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Treatment of Helicobacter pylori Infection

Digestion, General | December 15, 2015 | Author: The Super Pharmacist

general, Digestion

Treatment of Helicobacter pylori Infection

What Is Helicobacter pylori?             

Helicobacter pylori (H. pylori) is a spiral-shaped bacterium that is found in the mucous layer lining of the inner surface of the stomach or first part of the small intestine (“helico-,” means “spiral”). H. pylori is the main cause of ulcers occurring in the lining of the upper part of the small intestine (duodenal ulcers) and in the lining of the stomach (gastric ulcers). Initially, the bacterium causes inflammation (gastritis or duodenitis). Many people may be unaware of this inflammation, and only experience symptoms when an ulcer develops, perhaps years later. Not all people infected with H. pylori will develop an ulcer.1

How Common Is H. pylori Infection?

Currently, about half of the world’s population is infected by H. pylori, with rates in the developed world in the order of 70%.2 H. pylori may be detected in approximately 90% of individuals with peptic ulcer disease; however, less than 15% of infected persons may have peptic ulcer disease.3

What Illnesses Does H. pylori Cause?

The presence of H. pylori in the stomach or small intestine is usually asymptomatic. However, duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients.4 In 20% of cases, the infection may progress to pre-cancerous changes in the stomach and eventually to gastric cancer in 2% of those persons infected with the organism.5  Gastric lymphoma is an even rarer consequence of H. pylori infection, occurring in fewer than 1% of those who are infected.6

What Are the Symptoms of a Gastric or Duodenal Ulcer?

Treatment of Helicobacter pylori InfectionThe most common ulcer symptom is gnawing or burning pain in the epigastrium (the upper middle region of the abdomen). This pain typically occurs when the stomach is empty, between meals and in the early morning hours, but it can also occur at other times. It may last from minutes to hours and may be relieved by eating or by taking antacids. Less common ulcer symptoms include nausea, vomiting, and loss of appetite. Bleeding can also occur; prolonged bleeding may cause anemia leading to weakness and fatigue. If bleeding is heavy, bloody vomiting or bloody stools may occur.1

How Is H. pylori Infection Acquired?

The most common route of H. pylori infection is either oral-to-oral (stomach contents are transmitted from mouth to mouth) or fecal-to-oral (from stool to mouth) contact. Parents and siblings seem to play a primary role in transmission.3 However, it is thought that people infected with the bacterium are only capable of passing it to others for a short period (days or weeks). It may be passed via the fingers through contact with vomit or stools from an infected person. Therefore, good hygiene may decrease the risk of the bacterium being spread. However, it is thought that people living in the U.S. are unlikely to pass it on and do not need to take any special measures to avoid giving it to others.1

How Is H. pylori Infection Diagnosed?

The test usually used to diagnose an ulcer is an endoscopy. This is a procedure where a flexible fiber-optic tube, which relays images to a video camera, is passed through the mouth down into the stomach.   The oesophagus, stomach, and duodenum can be inspected in this manner and a biopsy can be obtained. This involves taking a sample of cells from the lining of the stomach or duodenum. The cells are then grown in a special culture to test for the presence of H. pylori. If there is growth of H. pylori, different antibiotics can then be tested on this culture to establish which is the most effective in treating the bacterium.1 Noninvasive tests are divided into the urea breath test (UBT), serology and stool antigen test (SAT). For the urea breath test, patients swallow urea labelled with an uncommon isotope, either radioactive carbon-14 or non-radioactive carbon-13. In the subsequent 10–30 minutes, the detection of isotope-labelled carbon dioxide in exhaled breath indicates that the urea was split; this indicates that urease (the enzyme that H. pylori uses to metabolize urea) is present in the stomach, and hence that H. pylori bacteria are present. Urea is an organic chemical compound, and is essentially the waste produced by the body after metabolising protein. Serological tests detect the presence of antibodies to H. pylori. Positive serology indicates current or past infection with H. pylori. A stool antigen test checks to see if substances that trigger the immune system to fight an H. pylori infection are present in the stool.

How Is H. pylori Infection Treated?

Triple therapy:7, 8

Treatment of Helicobacter pylori InfectionStandard treatment of an H. pylori infection consists of 3 drugs, the so-called ‘triple therapy’ plan which includes a proton pump inhibitor (PPI) (suppresses gastric acid) and two different antibiotics.

