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Helicobacter pylori (H.Pylori)

Condition

THE BASICS

Background:

Helicobacter pylori, also known as H. pylori, is a bacterium that is commonly found in the stomach. It is present in approximately one-half of the world's population.

The majority of people infected with H. pylori have no symptoms and may never develop problems. However it may cause digestive problems ranging from stomach inflammation (gastritis), small intestinal inflammation (duodenitis) to stomach cancer.

It is not clear why some people with H. pylori get these conditions and others do not, but it may be in part due to genetics, ethnicity and other environmental exposures.

As a result of these changes, the stomach and duodenum are more vulnerable to damage from digestive juices, such as stomach acid.

Symptoms:

Many patients with chronic (long-term) gastritis or duodenitis have no symptoms. However, some symptoms related to H.Pylori include:

  • Pain or discomfort (usually in the upper abdomen)
  • Bloating
  • Feeling full after eating a small amount of food
  • Lack of appetite
  • Nausea or vomiting
  • Dark or tar-coloured stools (indicative of bleeding)
  • Ulcers that bleed can cause a low blood count and fatigue

Chronic inflammation in the stomach can cause abnormal changes in the stomach lining, which can lead to certain forms of cancer. After years of infection, the stomach lining may begin to thin (atrophy), then start to change the lining to help protect it (intestinal metaplasia). These changes are the first, early changes to become gastric cancer (adenocarcinoma). If detected at an early stage, close surveillance and observation is suggested so that initial steps (dysplasia) can be identified and removed from the stomach.

Diagnosis:

There are several ways to diagnose H. pylori.

Stool tests — “H.Pylori faecal antigen” tests. Very accurate.

Blood tests — Blood tests can detect specific antibodies (proteins) that the body's immune system develops in response to the H. pylori bacterium. However, concerns over its accuracy have limited its use, including that it may remain positive for some time after successful eradication.

Breath tests – Not frequently performed in New Zealand

Biopsy test – H.Pylori organism seen and identified under the microscope in biopsies (samples) taken from the stomach lining during the gastroscopy

Who should be tested?

Patients with symptoms (see above). In addition, if you have had stomach or intestinal ulcers in the past, you may wish to be tested if you haven't already.

Some people recommend if you have to take blood thinners long term (in particular aspirin) or anti-inflammatories (such as ibuprofen, voltaren, diclofenac, neurofen) it is a good idea to get tested as you are at higher risks of gastritis or ulcers.

In addition, certain populations without symptoms should be considered for testing and eradication to prevent complications such as stomach cancer.

This includes:

-Patients of Asian, Maori or Pasifika ethnicity.

-Patients with a family history of gastric cancer.

 Treatment:

 Successful treatment of H. pylori can help the ulcer to heal, prevent ulcers from coming back, and reduce the risk of ulcer complications (like bleeding). 90% of duodenal ulcers may be related to H.Pylori and although they will heal with ant-acids, these ulcers may reoccur if the precipitant is not treated.

Treatment involves taking two (or three) antibiotics and an ant-acid for 7-14 days. This treatment may be tailored to you.

In New Zealand, H.Pylori has become more and more resistant to the standard treatments (including Amoxicillin, Metronidazole or Clarithyomycin). Initial treatment is over 80% successful. For H. pylori treatment to be effective, it is vital to take the entire course of all medications, even if you already start to feel better early in the treatment course. If we are not successful with eradication in the first instance, a second line regimen may be prescribed. Biopsies can also be taken with a gastroscopy, and the organism cultured (grown) and tested (sensitivity testing) to see which antibiotics will be effective.

Side effects — Up to 50 percent of patients have side effects while taking H. pylori treatment. Side effects are usually mild. It may be possible to make adjustments in the dose or timing of medication to help, or take things such as anti-nausea to help you through the course.  In particular, Metronidazole may cause a metallic taste in the mouth. Alcohol should not be consumed whilst taking this, as you can feel very unwell.

