Helicobacter pylori (Hp) is a bacteria which infects only stomach tissues. The source of the bacteria is not known but presumably it is acquired through food or water ingestion. The infection is generally chronic and most people are not aware of the initial infection.
Risk associations for being infected include advancing age such that less than 20% of young adults but at least 60% of Canadian seniors are infected. Growing up in very crowded conditions or in a less developed country are also risk factors.
Tests to diagnose the infection include blood or saliva tests for the antibody to Hp. One should be aware that the antibody can persist in the body for more than a year after complete eradication of the organism so that following antibody levels after treatment is not a useful way to confirm successful therapy. The organism can be seen microscopically on stomach biopsies taken at the time of scoping. Nuclear breath tests also indicate the presence of the bacteria but are not readily available, are expensive and not generally needed.
In most people, the bacteria does no discernible harm but simply lives in the stomach lining. However 15% of people with this infection will eventually develop an ulcer. The exact reason why some get an ulcer and others do not is not known. However, looked at the other way, almost everybody with a standard peptic ulcer will be infected. Furthermore the chance of getting a second ulcer within the year can be reduced from 60% to about 5% if the bacteria is eradicated after an episode of ulcer disease.
Ulcer disease is the only current symptomatic disease association with Hp. There is no association with heartburn, gas, belching, constipation, diarrhea or non-ulcer dyspepsia (the common complaint of intermittent, upper abdominal discomfort, without any signs of ulcers). Discussion has been raised about an association with stomach cancer but there is no proof for this and nobody is suggesting wholesale treatment simply for this theoretical concern.
Unfortunately the organism is difficult to treat. At the moment, the only indication for therapy is past or current duodenal or gastric ulcers not due to aspirin like drugs. There are many programs available for treatment but all have in common a combination of two antibiotics in high doses plus other agents. The most effective programs (90-95% eradication) use clarithromycin (Biaxin®) 500mg twice a day (bid), Metronidazole 500mg bid plus a proton pump inhibitor such as omeprazole (Losec®) 20mg bid, lansoprazole (Prevacid®) 30mg bid or pantoprazole (Pantoloc®) 40mg bid) for seven days. Alternatives include Amoxicillin 500mg bid, or Tetracycline 500mg four times a day (qid), plus bismuth subsalicylate (Pepto-Bismol®) 2 tabs qid for 10 days with eradication rates of about 80%. In addition a further 2-4 weeks of acid inhibition is used to heal acute ulcerations.
The need for confirmation of eradication is controversial. Most physicians rely on the good success rates of the latest treatment regimens rather than undertaking expensive or tedious tests to prove it. Perhaps the best news is that the recurrence of Hp infection is only about 1% per year after successful treatment.
In summary the approach to duodenal or gastric ulcers has radically changed over the last decade. Eradication of Helicobacter pylori in those with past or current ulcers will dramatically reduce the risk of recurrent disease and complications.
James Gray, MD, FRCPC
First published in the Inside Tract® newsletter issue 101 – May/June 1997
We have good and bad bacteria living in us at all times. What you might find surprising is that the human body contains symbiotic (of mutual benefit) bacteria that significantly outnumber the body’s own cells. For each cell in the body, at least 10 bacteria live within or on us. They work with and against the body and with and against each other. Maintaining the right balance of good and bad bacteria is important, and a variety of factors such as diet, disease, and medical treatments, can influence this balance.
While there may be up to 1,000 different species of bacteria living within our bodies at any one time, there are at least 30 to 40 species in regular residence. The relationships humans have with bacteria are usually mutually beneficial; however, in some cases, bacterial overgrowth can result in human death. Useful bacteria help us convert our food into energy, fight against harmful bacteria, and help modulate our immune systems. Bacteria comprise about 60% of the mass of our feces. While it may be possible to live without the bacteria, it might not be living well. Probiotics is the term used to include any and all beneficial bacteria. Newer disease treatments call for re-introduction of various probiotic strains into the body.
Helicobacter pylori (H. pylori) bacteria are present only in humans and have adapted to the stomach environment. The bacterium is extremely variable, and strains differ markedly in many aspects, such as adherence to gastric mucosa and ability to provoke inflammation. Even in a single infected individual, not all H. pylori bacteria are identical and, during the course of chronic infection, these bacteria adapt to the changing conditions in the stomach. Genetic variations among humans may affect their susceptibility to H. pylori.
H. pylori are responsible for more than 90% of duodenal ulcers and up to 80% of gastric (stomach) ulcers. Evidence links the bacteria to gastritis (inflammation of the stomach) and gastric cancer – the second-leading cause of cancer-related deaths in the world.
H. pylori linked to iron deficiency
A recent study in the American Journal of Epidemiology1, looking at data for 7,462 people, reveals that these bacteria might also contribute to one of the most common nutritional deficiencies in the world – iron.
