancer and has been associated with a wide range of other diseases although its role in the development of many of these other diseases requires further study. Humans infected with H. heilmannii s.s. may develop some of the same gastrointestinal diseases viz., stomach inflammation, stomach ulcers, duodenal ulcers, stomach cancers that are not lymphomas, and extranodal marginal B cell lymphomas of the stomach. Other non-H. pylori Helicobacter species that are known to be associated with these gastrointestinal diseases are Helicobacter bizzozeronii, Helicobacter suis, Helicobacter felis, and Helicobacter salomonis. Because of their disease associations, these four Helicobacter species plus H. heilmannii s.s. are often group together and termed Helicobacter heilmannii sensu lato.

Ranitidine bismuth citrate - drug, which has antisecretory and bactericidal action.

Vonoprazan/amoxicillin/clarithromycin, sold under the brand name Vonosap among others, is a co-packaged medication used for the treatment of Helicobacter pylori infection. It contains vonoprazan, a potassium-competitive acid blocker; amoxicillin, a beta-lactam antibiotic; and clarithromycin, a macrolide antibiotic.

<span class="mw-page-title-main">Vonoprazan/amoxicillin</span> Combination medication

Vonoprazan/amoxicillin, sold under the brand name Voquezna Dual Pak among others, is a co-packaged medication used for the treatment of Helicobacter pylori infection. It contains vonoprazan, a potassium-competitive acid blocker and amoxicillin, a beta-lactam antibiotic. It is taken by mouth.