Follow-up — After completing H. pylori treatment, repeat testing is usually performed to ensure that the infection has resolved. I typically do this with a H.Pylori stool test, 6 weeks after the end of the treatment. You have to stop taking any ant-acids for 2 weeks prior for this test to be accurate. 

 

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ADVANCED (including for medical professionals)

H.Pylori is the most common bacterial infection in the world, estimated to colonize nearly half of the world’s population. It infects humans (and animals) of all ages, and often persists long term. In up to 80%, it may lay dormant - never causing an issue. In some it may cause indigestion and abdominal pain. In others it will cause catastrophic gastrointestinal ulceration and bleeding, and as a class I carcinogen, is also responsible for nearly 90% of gastric cancer, which is the 3rd most common cause of cancer death worldwide.

 

In the last years, rates of testing for this infection in New Zealand (NZ) have increased by nearly 40%, with over 80% of these tests performed in primary care.  Yet there are no consensus guidelines on its management. Herein, I will attempt to add some background, context and clarity to this seemingly ubiquitous infection.

 

Background

 

Gastric organisms have been observed for over 100 years, linked to gastric inflammation for over 50 years and identified as what we now call Helicobacter Pylori for 40 years. Genetic sequencing suggests that humans have been infected with H.Pylori since they migrated from Africa over 58,000 years ago. Infection rates in Africa and South America are around 70%, West Asia 67% and Northern America 37%. The prevalence is comparatively lower in NZ, estimated at around 30%. It is more common in Māori (35%), Pacific (62%) and Asian (24%) people as opposed to NZ Europeans (18%).1,2 Prevalence is higher in the North Island, specifically Northland and Auckland compared to the South Island. However it is still important to remember that people who immigrate will retain a prevalence of H.pylori similar to their country of origin.

 

Infection and Transmission

 

In less developed countries, initial infection in childhood is common. In developed countries, it is more often acquired in adulthood with an increasing incidence with age. However although this is now thought to be slowly shifting to acquisition in younger years. Interestingly, the main mode of transmission is still not clear. Faecal-oral transmission via contaminated water is proposed as most likely. Oral-oral transmission has not been definitively shown.

 

The main risk factors for this acquisition relate to socioeconomic factors, particularly housing density, overcrowding and number of family members. This is particularly relevant in New Zealand where this has been demonstrated in particular in Māori and Pacifica communities. Certain ethnicities have a higher infection rate independent of socioeconomic status, although hereditary susceptibility to infection has never been conclusively proven.

 

Human adaption:

It is a gram negative bacteria with multiple flagella (tails) that help to propel it around the stomach lining and through its thick mucus where it lives. It is highly adapted to the human stomach, for example producing a urease enzyme that forms a protective ammonia cloud surrounding it to allow it to colonise and live in an acidic gastric environment.

 

Disease:

 

H.Pylori  alters gastric acid secretion, most commonly leading to a sequence of progressive inflammation. This long term, grumbling inflammation in the majority of people may be asymptomatic and will not progress to cause disease. In others, changes in acid and resultant tissue damage leads to stomach or duodenal ulceration. This may also lead to a course of events with stepwise progression over years (“The Correa cascade”) beginning with gastric atrophy (thinning of the stomach wall), intestinal metaplasia (transformation of cells lining the stomach), dysplasia (grossly abnormal cell changes) and finally frank malignancy.

 

The initial most common pattern of gastritis starts in the antrum of the stomach (distal or lower portion), progressing proximally up the gastric body. With persistent inflammation over years, gastrin and acid producing parietal cells are lost. The advancing inflammatory front causes a reduction of acid and overgrowth of other bacteria, leading to further chronic inflammation.

 

The mechanism by which this is caused is a complex interplay between the host, bacterium and the environment. Bacterial factors include different strains. These are not tested for in routine lab samples in NZ, however there are known functional differences that may contribute to outcomes. For example, the H.Pylori strain with expression of CagA is more likely to cause ulcerative disease (85-100% of patients with duodenal ulcers).In addition, different CagA subtypes and VacA strains carry different and higher risks of cancer development.

