Helicobcter pylori is very notorious.

Helicobacter pylori infection is an infectious disease caused by a gram-negative spiral bacterium. Once untreated, it is associated with devastating clinical outcomes such as peptic or duodenal ulcers, gastric B cell lymphoma (commonly known as gastric mucosa-associated lymphoid tissues (MALT) lymphoma), atrophic gastritis, and gastric cancer.

Helicobacter pylori infection affects close to 50% of the world’s population, with those in the developing world like Uganda being affected the most. It is typically acquired during childhood and transmitted within families. It can exist as an active infection or a latent infection. However, unlike other infectious diseases like tuberculosis and syphilis, H pylori infection continues to be transmitted from one person to another even in its latency.

Helicobacter pylori infection leads to chronic progressive damage to the stomach walls (gastric mucosa). What is baffling is the fact that this infection leads to such devastating clinical outcomes, yet the risk is not predictable for any given person. We can, however, see its effects in the fact that gastric cancer remains the fourth most common cause of cancer deaths around the globe. 

It is worth noting that less than 80% of the people treated for H pylori infection with the standard triple therapy get to have eradication of the bacteria. The resistance to metronidazole or clarithromycin has been skyrocketing in the 2000s. What is more amusing is the fact that close to 95% of these patients diagnosed with H pylori in Uganda aren’t aware whether they are harbouring an active infection or just exposed to it at some point in their lives. It is true due to an observation that almost all the health centres in the country diagnosed H pylori infection using serology markers like the antibody tests yet these tests cannot distinguish between the active disease and the exposure to the bacteria. It eventually adds more burden to the irrational use of antibiotics among this group of people.

However, the above scenarios aren’t occurring only in Uganda, even in the developed world like in the US physicians do not universally employ the tests for an active infection because many clinicians still harbour that knowledge gap. We present to you the latest guidelines about whom we

should test and who should be treated for H pylori as put forth by the Houston consensusLet’s get this started.

Upon a series of discussions backed up by evidence, the panel reached a consensus that health care providers should treat all people with an active H pylori infection. They also noted that all people that fall in the following categories should have the test for an active H pylori infection. 

People with;

  1. Current or past gastric or duodenal ulcers
  2. Uninvestigated dyspepsia (dyspepsia, been defined as predominant epigastric pain lasting at least one month).
  3. Reflux symptoms only if they are at high risk for H pylori-related disease.
  4. Gastric mucosa-associated lymphoid tissue (MALT) lymphoma
  5. Family history of gastric cancer
  6. 1st generation immigrants from regions with a high prevalence of H pylori in Latino and African American racial or ethnic groups 

The expert panel agreed that people with idiopathic thrombocytopenia, those receiving proton pump inhibitors (PPIs), family members residing in the same household of patients with active H pylori infection and a family history of peptic ulcer disease, should be tested.

Because of the high rates of treatment failure and issues with antibiotic susceptibility testing, the panel agreed that;

  1. Base empiric eradication therapy for H pylori on a region or population-specific antibiotic susceptibility data.
  2. Consult an expert following two proven unsuccessful treatment attempts with different antibiotics suggesting multidrug resistance.
  3. Validated diagnostic testing of stool or gastric mucosal biopsy by culture and susceptibility or molecular analysis be universally available.
  4. You may evaluate antibiotic susceptibility on a routine basis. Include amoxicillin, clarithromycin, levofloxacin, metronidazole, and tetracycline.
  5. Professional societies should provide the research to support evidence-based reimbursement decisions for antibiotic testing for H pylori.

Due to the inconsistencies in the testing and confirmation of eradication of the infection, the panel agreed that;

  1. Use the tests that show evidence of active infection for the initial diagnosis. These include Urea Breath Test (UBT) and H pylori stool antigen assay (HpSAg).
  2. Obtain biopsies (2 each) from the antrum, and corpus (+/- incisura) when performing endoscopy.
  3. Stop Bismuth and antibiotics at least four weeks before H pylori testing with tests for active infection.
  4. Discontinue PPIs at least four weeks before UBT and HpSAg.
  5. Utilize H2 blockers and antacids without affecting the accuracy of UBT and HpSAg.
  6. Consider a positive test for active infection positive even when you discontinued the PPIs. However, if the test is negative, repeat it four weeks after you stop the PPIs, to rule out false negatives.
  7. Do posttreatment confirmation for eradication in all patients treated for H pylori.
  8. Do not perform further H pylori testing if once appropriate testing has confirmed eradication.

Related article: Terminal care: It is a task for every district hospital: from the book that matters.

It is worth noting that the absence of gastric atrophy, intestinal metaplasia or dysplasia at the time of initial biopsy doesn’t rule out the development of catastrophic pathology if Helicobacter pylori infection persists.

You can get the full report to understand the details of how and why the recommendations were made by clicking here. For now, share this article with a colleague to spread the knowledge.

 

By IAmDrSsekandi

I am a medical officer interested in maternal and child health. I am a content creator, author and founder of https://ssekandima.com. I do private practice with a public touch. I am a certified digital marketer. I earned certificates in Understanding Clinical Research and Writing in Sciences from the University of Cape Town and Stanford University respectively.

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