Eradication of <i>Helicobacter pylori</i> Does Not Reduce the Incidence of Gastroduodenal Ulcers in Patients on Long‐term NSAID Treatment: Double‐Blind, Randomized, Placebo‐Controlled Trial

Leest, H.T.J.I. de; Steen, K.S.S.; Lems, Willem F.; Bijlsma, J. W. J.; Laar, Mart A F J van de; Huisman, André; Vonkeman, Harald E.; Houben, Harry; Kadir, S.W.; Kostense, Piet J.; Tulder, Maurits W. van; Kuipers, Ernst J.; Boers, Maarten; Dijkmans, Ben A. C.

doi:10.1111/j.1523-5378.2007.00543.x

Cited by 57 publications

(35 citation statements)

References 34 publications

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“…Th e benefi t of H. pylori eradication in patients already taking NSAIDs is less clear ( 68 ). RCTs suggest that H. pylori eradication does not reduce the incidence of new peptic ulcers in chronic NSAID users ( 69 ) and that PPI therapy provides a more eff ective ulcer risk reduction strategy than H. pylori eradication in patients on chronic NSAIDs ( 66 ).…”

Section: Non-steroidal Anti-infl Ammatory Drug (Nsaid) Usementioning

confidence: 99%

ACG Clinical Guideline: Treatment of Helicobacter pylori Infection

Chey

Leontiadis

Howden

et al. 2017

American Journal of Gastroenterology

1,319

1,505

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Helicobacter pylori ( H. pylori ) infection is a common worldwide infection that is an important cause of peptic ulcer disease and gastric cancer. H. pylori may also have a role in uninvestigated and functional dyspepsia, ulcer risk in patients taking low-dose aspirin or starting therapy with a non-steroidal anti-infl ammatory medication, unexplained iron defi ciency anemia, and idiopathic thrombocytopenic purpura. While choosing a treatment regimen for H. pylori , patients should be asked about previous antibiotic exposure and this information should be incorporated into the decision-making process. For fi rst-line treatment, clarithromycin triple therapy should be confi ned to patients with no previous history of macrolide exposure who reside in areas where clarithromycin resistance amongst H. pylori isolates is known to be low. Most patients will be better served by fi rst-line treatment with bismuth quadruple therapy or concomitant therapy consisting of a PPI, clarithromycin, amoxicillin, and metronidazole. When fi rst-line therapy fails, a salvage regimen should avoid antibiotics that were previously used. If a patient received a fi rst-line treatment containing clarithromycin, bismuth quadruple therapy or levofl oxacin salvage regimens are the preferred treatment options. If a patient received fi rst-line bismuth quadruple therapy, clarithromycin or levofl oxacin-containing salvage regimens are the preferred treatment options. Details regarding the drugs, doses and durations of the recommended and suggested fi rst-line and salvage regimens can be found in the guideline. Asia and Central and South America ( 8,22 ). Th ere is, however, preliminary evidence that it may be falling in some previously high prevalence areas ( 22 ). People immigrating to North America from Asia and other parts of the world have a much higher prevalence of the infection than people born in North America ( 23 ). In one study, the seroprevalence among immigrants from East Asia was 70.1% ( 24 ). Hispanic immigrants to North America have higher rates of the infection than fi rst-or second-generation Hispanics who were born here ( 25 ). QUESTION 2: WHAT ARE THE INDICATIONS TO TEST FOR, AND TO TREAT, H. PYLORI INFECTION? RecommendationsSince all patients with a positive test of active infection with H. pylori should be off ered treatment, the critical issue is which patients should be tested for the infection (strong recommendation, quality of evidence: not applicable), All patients with active peptic ulcer disease (PUD), a past history of PUD (unless previous cure of H. pylori infection has been documented), low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma, or a history of endoscopic resection of early gastric cancer (EGC) should be tested for H. pylori infection. Th ose who test positive should be off ered treatment for the infection (strong recommendation, quality of evidence: high for active or history of PUD, low for MALT lymphoma, low for history of endoscopic resection of EGC).In patients with uninvestigated d...

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Section: Non-steroidal Anti-infl Ammatory Drug (Nsaid) Usementioning

confidence: 99%

ACG Clinical Guideline: Treatment of Helicobacter pylori Infection

Chey

Leontiadis

Howden

et al. 2017

American Journal of Gastroenterology

1,319

1,505

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“…There have been contradictory reports about whether infection with H. pylori increases the risk of developing NSAID-induced gastric lesions (in other words, whether eradication of H. pylori reduces the risk of developing NSAID-induced gastric lesions) (1)(2)(3)(4)(5)(6)54). This may be due to differences in diagnostic criteria (endpoints), standards for patient recruitment, and populations used for these studies.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, an important question is whether infection with H. pylori increases the risk of developing NSAID-induced gastric lesions (in other words, if eradication of H. pylori would reduce the risk of developing NSAID-induced gastric lesions). Recent clinical studies suggest that infection with H. pylori increases the risk of developing NSAID-induced gastric lesions (1-4); however, some studies have shown the opposite effect (5,6). Animal models could be useful to address this issue.…”

mentioning

confidence: 99%

Suppression of Expression of Endoplasmic Reticulum Chaperones by Helicobacter pylori and Its Role in Exacerbation of Non-steroidal Anti-inflammatory Drug-induced Gastric Lesions