 

Symptoms and Conditions

 

Acute infection:

Acute infection in the adult often may be asymptomatic or lead to mild self-limiting dyspeptic symptoms. However this acute infection and subsequent inflammation almost always leads to a degree of chronic gastritis unless treated. Despite H.Pylori sitting in the gastric mucus layer and is therefore classified as ‘non-invasive’, it stimulates a varied host inflammatory and immune response, with cytokine release and antibody response. Occasionally patients will have a very vigorous reaction including severe pain, nausea and vomiting with intense inflammation that can be seen at gastroscopy. These were noted during its discovery and voluntary self experiments with ingestion of bacterial broths.

 

Gastritis:

Inevitably chronic gastritis develops which may lead to a number of symptom complexes, in particular dyspepsia. It is now understood that there are 3 main different patterns of gastritis that develop in patients that lead to the different disease states. These include the “duodenal ulcer” phenotype (10-15% of patients) with antral gastritis leading to high acid output and ulceration. This state may actually be protective from gastric cancer. There is a “simple gastritis” phenotype, with mild, mixed gastritis with no change in acid production and no significant clinical outcome. This is the majority of patients. Finally there is the least common “gastric cancer” phenotype, with gastric body predominant gastritis, with chronic multifocal inflammation, reduction in acid production and development of cancer via the Correa cascade. Practically speaking, these 3 states are only relevant at gastroscopy where these changes can be seen and identified with consequent risk stratification, but I do feel this helps to explain the heterogenous differences in clinical outcomes.

 

Dyspepsia / non-ulcer dyspepsia:

 

Dyspepsia is often ascribed to H.Pylori, and is a very common presenting complaint with a wide differential diagnosis. Symptoms may include epigastic pain, burning, postprandial fullness, early satiation, bloating, nausea, vomiting, and belching. It is known that H.Pylori occurs 60% more commonly in these patients than in matched controls.3

 

The pathogenesis of this is complex and multifactorial. It may include increased acid production, impaired accommodation (ability of the stomach to expand and stretch), slower gastric emptying and visceral hypersensitivity. It is known that these occur more frequently in patients with functional dyspepsia.

 

There are therefore considerable differences with regard to outcome of treatments of H.Pylori and these symptoms. The overall number needed to treat (NNT) to resolve symptoms is 14 (95% CI, 10 to 25) which is surprisingly high to many, but in my view reinforces the difficulty of dyspepsia diagnosis and management.4  In Asian patients where infection and this condition is more common, the odds ratio for improvement in symptoms after eradication was 3.6, suggesting that the role of this infection in causing dyspepsia is much larger in the Chinese population than in Western populations.

 

Workup and management of dyspepsia will be discussed in another article. However, as above, although common and concurrent, should not always be ascribed to H.Pylori. If symptoms persist post eradication, which will be in the majority of patients, a wider differential diagnosis should be sought.

 

Gastroduodenal ulceration:

Overall ulcer incidence has been dramatically falling due to H.Pylori identification and eradication, with prevalence rates related directly to its presence. The incidence is 1% per year, with an up to 20% lifetime risk. This is up to 10x higher than for non-infected individuals.5 The other major risk factor for ulcers is non-steriodal anti-inflammatory use, which also acts synergistically with infection to cause ulceration. Because of this, some even suggest testing and treating for H.Pylori prior to beginning non-steroidal anti-inflammatories including aspirin, although this is not currently the standard of care.

 

Additional exacerbating risk factors for H.Pylori driven ulcer disease include smoking, alcohol and genetic factors that lead to variations in pro-inflammatory cytokine production which drives damage to the gastric mucosal barrier. Psychological factors, in particular stress and the patients physiological response has been seen to alter acid secretion and correspondingly healing or relapse of ulceration.

 

Around 80% of duodenal (small intestine) ulcers are related to H.Pylori. Eradication results in a reduction in recurrence rate in the first 6 months from 67% to 6%.

 

Gastric Cancer

H.Pylori was established by the World Health Organisation (WHO) as a class I carcinogen in 1994. It has a number of proteins that modify and interact with receptors and cell signalling involved with inflammation and cell growth. Infection may lead to gene methylation and increased exposure to free radicals leading to dysplastic change.