  1. Proton pump inhibitor options:
  • omeprazole 20 mg twice a day
  • lansoprazole 30 mg twice a day
  • esomeprazole 40 mg daily
  • pantoprazole 40 mg daily
  • rabeprazole 20 mg twice a day


  1. Clarithromycin 500 mg twice a day (first-line) OR Metronidazole 500 mg twice a day (when resistance to clarithromycin is increasing)


  1. Amoxicillin 1000 mg twice a day OR Metronidazole 500 mg twice a day (if not used above)

Duration options are as follows (each duration below yields good outcomes of around 80% and is associated with similar risks because of good tolerance):

  • 14 days (deemed the most prudent recommendation based on a meta-analysis of 7 studies and confirmed by a large Italian randomized single-center trial)
  • 7 days (no significant difference from 14 days based on a prospective randomised comparative trial in Nairobi)
  • 10 days (also showed high cure rates with metronidazole 500 mg three times a day and high-dose esomeprazole (40 mg twice a day) based on a pilot study

Sequential therapy

Standard triple therapy started from eradication rates of more than 90%, and has now decreased to 70–80%.9,10 Treatment of H. pylori infection is challenged by a dramatic fall in eradication rates all over the world. Over the past few decades, the efficacy of the standard first-line triple therapy has experienced a steady decline. There are several reasons for the loss of eradication efficacy, but the far most important is the increasing rate of H. pylori resistance to antibiotics. The resistance to clarithromycin has the highest impact on treatment failure and the rate of resistance to clarithromycin has dramatically risen in many countries. Newer treatment regimens have been introduced including sequential, quadruple therapies. In sequential therapy for H. pylori, more antibiotics are added to the treatment regimen in sequence rather than giving all 4 drugs together. Typically, this involves an initial 5-day therapy with a benign combination (e.g. pantoprazole 40 mg twice daily, with amoxicillin 1 g twice daily) followed by 5 days of 2 further antibiotics plus a proton pump inhibitor (PPI) (e.g. clarithromycin 500 mg twice daily, and tinidazole 500 mg twice daily, plus pantoprazole 40 mg twice daily).11 In a large prospective, controlled study,12 researchers showed a 90% cure rate for this “new” treatment versus 80% for the “old.” Sequential therapy is considered superior to standard triple therapy based on 2 systematic reviews.13,14   The confirmation of cure should be performed by noninvasive tests, except in cases when a follow-up endoscopy is indicated from a clinical perspective (gastric ulcer, preneoplastic lesions, lymphoma). As a noninvasive test, the UBT should be employed, if available. Australia's best online pharmacy


  1. Helicobacter Pylori Infection Patient Fact Sheets. Monthly Prescribing Reference. Updated May 2013. Accessed 1 Dec 2014.
  2. Suerbaum S, Michetti P. Helicobacter pylori N Engl J Med. 2002;347:1175–1186.
  3. Santacroce L. Helicobacter Pylori Infection Treatment & Management. Updated 14 Sept 2014. Accessed 1 Dec 2014.
  4. Barclay L. Diagnosis and Management of H pylori Infection. 28 Apr 2010. Accessed 1 Dec 2014.
  5. Peek RM, Jr, Blaser MJ. Helicobacter pylori and gastrointestinal tract adenocarcinomas. Nat Rev Cancer. 2002;2:28–37.
  6. Sung Soo Kim, SS, Ruiz, VE, Carroll, JD, et al. Helicobacter pylori in the pathogenesis of gastric cancer and gastric lymphoma. Cancer Lett. 28 Jun 2011; 305(2): 228–238.
  7. O'Connor A, Molina-Infante J, Gisbert JP, O'Morain C. Treatment of Helicobacter pylori infection 2013. Helicobacter. Sep 2013;18 Suppl 1:58-65.
  8. Joseph Adrian Lumawig Buensalido, Pranatharthi Haran Chandrasekar. Helicobacter pylori Infection Treatment. Updated 8 Aug 2014. Accessed 1 Dec 2014.
  9. Paoluzi OA, Visconti E, Andrei F, et al. Ten and eight-day sequential therapy in comparison to standard triple therapy for eradicating Helicobacter pyloriinfection: a randomized controlled study on efficacy and tolerability. J Clin Gastroenterol 2010; 44:261–266.
  10. Kearney DJ, Brousal A. Treatment of Helicobacter pyloriinfection in clinical practice in the United States: results from 224 patients. Dig Dis Sci 2000; 45:265–271.
  11. Marshall B. Sequential Therapy for Helicobacter pylori: A Worthwhile Effort for Your Patients. Ann Intern Med. 2008;148(12):962-963.
  12. Vaira D et al. Sequential therapy versus standard triple-drug therapy for Helicobacter pylori eradication: A randomized trial. Ann Intern Med 2007 Apr 17; 146:556-63.
  13. Zullo A, De Francesco V, Hassan C, et al. Modified sequential therapy regimens for Helicobacter pylori eradication: a systematic review. Dig Liver Dis. Jan 2013;45(1):18-22.
  14. Zullo A, Hassan C, Ridola L, De Francesco V, Vaira D. Standard triple and sequential therapies for Helicobacter pylori eradication: an update. Eur J Intern Med. Jan 2013;24(1):16-9.
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