Helicobacter pylori (H. pylori) infection.

The Nutrition Practitioner. Spring 2007

H. pylori may be found in up to 50% of the world’s population, which would make it the most common infectious agent worldwide 1. The World Health Organisation (WHO) has classed H. pylori as a type 1 carcinogen, yet it is mainly only patients with gastric ulcers who get tested and treated. Non-invasive breath testing is reliable, safe and inexpensive 2.  Re-infection is virtually absent after successful eradication 3.  At present, antibiotic therapy remains the standard care for patients with H. pylori infection. Nutritional support may help to improve antibiotic     efficacy 4,5, suppress H. pylori activity 6,7 and reduce gastric symptoms.   


H. pylori may be found in up to 50% of the world’s population making it the most common infectious agent worldwide1.  H. pylori is a Gram-negative spiral-shaped bacterium. In humans, it colonises the stomach and infection is known to be the likely cause of:

o Duodenal ulcers – 70% to 90% of cases are caused by H. pylori.
o Gastric ulcers – 60% to 80% of cases are infected by H. pylori.
o Chronic gastritis – caused by a decrease of stomach acid, a reflection of H. pylori infection.
o Mucosa-associated lymphoid tissue (MALT) lymphomas which account for around 5% of all cancers.
o Gastric cancer is the second most common cancer in the world, and H. pylori is present in >80% of cases.
o Non-ulcer dyspepsia – up to 87% of cases are related to H. pylori. 8,9


H. pylori infection is known to produce peptic ulcers and gastritis associated with gastric acid hypersecretion.  However, not all H. pylori infected individuals have ulcers or gastric symptoms; there are a variety of additional, external factors, including genetic background and environmental factors, such as cigarette smoking 10, which are known to increase the likelihood of ulcerogenesis.  Certain pathogenic strains of H. pylori are also more associated with peptic ulcer disease.11 


H. pylori can also result in gastric acid hyposecretion if the infection is chronic in nature 8.  Both hyperchlorhydria and hypochlorhydria may produce symptoms including heartburn, indigestion and dyspepsia.  However, indigestion is so prevalent that patients often self-medicate with over-the-counter remedies (a multimillion-pound-a-year industry) that suppress symptoms by neutralising acidity in the stomach.  The symptoms of indigestion are rarely treated seriously unless accompanied with pronounced pain. 


Since the discovery of H. pylori in 1982 by Robin Warren and Barry Marshall there have been numerous studies conducted regarding its epidemiology, transmission, testing, treatment and associations with disease.   It is now apparent that H. pylori can also infect the skin, liver and heart and that these infections may produce a number of different disease states 8. As well as the previously mentioned gastric symptoms, previous studies have reported an association between H. pylori infection and:

o Liver disease: a higher prevalence of H. pylori infection has been described in patients with liver cirrhosis 12.  Causal mechanisms are unclear but H. pylori has strong urease activity 13.
o Iron deficiency anaemia: some strains of H. pylori are able to acquire iron, competing with the host 14
o Hypertension: this may be due to the cytotoxic substances produced by the bacteria or produced by the host in response to infection15. Diastolic blood pressure values significantly decrease after H. pylori eradication.15 
o Autoimmune diseases, such as Henoch-Schönlein purpura, Sjögren’s syndrome, and autoimmune thrombocytopenia, which may be due to cross mimicry between bacterial and host antigens.12
o Rosacea:  patients have various gastrointestinal symptoms and a higher prevalence of infection which may be mediated by H. pylori related cytotoxins and cytokines.16
o Diabetes:  although controversial, the increased production of cytokines could be deleterious for the control of the glycaemia.17
o Hyperparathyroidism: patients have a higher prevalence of infection 18 and it results in increased acidity of gastric juice which may intensify H. pylori infection.19
o Cardiovascular disease:  chronic infection may act as a risk factor due to low grade, persistent inflammatory stimulation.12,20,21 
o Parkinson’s disease: H. Pylori may be involved with the development of this neurological condition and eradication appears to help the physical abilities of people with this disease,22 this may be due to improved drug absorption and response to levodopa after eradication 23,24 
o Chronic Urticaria:  although the reason is unknown cytotoxins may act as a trigger in some individuals.11,12 
o Cobalamin deficiency:  H. pylori gastritis leads to the impairment of the production of pepsinogen and acid which are essential to cobalamin absorption25.  Serum haemoglobin and cobalamin levels increase after treatment.26


The National Institutes of Health (NIH) Consensus Development Conference guidelines recommends H. pylori should be eradicated in peptic ulcer disease, functional dyspepsia, gastroesophageal reflux disease (GERD) and mucosa-associated lymphoid tissue (MALT) lymphoma but the prophylactic eradication of H. pylori was not recommended 27.  Even though an epidemiological study 28 showed that half of an asymptomatic healthy population were infected with H. pylori, and the World Health Organisation has classed H. pylori as a type 1 carcinogen, current data does not support treatment of asymptomatic patients and this has set precedence so that only patients with severe gastric symptoms are tested and treated.