 

It is associated with an approximately 3-fold increased risk of gastric cancer, which is the 5th most common cancer worldwide and 3rd leading cause of cancer death.6,7 H.Pylori accounts for nearly 90% of non-cardia cancers, with a lifetime risk of development of gastric cancer of up to 3%.8

 

In NZ, there are over 400 new cases diagnosed each year. Māori have an incidence 3 times that of non-Māori (15.8 vs 4.8 /100,000). They have an average age of diagnoses 10 years younger yet are 22% more likely to die than non-Māori patients. It is only second behind lung cancer as the most significant contributor to ethnic inequality in cancer mortality. It is estimated that more than half of the excess cancer incidence in Māori men, and more than two thirds in Pacifica men in NZ is explained by H.Pylori infection.9

 

Treatment of H.Pylori may reduce this risk of progression by over 30%. Furthermore, eradicating H.pylori in patients treated via endoscopic excision for early gastric cancer reduces the rate of futher metachronous gastric cancer development by 50%.10

 

Mucosa-associated lymphoid tissue (MALT) lymphoma.

H.Pylori is responsible for 90% of MALT lymphoma. 75% of Stage I H. pylori-positive gastric lymphomas achieve complete remission by eradication alone. Its association with H.Pylori is so strong that even in H. pylori-negative gastric MALT lymphoma patients, antibiotic eradication therapy is suggested as first line and may still be effective in treatment for nearly 50%.11

 

Iron and B12 deficiency

This association is thought to be related to the gastric atrophy (thinning) of the lining and resultant reduction in acid which reduces absorption.  

 

ITP (Idiopathic thrombocytopenic purpura)

Molecular mimicry with cross reactive antibodies may explain improvement in platelet count with eradication.

 

Rosacea

This inflammatory disease affecting the face characterized by erythematous rash and pustules in some patients may be related to H.Pylori mediated inflammatory immune stimulation. It should be checked and treated in these patients.

 

Gastrooesophageal reflux disease (GORD)

Patients may present with typical reflux (rising, burning pain the upper abdomen or chest), and investigations including testing for H.Pylori undertaken. However, eradication is actually often associated with worsening of GORD in those with gastric body or whole stomach gastritis, where H.Pylori decreases acid production in the stomach. Reversal of this therefore has the potential to increase acid production.

 

In patients with antral (lower stomach) gastritis, where acid production is maintained or increased, it may improve symptoms. Practically speaking, in a consultation it is not possible to tell which is which and what will happen. My advice is that isolated GORD is not often caused or related to H.Pylori infection. It should be noted that acute symptomatic improvement following a treatment regimen may be related to the omeprazole component as part of the triple therapy, and therefore further follow-up is suggested.

 

Testing

 

Testing in NZ has increased by nearly 40%. The majority (82%) of this was done in primary care.12 All non-invasive tests require patients to stop taking antibiotics and proton pump inhibitors (PPI) which may lead to a higher rate of false negatives via a temporary suppression of bacterial growth. They should be stopped for at least 14 days.

 

  1. Stool test (Faecal antigen)

 

This is the recommended test to detect H.Pylori in NZ. It has a sensitivity and specificity exceeding 95%. It is cost effective. This is also the preferred method to test for successful eradication post treatment. It must be provided to the lab within 48 hours.

 

  1. Blood test (Serology)

 

This detects bacterial antibodies (IgG) and is still widely performed but has the significant drawback in that it cannot distinguish between current or past infection. It cannot be used to check for successful eradication, and has a lower accuracy than stool antigen testing. Despite this and that it is not really recommended in many clinical scenarios, it is the most frequent test ordered in NZ. This can lead to confusion with unnecessary duplicate testing and treatment regimens.