References

  1. ↑ Chan FK, To KF, Wu JC, Yung MY, Leung WK, Kwok T, Hui Y, Chan HL, Chan CS, Hui E, Woo J, Sung JJ (5 January 2002). "Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-term treatment with non-steroidal anti-inflammatory drugs: a randomised trial". Lancet. 359 (9300): 9–13. doi:10.1016/s0140-6736(02)07272-0. PMID   11809180. S2CID   26114789.
  2. ↑ Sonnenberg A (June 2007). "Time trends of ulcer mortality in Europe". Gastroenterology. 132 (7): 2320–7. doi: 10.1053/j.gastro.2007.03.108 . PMID   17570207.
  3. 1 2 3 Gatta L, Vakil N, Vaira D, Scarpignato C (7 August 2013). "Global eradication rates for Helicobacter pylori infection: systematic review and meta-analysis of sequential therapy". BMJ (Clinical Research Ed.). 347: f4587. doi:10.1136/bmj.f4587. PMC   3736972 . PMID   23926315.
  4. 1 2 Malfertheiner P, Megraud F, O'Morain CA, Atherton J, Axon AT, Bazzoli F, Gensini GF, Gisbert JP, Graham DY, Rokkas T, El-Omar EM, Kuipers EJ (5 April 2012). "Management of Helicobacter pylori infection—the Maastricht IV/ Florence Consensus Report". Gut. 61 (5): 646–664. doi: 10.1136/gutjnl-2012-302084 . hdl: 1765/64813 . PMID   22491499.
  5. ↑ Molina-Infante J, Romano M, Fernandez-Bermejo M, Federico A, Gravina AG, Pozzati L, Garcia-Abadia E, Vinagre-Rodriguez G, Martinez-Alcala C, Hernandez-Alonso M, Miranda A, Iovene MR, Pazos-Pacheco C, Gisbert JP (July 2013). "Optimized nonbismuth quadruple therapies cure most patients with Helicobacter pylori infection in populations with high rates of antibiotic resistance". Gastroenterology. 145 (1): 121–128.e1. doi:10.1053/j.gastro.2013.03.050. PMID   23562754.
  6. ↑ Malfertheiner P, Megraud F, O'Morain C, Bazzoli F, El-Omar E, Graham D, Hunt R, Rokkas T, Vakil N, Kuipers EJ (June 2007). "Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report". Gut. 56 (6): 772–81. doi:10.1136/gut.2006.101634. PMC   1954853 . PMID   17170018.
  7. ↑ Wang H, Kong QZ, Li YY, Yang XY, Zuo XL (March 2024). "High-dose dual therapy versus bismuth-containing quadruple therapy for the eradication of Helicobacter pylori: A systematic review and meta-analysis". J Dig Dis. 25 (3): 163–175. doi:10.1111/1751-2980.13263. PMID   38577962.
  8. ↑ Urgesi R, Cianci R, Riccioni ME (2012). "Update on triple therapy for eradication of Helicobacter pylori: current status of the art". Clinical and Experimental Gastroenterology. 5: 151–157. doi: 10.2147/CEG.S25416 . PMC   3449761 . PMID   23028235.
  9. ↑ Rimbara E, Fischbach LA, Graham DY (2011). "Optimal therapy for Helicobacter pylori infections". Nat. Rev. Gastroenterol. Hepatol. 8 (2): 79–88. doi:10.1038/nrgastro.2010.210. PMID   21293508. S2CID   23529476.
  10. ↑ Zhou BG, Jiang X, Ding YB, She Q, Li YY (2024). "Vonoprazan-amoxicillin dual therapy versus bismuth-containing quadruple therapy for Helicobacter pylori eradication: A systematic review and meta-analysis". Helicobacter. 29 (1): e13040. doi:10.1111/hel.13040. PMID   37983865. S2CID   265308205.
  11. ↑ Ren Q, Yan X, Zhou Y, Li WX (7 February 2016). "Periodontal therapy as adjunctive treatment for gastric Helicobacter pylori infection". The Cochrane Database of Systematic Reviews. 2016 (2): CD009477. doi:10.1002/14651858.CD009477.pub2. PMC   8255095 . PMID   26852297.
  12. ↑ Szajewska H, Horvath A, Piwowarczyk A (2010). "Meta-analysis: the effects of Saccharomyces boulardii supplementation on Helicobacter pylori eradication rates and side effects during treatment". Aliment Pharmacol Ther. 32 (9): 1069–1079. doi: 10.1111/j.1365-2036.2010.04457.x . PMID   21039671. Archived from the original on 2019-09-02. Retrieved 2019-09-02.
  13. ↑ B Y, H A (2010). "Efficacy of probiotics in Helicobacter pylori eradication therapy". Turk J Gastroenterol. 21 (3): 212–217. doi:10.4318/tjg.2010.0090. PMID   20931422.
  14. ↑ Borody TJ, P. Cole, S. Noonan, A. Morgan, J. Lenne, L. Hyland, S. Brandl, E. G. Borody, L. L. George (October 16, 1989). "Recurrence of duodenal ulcer and Campylobacter pylori infection after eradication". Medical Journal of Australia. 151 (8): 431–435. doi:10.5694/j.1326-5377.1989.tb101251.x. PMID   2687668. S2CID   26066525.
  15. 1 2 Mirbagheri SA, Mehrdad Hasibi, Mehdi Abouzari, Armin Rashidi (August 14, 2006). "Triple, standard quadruple and ampicillin–sulbactam-based quadruple therapies for H pylori eradication: A comparative three-armed randomized clinical trial". World Journal of Gastroenterology. 12 (30): 4888–4891. doi: 10.3748/wjg.v12.i30.4888 . PMC   4087627 . PMID   16937475.
  16. ↑ Cammarota G, Branca G, Ardito F, Sanguinetti M, Ianiro G, Cianci R, Torelli R, Masala G, Gasbarrini A, Fadda G, Landolfi R, Gasbarrini G (2010). "Biofilm Demolition and Antibiotic Treatment to Eradicate Resistant Helicobacter pylori: A Clinical Trial". Clinical Gastroenterology and Hepatology. 8 (9): 817–820.e3. doi:10.1016/j.cgh.2010.05.006. PMID   20478402.
  17. ↑ Kanu JE, Soldera J (March 2024). "Treatment of Helicobacter pylori with potassium competitive acid blockers: A systematic review and meta-analysis". World J Gastroenterol. 30 (9): 1213–1223. doi: 10.3748/wjg.v30.i9.1213 . PMC   10989498 . PMID   38577188.

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