The source of H. pylori is not yet known but it appears to be mainly acquired during childhood 29 and the bacteria are most likely spread from person to person through faecal-oral or oral-oral routes 9 but why some patients become symptomatic, while others do not, is not known.  Further research is required to develop understanding regarding its transmission, symptomology, pathophysiology and its role in different disease states.


Tests used to identify H. pylori infection include:
• Endoscopic biopsy of the gastric mucosa
• The urea breath test
• Stool antigen assessment (HpSA)
• Blood antibodies enzyme-linked immunosorbent assay (ELISA)
o Via a venous blood sample
o Via a fingerstick blood sample


Diagnosis of H. pylori can be made by urease testing, histology and/or culture from biopsy specimens of the stomach and duodenum 30. Endoscopic biopsy is considered the reference method of diagnosis but it is costly and invasive.


In a urea breath test (UBT), the patient is given an oral preparation of either non-radio isotope carbon 13 (13C)-labelled urea or radioactive isotope carbon 14 (14C)-labelled urea.  In the presence of H. pylori infection, bacterial ureases metabolise the urea to produce labelled carbon dioxide and ammonia.  The labelled carbon dioxide diffuses into the blood stream and is excreted by the lungs.  This labelled carbon can then be measured as CO2 in the patient’s expired breath to determine the presence of H. pylori.  The 13C-labelled urea is detected by mass spectrometry and the 14C-labelled urea by liquid scintillation.  The sensitivity and specificity of UBT ranges from 94-98% 9, 30.  Urea breath testing is considered to be a safe, simple, inexpensive and non-invasive method of accurately testing for H. pylori 2 but acid-suppression treatment should be withheld for two weeks prior to testing, as false negatives may result if it is continued. 


Stool antigen serology identifies active infection.  A study of 102 patients 31, where stool immunoassays were compared to endoscopy biopsy, showed the stool testing had excellent sensitivity and specificity (92-98%). The cost is cheaper than urea breath testing and stool tests are approved by the United States Food and Drug Administration (FDA) for diagnosis of active infection, monitoring effectiveness of antibiotic therapy during treatment and confirmation of eradication after treatment. 32 Although this is the only method which may be used to monitor therapy effectiveness during treatment, it can only indicate treatment failure with a positive result, eradication cannot be confirmed at this point as specificity may be reduced. 32, 33


Serological assays measure specific H. pylori immunoglobulin antibodies that can determine if an individual has been infected. An evaluation of commercially available serology kits 34 concluded that serology kits which measured IgA, IgG and IgM simultaneously or IgA alone did not perform as well as those that measures only IgG H. pylori antibodies in serum.  This may be because most patients infected with H pylori produce a measurable systemic immune response, composed primarily of IgG 35. Serum IgA may be detected in fewer than half (range, 39%-82%) of infected patients, and serum IgM is found rarely 35.  The sensitivity and specificity of the IgG serology assays range from 80-95% depending on the assay used.9,30


Whole-blood finger-stick antibody tests offer a simple near patient test with more rapid results 36. Specificity among different test varies between 79% and 90% but these tests proved only marginally sensitive in detecting patients infected with H. pylori. 37


The urea breath test may be the most reliable, non-invasive test for H. pylori infection, including follow up testing after treatment. Post-therapy confirmation of bacterial eradication is important because of the growth of resistant H. pylori strains and the continuation of symptoms that may occur with incomplete eradication 38. Retesting should be done four weeks after completion of therapy 30,32,38 but biopsy and serological tests should not be used after H pylori treatment.30,31