 

  1. Breath Test (Urea detection)

 

This may requested by patients who have immigrated or had family tested using this method overseas as it is more clinically acceptable than a stool test with similarly high sensitivity and specificity. It tests for an increase in exhaled CO2 after consumption of a drink containing urea, which is broken down by H.Pylori if present into CO2. However this is not offered in the public system in NZ, with associated expense of the testing equipment.

 

Invasive testing

Performed with a gastroscopy and biopsy for urease assessment or histology, this is generally reserved for patients with symptoms that require direct visualisation (i.e. dyspepsia with red flags such as: older age of symptom onset, family history of gastric cancer, signs or symptoms of bleeding, weight loss, vomiting etc). H.Pylori infection can be patchy and biopsy may also have a false negative result, therefore multiple samples should be taken. The benefit of a biopsy may be that a sample can be taken for culture and sensitivity. If 2 eradication attempts are unsuccessful, this should be requested to assess resistance patterns to guide treatment (see treatment below).

 

Testing and treatment of Children

 

This is controversial. Most infections in the world occur before the age of 10. Disease and symptoms in this age group is uncommon, in particular gastroduodenal ulcerative disease, non-ulcer (functional) dyspepsia or of course dysplasia and cancer, which takes many years to develop. Children also have a much higher rate of reinfection (up to 20%) in high prevalence areas.

 

It is generally agreed upon that children of parents with H.Pylori should not be screened and treated. Children with non-specific symptoms deemed to be functional dyspepsia or with conditions such as poor growth or iron deficiency do not predict the presence of H.Pylori. If detected, these conditions are unlikely to improve with treatment. However, this area is not well studied.

 

Children with confirmed disease such as gastroduodenal ulcer disease and alarm features (night-time wakening, occult blood in stool, weight loss or vomiting) should be referred and considered for investigation with endoscopy, as opposed to non-invasive testing.13,14 It is not suggested to test (i.e. stool test or blood test) unless you are intending to treat.

 

Treatment:

 

Treatment, in my opinion, should always be based only on confirmed infection. I do not often suggest empirical eradication, even in a hospital setting with acute ulceration or bleeding seen at gastroscopy. Treatment of H.Pylori is never an emergency, and, as discussed further below, should be a considered discussion with the patient to allow for maximum possible adherence to what is a fairly rigorous regimen.

 

Anticipatory guidance

 

Given the complexity of treatment regimens, it is suggested to provide patients and families additional background information which can assist with improved treatment success. Although not always possible, ideally this is done face to face. Clear communication is crucial. Some things I mention include:

 

  1. Effective treatment requires close adherence to a regimen of three medicines for 10-14 days.
  2. Missed doses are the highest cause of treatment failure
  3. Even with strict adherence, first line treatment still has a 10-20% failure rate with rising rates of resistance, both in NZ and internationally to both clarithromycin and metronidazole.
  4. You can except to have some treatment adverse effects from the antibiotic including nausea or indigestion. Rates may be as high as 50%. Alcohol cannot be consumed whilst taking metronidazole as this causes significant gastrointestinal reactions. It may also cause dysgeusia with a metallic taste in the mouth. Colloidal bismuth as part of second line quadruple therapy may cause darkening of the tongue, urine and stools which can be particularly concerning if not forewarned. Without this pre-emptive advice, patients may believe treatment is exacerbating their condition, or that the ‘cure is worse than the disease’ and stop treatment early. Advice to call through to the practice for assistance can be useful and reassuring for patients. Occasionally patients may require a script of anti-nausea medication.
  5. If asked, I mention that probiotics added to H. pylori treatment regimens have a small and inconsistent effect on eradication rates but may reduce adverse effects.9
  6. This can also be a good time to mention smoking cessation as this decreases treatment efficacy
  7. Explanation for rationale of treatment (i.e. treatment of symptoms / disease they are experiencing, prevention of recurrence, reduction of stomach cancer risk).

 

Triple therapy

 

Local guidelines or pathways may vary depending on local resistance data. Please refer to these if available.

