Helicobacter pylori: Difference between revisions

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==Diagnosis==
==Diagnosis==

Revision as of 09:49, 10 March 2008


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Diagnosis

Prior infection

Detection of serum antibodies against H. pylori indicate prior infection. The probability of having positive antibody test is approximately the same as the age of the patient.[1] For example, a 50 year old male has approximately a 50% chance of having antibodies against H. pylori.

Active infection

There is no one test that detects all patients infected with H. pylori.

Non-invasive tests

Clinical practice guidelines by the American Gastroenterological Association state "H. pylori testing is optimally performed by a 13C-urea breath test or stool antigen test."[2] Details of test accuracy have been reviewed.[3]

If a patient is taking anti-secretory therapy, the breath test may be falsely negative for 3-9 days after stopping pantoprazole. For patients on ranitidine, if they have been taking it for at least 30 days, they do not need a washout period.[4]

Invasive tests

H. pylori can be detected during esophagogastroduodenoscopy (EGD) by biopsy, culture, or rapid urease testing.

Treatment

Clinical practice guidelines[5] by the American College of Gastroenterology and systemical review by the UK Clinical Evidence[6] guide treatment. The recommendations conflict on treating non-ulcer dyspepsia.

Regarding which patient to treat:

  • Patients with duodenal or gastric ulcer, non-ulcer dyspepsia, people with uninvestigated dyspepsia.[6]
  • "Testing is uncertain among patients with functional dyspepsia, gastroesophageal reflux disease (GERD), patients taking nonsteroidal antiinflammatory drugs, with iron deficiency anemia, or who are at risk of developing gastric cancer".[5] A subsequent randomized controlled trial showed benefit of eradication to prevent gastric cancer in a high risk region.[7] Regarding gastritis and gastric erosions, patients with antral predominant gastritis are more likely to improve whereas patients with corpus-predominant gastritis are less likely to improve.[8] This may be due to antral erosions being due to hyperacidity the is corrected by treatment whereas corpus erosions are hypoacidic and treating this may increase the ability of the stomach to produce acid. [8] Another study found that patients with gastritis or erosions were less likely to respond[9], but this study did not separate patients with antral versus corpus erosions.

Regarding how to treat:[5]

  • "Eradication rates achieved by first-line treatment with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin have decreased to 70-85%, in part due to increasing clarithromycin resistance".
  • "Eradication rates may also be lower with 7 versus 14-day regimens."

Regarding follow-up of treatment[5], H. pylori antibiotic resistance is increasing[10] due to prior exposure of patients to macrolide antiobiotics and metronidazole.[11]

  • "Testing to prove eradication should be performed in patients who receive treatment of H. pylori for peptic ulcer disease, individuals with persistent dyspeptic symptoms despite the test-and-treat strategy, those with H. pylori-associated MALT lymphoma, and individuals who have undergone resection of early gastric cancer".
  • "For patients with persistent H. pylori consider bismuth quadruple therapy. A PPI, levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori".

A complication of treatment is selecting for "highly resistant enterococci that can persist for at least 3 years ".[12]

Prevention

It has been recommended to eradicate H. pylori world wide as was done for smallpox.[13]

History

Barry Marshall and Robin Warren won the 2005 Nobel Prize in Physiology or Medicine for discovery of Helicobacter pylori in 1983.[14][15]

References

  1. ↑ Soll AH (1990). "Pathogenesis of peptic ulcer and implications for therapy". N. Engl. J. Med. 322 (13): 909–16. PMID 2179722. [e]
  2. ↑ Talley NJ (2005). "American Gastroenterological Association medical position statement: evaluation of dyspepsia". Gastroenterology 129 (5): 1753–5. DOI:10.1053/j.gastro.2005.09.019. PMID 16285970. Research Blogging. National Guideline Clearinghouse
  3. ↑ Logan RP, Walker MM (2001). "ABC of the upper gastrointestinal tract: Epidemiology and diagnosis of Helicobacter pylori infection". BMJ 323 (7318): 920–2. PMID 11668141. [e]
  4. ↑ Dulbecco P, Gambaro C, Bilardi C, et al (2003). "Impact of long-term ranitidine and pantoprazole on accuracy of [13C]urea breath test". Dig. Dis. Sci. 48 (2): 315–21. PMID 12643609. [e]
  5. ↑ 5.0 5.1 5.2 5.3 Chey WD, Wong BC (2007). "American College of Gastroenterology guideline on the management of Helicobacter pylori infection". Am. J. Gastroenterol. 102 (8): 1808–25. DOI:10.1111/j.1572-0241.2007.01393.x. PMID 17608775. Research Blogging.
  6. ↑ 6.0 6.1 Delaney B, Moayyedi P, Forman D (2005). "Helicobacter pylori infection". Clinical evidence (13): 518–34. PMID 16135272. [e]
  7. ↑ Wong BC, Lam SK, Wong WM, et al (2004). "Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial". JAMA 291 (2): 187–94. DOI:10.1001/jama.291.2.187. PMID 14722144. Research Blogging.
  8. ↑ 8.0 8.1 Vakil N, Talley NJ, Stolte M, Sundin M, Junghard O, Bolling-Sternevald E (2006). "Patterns of gastritis and the effect of eradicating Helicobacter pylori on gastro-oesophageal reflux disease in Western patients with non-ulcer dyspepsia". Aliment. Pharmacol. Ther. 24 (1): 55–63. DOI:10.1111/j.1365-2036.2006.02964.x. PMID 16803603. Research Blogging.
  9. ↑ Mazzoleni LE, Sander GB, Ott EA, et al (2006). "Clinical outcomes of eradication of Helicobacter pylori in nonulcer dyspepsia in a population with a high prevalence of infection: results of a 12-month randomized, double blind, placebo-controlled study". Dig. Dis. Sci. 51 (1): 89–98. DOI:10.1007/s10620-006-3090-6. PMID 16416218. Research Blogging.
  10. ↑ Mégraud F (2004). "H pylori antibiotic resistance: prevalence, importance, and advances in testing". Gut 53 (9): 1374–84. DOI:10.1136/gut.2003.022111. PMID 15306603. Research Blogging.
  11. ↑ McMahon BJ, Hennessy TW, Bensler JM, et al (2003). "The relationship among previous antimicrobial use, antimicrobial resistance, and treatment outcomes for Helicobacter pylori infections". Ann. Intern. Med. 139 (6): 463–9. PMID 13679322. [e]
  12. ↑ Sjölund M, Wreiber K, Andersson DI, Blaser MJ, Engstrand L (2003). "Long-term persistence of resistant Enterococcus species after antibiotics to eradicate Helicobacter pylori". Ann. Intern. Med. 139 (6): 483–7. PMID 13679325. [e]
  13. ↑ Graham DY (1997). "Can therapy even be denied for Helicobacter pylori infection?". Gastroenterology 113 (6 Suppl): S113–7. PMID 9394771. [e]
  14. ↑ Parsonnet J (2005). "Clinician-discoverers--Marshall, Warren, and H. pylori". N. Engl. J. Med. 353 (23): 2421–3. DOI:10.1056/NEJMp058270. PMID 16339090. Research Blogging.
  15. ↑ Marshall BJ, Warren JR (1984). "Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration". Lancet 1 (8390): 1311–5. PMID 6145023. [e]
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