Conventional treatment for H. pylori includes varied combinations of antibiotics, proton pump inhibitors and histamine H2 receptor antagonists for a period of one to two weeks. The antibiotics omeprazole, clarithromycin and metronidazole are commonly used as they are cost-effective and have a 97% eradication rate 39. Acid suppression by the H2 blocker or proton pump inhibitor (PPI) in conjunction with the antibiotics helps to alleviate ulcer-related symptoms, helps to heal gastric mucosal inflammation and may enhance the efficacy of the antibiotics against H. pylori at the gastric mucosal surface.9


Eradication rates range from 61% to 94% depending on the regime used 9,40. Antibiotic resistance and patient non-compliance are the two major reasons for treatment failure 9. Overall, triple therapy regimes, which involve the use of a PPI and two antibiotics, have shown better eradication rates than dual therapy and longer length of treatment may result in better eradication rates 9. However, if the triple therapy regime is not initially effective there may be increased antibiotic resistance leading to limited treatment choices available afterwards; treatment should therefore start with dual therapy to avoid this. 40 


Clinical trials indicate that L. acidophilus probiotics produce a suppressive activity against H. pylori 6,7.  Some probiotics may also improve efficacy of antibiotic therapies 4,5 and reduce the incidence of antibiotic-associated gastrointestinal side effects, which could help to improve compliance 5,41,42.  The mechanisms by which Lactobacilli participate in protecting against enteric infections are, however, unclear.5


Honey is a traditional remedy for dyspepsia. One in vitro study using isolates from biopsies of gastric ulcers concluded that the antibacterial effects of manuka honey may be effective against H. pylori 43. Some sources indicate grapefruit seed extract, berry extracts, cranberry juice, mastic gum, vitamin C, thyme, cinnamon, ginger, garlic, liquorice and hot chillis may also have inhibitory effects 44-52 but evidence is limited and inconclusive, and further research is required.


A 1995 clinical trial of 3,365 adults 53 tested the effects of:
1. 2-week amoxicillin and omeprazole treatment vs.placebo
2. long-term vitamin C, E and selenium treatment vs. placebo
3. aged garlic supplements vs. placebo
in reducing the prevalence of advanced precancerous gastric lesions.


The results showed that conventional antibiotic treatment reduced the prevalence of severe chronic atrophic gastritis, intestinal metaplasia, dysplasia and gastric cancer but no statistically significant beneficial effects were seen for garlic or vitamin supplements. The researchers concluded that treatment of H. pylori infection reduces the risk of precancerous changes to the stomach 53. As re-infection of H. pylori is virtually absent after successful eradication 3, conventional treatment is therefore important. 


Case Studies
In one year of practice I have asked two patients to go to their GPs to be tested for H. pylori infection.   The first was a 33 year old female with poor digestion, increased gut permeability, food allergies, urticaria and a family history of H. pylori. Her father had stomach ulcers for years and he had tested positive for H. pylori and been successfully treated. She tested positive with the urea breath test and her GP prescribed an antibiotic treatment regime.  Nutrition support included a probiotic course immediately after antibiotic therapy and then a gastro-intestinal support program to help normalise gut function and regain mucosal integrity.  The approach included a four step clinical program which aimed to:

o Remove allergens and toxins from the GI tract.
o Replace enzymes and other digestive factors that may have been lacking or insufficient.
o Re-inoculate the GI tract with desirable bacteria and gain microfloral balance.
o Repair the intestinal wall structure and function via nutritional support.


This patient was not re-assessed by her GP for confirmation of bacterial eradication.  Her urticaria and digestion improved after therapy.  After being informed that H. pylori infection clusters within families 54, she advised other family members to get tested.  Her mother tested positive but her brother’s GP refused to test him. It may be that some GP surgeries do not have access to non-invasive methods of testing and/or they lack funding or rationale for testing patients without ulcers or chronic gastritis.


The second case is of a 48 year old female with numerous digestion and elimination issues, as well as a history of duodenal pain, hiatus hernia, heartburn and antacid consumption.  Unfortunately her GP also refused to test her.  We will proceed with a urea breath test from Individual Well-being Diagnostics Laboratory (IWDL) or The Doctors’ Laboratory (TDL). 


Since the source of H. pylori infection is not yet known recommendations for avoiding infection have not been made.  However, prevention strategies, such as washing hands, should be encouraged in children and adults. At present, antibiotic therapy remains the standard care for patients with H. pylori infection. Benefits of nutritional support with probiotics during and after antibiotic therapy are indicated and a nutrient-dense, fibre-rich diet of whole, unprocessed foods rich in bioflavonoids, anti-inflammatory and antibacterial foods may be beneficial in helping to reduce symptoms.

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