 

In Auckland where I work, my first line treatment suggested is triple therapy consisting of:

 

  • Omeprazole 40 mg twice a day (some suggest just 20mg twice a daily – see below)
  • Amoxicillin 1g twice a day
  • Clarithromycin 500mg twice a day

 

for 10 days total (some suggest 14 days, but 7 days is now considered too short).15


Two additional caveats:

 

  • Resistance to clarithromycin is increasing. Patients with previous macrolide treatments (azithromycin, clarithromycin, erythromycin) are at higher risk of this and metronidazole should be considered as a substitute for erythromycin. Clarithromycin resistance has a greater effect on treatment efficacy as compared with metronidazole resistance, which has a lesser effect on eradication efficacy.

 

  • For patients with penicillin allergy, use metronidazole 400mg twice a day. However it is important to know that amoxicillin is an important part of the triple therapy, as resistance is very low (<5% in NZ). Therefore identification of true penicillin allergy is critical, as up to 90% of patients reporting an allergy are actually able to tolerate penicillin.

 

Second line quadruple therapy for first line failures is:

 

  • Omeprazole 40mg twice a day
  • Tripotassium dicitratobismuthate (Colloidal bismuth) 120 mg four times daily, taken 30 minutes prior to meals and then 2 hours after dinner.
  • Tetracycline 500 mg four times daily (requires separate special authority but fully subsidised)
  • Metronidazole 400 mg three times a day

 

Taking a medication four times per day can be extremely difficult to remember. Using phone applications or setting reminder alarms can be useful.

 

I prefer to use full dose (40mg twice per day) omeprazole treatment. This is because the risk of side effects from PPI therapy is low. Inadequate acid suppression is associated with treatment failure. In addition to optimising the stability and bioavailability of the antibiotics, H.Pylori enters a replicative stage at neutral pH of 6-8, where it is then most susceptible to growth-dependent antibiotics, particularly amoxicillin. Although 20mg twice daily in most may have this effect, variability in adherence, times taken and individual patient pharmacodynamics and medication metabolism may lead to treatment failure.

 

Doxycycline (100mg twice per day) should not be substituted if possible for tetracycline as the efficacy is lower.

 

Pregnancy

Generally symptoms in pregnancy such as dyspepsia and reflux, and therefore treatment is directed at acid suppression with PPI. Usually H.Pylori treatment can be deferred until after delivery. However in cases where H.Pylori is identified and treatment is required (severe nausea or vomiting, worrisome recurrent bleeding ulcers not responding to standard treatment) first line treatment as above is low risk, especially after week 14.  

 

Confirmation of Eradication

This is somewhat controversial. Auckland guidelines suggest that “resolution of symptoms is correlated with successful eradication and re-testing is not required”.

 

However, due to increasing antibiotic resistance and all of the disease possibilities above, my personal practice (especially in high risk patients) is to check and confirm clearance. In addition, some patients have a temporary improvement of symptoms with the acid suppression from the omeprazole. Faecal antigen testing to confirm eradication should be performed at least two weeks, preferably four weeks after completion of antibiotic treatment, and must be done with the patient off PPI. If the patient requires PPI for reflux disease, an histamine (H2) blocker such as famotidine 20mg twice daily can be used as a temporary substitute.

 

Treatment failure:

Management of patients who have failed multiple regimens is an increasingly frequent challenge. After 2 trials of treatment, referral for gastroscopy with biopsy for culture and sensitivity is suggested. Rarely in NZ, other antibiotics such as levofloxacin may be required.

 

Reinfection following treatment:

This is not common in adults, perhaps <1-2%. This risk is again mostly dictated by socio-economic status. Confirmed clearance on stool testing, followed by a repeated positive test later on is more likely to represent an originally suppressed, but not completely eliminated bacteria.

 

Future directions:

 

  1. Further local updated data on prevalence and primary and secondary resistance patterns required

 

International data and treatment guidelines and suggestions must be taken with a grain of salt, with considerable differences in patient population and prescribing practices.  A recently published meta-analysis examining antibiotic resistance of H.Pylori in Australia and New Zealand demonstrated an increase in primary clarithryomycin resistance with stable or low resistance to other used antibiotics.16 However, there were only 15 total studies, including 3 from New Zealand published between 1996-2013, and none in the last 10 years.