Iron deficiency affects mainly older infants, young children, adolescents, and pre-menopausal women. Our bodies need iron to manufacture hemoglobin, a substance in red blood cells that carries oxygen to the cells via the lungs. When insufficient iron is present, the body produces smaller and fewer red blood cells, resulting in less oxygen fuelling the body. This can cause impairments in immune, cognitive, and reproductive body functions, and in work performance.
Researchers looked at a representative sample of the American population, aged three and over, covering the years 1999 and 2000, for three factors:
- iron deficiency, defined as at least two abnormal results out of three measures of iron stores,
- iron deficient anemia (IDA), defined as low hemoglobin levels in the presence of iron deficiency, and
- H. pylori infection.
In the study population, 35% of the cases of iron deficiency and 51% of the cases of IDA occurred in H. pylori-infected subjects.
The biochemical mechanism whereby H. pylori cause iron deficiency and anemia is unknown. However, the researchers suggest that the reduced iron could be due one or more of these factors:
- Use of iron by the bacteria to reproduce,
- Micro-bleeding resulting from H. pylori attachments to the stomach wall, and/or
- Decreased iron absorption due to an affect of H. pylori on the stomach.
The majority of people infected with H. pylori were born outside the US, where higher infection rates with the bacteria typically exist. These researchers suggest that H. pylori is the second leading cause of communicable iron deficiency, next to worm infestation.
To conclude, the researchers point out that H. pylori infection raised the risk of iron deficiency by 40% and of IDA by 160%. This was after ruling out patients with peptic ulcer disease – a known contributor to anemia due to blood loss.
Yoghurt helps in the fight against Helicobacter pylori
Doctors treat H. pylori infection with “triple therapy,” consisting of two antibiotics and a proton pump inhibitor. When followed as prescribed, this treatment can prevail over 80-90% of infections. For the remaining 10-20% of resistant cases, quadruple therapy may be necessary, adding other antibacterial medications. Unfortunately, this course of action still does not completely eradicate the bacteria in all cases, and the downside of antibiotic treatment is that it destroys both the bad and the good bacteria.
Two studies, led by the same principal investigator in Taiwan, done four years apart, show better results for both the triple and quadruple therapy by adding AB-yoghurt consumption to the melee. AB-yoghurt contains Lactobacillus acidophilus (acidophilus) and Bifidobacterium bifidus (bifidus), naturally occurring probiotics of the human digestive system.
During the first look at AB-yoghurt, published in the journal, Alimentary Pharmacology and Therapeutics3, in 2002, researchers divided 160 H. pylori-infected patients into two groups. Both groups underwent one-week of “triple therapy” with two antibiotics and one proton pump inhibitor. One group also consumed 200mL of AB-yoghurt, containing at least 5×109 organisms, twice a day, for the week of triple therapy, and for the subsequent four weeks. The other group abstained from all yoghurt products.
The eradication rate of H. pylori was significantly higher in the triple therapy-plus-yoghurt group at 91%, compared to 78% for the triple therapy-only group. Common side effects of triple therapy, such as vomiting, constipation, diarrhea, and metallic taste were less common in the yoghurt-eating group.
In addition, researchers analyzed stool samples from participants four weeks after triple therapy for the quantity of bifidus and found that the numbers were nearly restored to pre-treatment levels in the yoghurt-consuming group, whereas those who did not eat yoghurt showed depleted levels of bifidus.
For the second study, which was published in early 2006 in the American Journal of Clinical Nutrition2, researchers tested whether, after failed triple therapy, yoghurt consumption could improve the efficacy of the next treatment option, quadruple therapy. The researchers worked with 138 patients whose triple therapy had failed to eradicate their H. pylori infection. They assigned patients to either quadruple therapy only or to a group that ate 200mL of AB-yoghurt twice a day for four weeks prior to quadruple therapy.
In those patients who had taken a course of triple therapy that did not eradicate the H. pylori infection, the subsequent eradication rate of H. pylori was close to 91% in the yoghurt-before-quadruple-therapy group, and 77% among quadruple-therapy-only patients.
How does AB-yoghurt work at diminishing H. pylori loads?
The researchers suggest at least six possible mechanisms of action for this:
- H. pylori and the acidophilus and bifidus may directly compete for nutrients in the yoghurt, and H. pylori could be the loser in the battle for nutrients.
- Acidophilus may directly inhibit H. pylori attachment to the stomach wall.
- Attachment of acidophilus and bifidus to the stomach wall may produce a barrier that the H. pylori cannot penetrate.
- Acidophilus and bifidus may exert an immune-modulating effect in the gut that could suppress H. pylori loads.
- Consumption of bifidus-containing yoghurt counteracts the hydrogen-producing action of coliform bacteria in the bowels, which keeps the H. pylori population under control.
- The direct inhibition of urease, which is an important colonization factor for H. pylori, by acidophilus and bifidus may have played some role.
The study authors conclude that AB-yoghurt supplementation – in lactose tolerate patients – may help improve H. pylori eradication and that this supplementation offers some protection against the treatment’s unpleasant side effects.