Namba

Hoshino

Suemasu

et al. 2010

Journal of Biological Chemistry

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Both the use of non-steroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, and infection with Helicobacter pylori are major causes of gastric ulcers. Although some clinical studies suggest that infection with H. pylori increases the risk of developing NSAID-induced gastric lesions, the molecular mechanism governing this effect is unknown. We recently found that in cultured gastric cells, expression of endoplasmic reticulum (ER) chaperones (such as 150-kDa oxygenregulated protein (ORP150) and glucose-regulated protein 78 (GRP78)) is induced by NSAIDs and confers protection against NSAID-induced apoptosis, which is important in the development of NSAID-induced gastric lesions. In this study we have found that co-culture of gastric cells with H. pylori suppresses the expression of ER chaperones. This suppression was regulated at the level of transcription and accompanied by a reduction in the level of activating transcription factor 6 (ATF6), one of the transcription factors for ER chaperone genes. In vivo, inoculation of mice with H. pylori suppressed the expression of ER chaperones at gastric mucosa both with and without administration of indomethacin. Inoculation with H. pylori also stimulated formation of indomethacin-induced gastric lesions and mucosal cell death. In addition, we found that heterozygous ORP150-deficient mice are sensitive to the development of indomethacin-induced gastric lesions and mucosal cell death. The results of this study suggest that H. pylori exacerbates NSAID-induced gastric lesions through suppression of expression of ER chaperones, which stimulates NSAID-induced mucosal cell death.The balance between aggressive and defensive factors determines whether gastric ulcers develop. The gastric mucosa is challenged by a variety of aggressive factors, and of these, both non-steroidal anti-inflammatory drugs (NSAIDs) 2 and Helicobacter pylori are major causes of gastric lesions. Therefore, an important question is whether infection with H. pylori increases the risk of developing NSAID-induced gastric lesions (in other words, if eradication of H. pylori would reduce the risk of developing NSAID-induced gastric lesions). Recent clinical studies suggest that infection with H. pylori increases the risk of developing NSAID-induced gastric lesions (1-4); however, some studies have shown the opposite effect (5, 6). Animal models could be useful to address this issue. For example, some reports have demonstrated that NSAID-induced gastric lesions in mongolian gerbils are exacerbated by infection with H. pylori (7-9), although the molecular mechanism governing this exacerbation is unclear.An inhibitory effect of NSAIDs on cyclooxygenase (COX) activity and the resulting decrease in the gastric level of prostaglandins (PGs), especially PGE 2 , was believed to be the only explanation for the gastric side effects of NSAIDs because PGE 2 is a strong protective factor for gastric mucosa (10). However, the increased incidence of gastrointestinal lesions and the decrease in PG levels induced by NSA...

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“…Hence, the results of our study need to be confirmed in locally conducted prospective clinical studies. Secondly, we limited our analysis to patients who were not on non-steroidal anti-inflammatory drugs (NSAIDs) since the exact benefit of H. pylori eradication with respect to PUH prevention in NSAID-positive patients is unclear [48].…”

Section: Discussionmentioning

confidence: 99%

Non-invasive Testing for Helicobacter pylori in Patients Hospitalized with Peptic Ulcer Hemorrhage: A Cost-Effectiveness Analysis

Atreja

Sanaka

et al. 2009

Dig Dis Sci

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Eradication of Helicobacter pylori Does Not Reduce the Incidence of Gastroduodenal Ulcers in Patients on Long‐term NSAID Treatment: Double‐Blind, Randomized, Placebo‐Controlled Trial

Abstract: H. pylori eradication therapy in patients on long-term NSAID treatment had no beneficial effect on the occurrence of ulcers, erosions, or dyspepsia. Ulcer rates in both study arms are remarkably low, in both patients with and without gastroprotective therapy.

Cited by 57 publications

References 34 publications

ACG Clinical Guideline: Treatment of Helicobacter pylori Infection

ACG Clinical Guideline: Treatment of Helicobacter pylori Infection

Suppression of Expression of Endoplasmic Reticulum Chaperones by Helicobacter pylori and Its Role in Exacerbation of Non-steroidal Anti-inflammatory Drug-induced Gastric Lesions

Non-invasive Testing for Helicobacter pylori in Patients Hospitalized with Peptic Ulcer Hemorrhage: A Cost-Effectiveness Analysis

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