 

The last paper from NZ was from 2012 in 100 patients in Auckland which demonstrated an overall 16% clarithyomycin resistance, 49% metronidazole resistance, 5.5% amoxicillin resistance and no resistance to tetracycline2. A study of 50 patients in 2004 showed no resistance to any antibiotics other than 20% to metronidazole.17

 

Updated prevalence data and primary resistance data, stratified by ethnicity and locality is required. Already underway, our group will aim to publish secondary resistance data on over a thousand isolates from previous years in Auckland shortly.

 

  1. H. pylori screening: test-and-treat as a strategy for stomach cancer prevention in high risk populations

 

In 2001 there was the first prospective clinical study to prove Pylori as the key factor in gastric cancer development. This key development presented the opportunity for preventive screen-and-treat strategies. We now have randomised controlled trial data with over 20 years of follow-up for eradication regimens as a method of population gastric cancer prevention. Data from one study show that participants receiving H.pylori treatment had a 43% lower incidence of gastric cancer compared with their placebo counterparts, which increased to 63% in patients without pre-cancerous lesions at baseline.18 A number of reports have suggested this to be a cost effective.

 

It is established that H.Pylori is the major contributor to excess gastric cancer incidence in high risk NZ groups. In my opinion, eradication strategies, successfully studied and implemented elsewhere, can and should be considered in these groups. These benefits do have to be weighed against cost and in particular, concerns around antibiotic usage and resistance.

 

  1. Vaccine development

 

A vaccine would certainly be a powerful method for prevention of gastric cancer and the other diseases caused by H.pylori. Despite first experimental research since 1992 with multiple subsequent trials, there are unfortunately no advanced vaccine candidates for treatment either prophylactically or therapeutically.

 

SUMMARY:

 

  • Pylori infects half of the worlds population, with extremely variable gastroduodenal pathologies including ulcer disease, gastric cancer and lymphoma.
  • Only test if you intend to treat
  • Only treat if you have a positive test result (i.e. there is no need for empirical eradication)
  • Use H.Pylori stool antigen testing for initial diagnosis and also confirmation of treatment. Blood testing for serology does not distinguish present and past infection
  • Have an anticipatory discussion with patients to advise them of the treatment regimen, the importance of strict compliance, the likelihood of minor adverse effects with triple therapy.
  • Triple therapy has an 80% first line success and should be taken for 10 to 14 todays.

 

REFERENCES: 

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  2. Hsiang J, Selvaratnam S, Taylor S, Yeoh J, Tan YM, Huang J, et al. Increasing primary antibiotic resistance and ethnic differences in eradication rates of Helicobacter pylori infection in New Zealand--a new look at an old enemy. N Z Med J. 2013 Oct 18;126(1384):64–76.
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  10. Zhao B, Zhang J, Mei D, Luo R, Lu H, Xu H, et al. Does Helicobacter pylori Eradication Reduce the Incidence of Metachronous Gastric Cancer After Curative Endoscopic Resection of Early Gastric Cancer. J Clin Gastroenterol. 2020 Mar;54(3):235–41.
  11. Raderer M, Wöhrer S, Kiesewetter B, Dolak W, Lagler H, Wotherspoon A, et al. Antibiotic treatment as sole management of Helicobacter pylori-negative gastric MALT lymphoma: a single center experience with prolonged follow-up. Ann Hematol. 2015 Jun 13;94(6):969–73.
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  14. Bontems P, Kalach N, Vanderpas J, Iwanczak B, Casswall T, Koletzko S, et al. Helicobacter pylori Infection in European Children with Gastro-duodenal Ulcers and Erosions. Pediatric Infectious Disease Journal. 2013 Dec;32(12):1324–9.
  15. Yuan Y, Ford AC, Khan KJ, Gisbert JP, Forman D, Leontiadis GI, et al. Optimum duration of regimens for Helicobacter pylori eradication. Cochrane Database of Systematic Reviews. 2013 Dec 11;
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