H. pylori has been found to play a role in chronic gastritis, peptic ulcer, mucosa-associated lymphoid tissue lymphoma, and gastric carcinoma.[1] It is estimated that 50% of the world’s population is infected with H. pylori [2] and 30% of North Americans with dyspepsia are infected with H. pylori.[3] Yet most people with H. pylori are asymptomatic.[4].

We get this question from doctors frequently: What does it mean if my patient has Helicobacter pylori (H. pylori) detected in his/her stool?

This question is common because stool H. pylori detected using DNA technology (also polymerase chain reaction or PCR) is a very new tool, especially in the clinical arena. Researchers test for H. pylori DNA in all kinds of specimens and fluids [2,5,6] but it has not yet become part of routine clinical practice.

H. pylori detected on a Metametrix stool test; 1.2E+006 represents 1.2x10⁶ CFU/g in scientific notation.

Frequency

H. pylori is a common finding on the GIfx stool test. We report it in approximately 16%–23% of specimens.[7,8] When we do detect H. pylori above the reference limit of 100,000 colony forming units/gram stool (CFU/g), it is designated as high (H) on the report. For people who have H. pylori in their stool, it is typically detected between 410,000–1,700,000 CFU/g (4.1x10⁵–1.7x10⁶). The median for an H. pylori result is around 6.2x 10⁵ or 620,000 CFU/g stool.[8]

How do the Different H. pylori Tests Measure Up?

H. pylori diagnostic tests can be broken down into two categories: invasive testing (endoscopy with biopsy, histology, culture, and rapid urease test) and non-invasive testing (serology, I3C urea breath test, and H. pylori stool antigen).[9] Endoscopy with biopsy, histology, culture, and rapid urease test is considered the “gold standard” for diagnosing H. pylori.[10]

Urea breath test (UBT) and H. pylori stool antigen (HpSA) are recommended by the American Gastroenterological Association for optimal noninvasive H. pylori testing.[3] HpSA is comparable to UBT in terms of accuracy.[1] However, urea breath test can be difficult to use in very young children, making noninvasive stool tests more desirable.[2] In addition, patients must discontinue use of proton pump inhibitors, bismuth products, and antibiotics prior to testing UBT.[4] Antibiotics, bismuth products, and PPIs may decrease the sensitivity of HpSA testing as well.[4]

Serum antibodies are the least sensitive and specific for H. pylori testing. Further, H. pylori serum antibodies cannot differentiate between a past or current infection.[3,4] HpSA is a better predictor of active H. pylori infection than IgG antibodies.[2]

Table adapted from “Update on Helicobacter pylori Treatment.”[3] Sensitivity and specificity values for H. pylori stool PCR are listed in order of lowest to highest with the corresponding reference.

There is no contest to the sensitivity and specificity of microbe detection using PCR. In fact, DNA identification of H. pylori in a biopsy specimen is superior to standard culture and histology.[10,12,13] H. pylori stool PCR is comparable with H. pylori stool antigen for sensitivity and specificity (see Table). In one study, H. pylori stool PCR, “showed sensitivities and specificities comparable to that of the ‘gold standard’ reference diagnostic methods: the rapid urease test, histology, and culture.”[10]

In patients suffering from abdominal pain,[10] persistent gastrointestinal problems,[5,11] and dyspepsia,[13,14] stool PCR accurately detected H. pylori when compared to endoscopy and biopsy.  Detecting H. pylori in stool by PCR was considered an effective diagnostic for patients with dyspeptic symptoms both before and after treatment when compared to biopsy and rapid urease test.[14] 

H. pylori stool PCR is not as sensitive as gastric biopsy and therefore a patient may be negative for stool H. pylori but positive by biopsy.[5,15] After H. pylori eradication (using triple therapy), endoscopy and biopsy are more sensitive and specific than HpSA or H. pylori stool PCR, suggesting that eradication in the stomach isn’t reflected in the stool immediately. Authors suggest waiting more than one month after eradication therapy to retest for H. pylori with stool PCR or HpSA.[14,16]

Clinicians have sometimes seen cases that are positive for stool H. pylori, yet the UBT is negative. Differences in results for H. pylori tests may be caused by low bacterial density and a patchy distribution of the pathogen.[10] A false negative UBT can be caused by medications taken weeks before the test (proton pump inhibitors, bismuth products, etc.) or incorrect administration of the test. More information can be found here:

• Metametrix Learning Center - Discrepancies in H. pylori Testing. Diagnostic Insight white paper. 2009.
• Explanations for Negative 13C-Urea Breath Test & Positive PCR Stool Test for H. pylori

To Treat or Not To Treat?

Most clinicians carefully weigh the patient’s clinical presentation to determine if H. pylori needs to be treated. Treatment is only warranted if lab data, symptoms, and clinical history are consistent with H. pylori infection. Adjunctive or repeat testing should be ordered to verify the presence of H. pylori. Stenstrom et. al. point out, “As no test is 100% accurate, there may be a case for using a concordance of two tests with different mechanisms, i.e. urea breath test together with stool test or serology, in order to prove if the patient’s H. pylori status is negative or positive.”[17]

Most people infected with H. pylori are asymptomatic and never develop a complication.[4] Some experts have suggested that H. pylori may be a normal, commensal bacterium and should not be treated in asymptomatic individuals. In fact, non-ulcer dyspepsia and GERD have not been shown to improve with H. pylori eradication.[3] Patients who were seropositive for H. pylori had markedly lower risk of developing Barrett’s esophagus,[18] suggesting that H. pylori may even have a protective effect against certain illnesses.

H. pylori-Associated Symptoms and Conditions:

• Chronic gastritis
• Peptic ulcer
• Mucosa-Associated Lymphoid Tissue Lymphoma
• Gastric carcinoma[1]
• Refractory iron deficiency anemia
• Chronic Idiopathic Thrombocytopenic Purpura[1]
• Antral gastritis and Duodenal Ulcer Disease in children, which is likely to present as chronic abdominal pain[5]
• Note: Non-ulcer dyspepsia and GERD have not been shown to improve with H. pylori eradication[3]

When the clinical history and lab tests suggest that H. pylori is causing symptoms for the patient, doctors often use natural anti-H. pylori formulas. Ingredients may include: mastic gum, bismuth, zinc carnosine, ginger root extract, deglycyrrhizinated licorice, Methylmethioninesulfonium (vitamin U), Pistacia leiscus, berberine, goldenseal, oregano oil, barberry, oregon grape root extract, and/or Coptis chinensis extract.

Five gram doses of vitamin C,[19] probiotics (before, during, and after treatment), an anti-inflammatory diet, stress reduction, and gut-healing formulas have also been used in comprehensive programs to effectively eradicate H. pylori. Some doctors use triple therapy[3] to eradicate H. pylori, especially if the patient is presenting with ulcer or severe GI symptoms and natural treatments were ineffective.  H. pylori is transmissible between humans and therefore strategies to avoid reinfection may be helpful, yet some studies showed patients with infected spouses were not at higher risk of reinfection.[3]

In a Nutshell

• More than one H. pylori test is recommended to determine if the patient’s H. pylori status is positive or negative
• Treatment of H. pylori is only warranted if lab data, symptoms and clinical history are consistent with H. pylori infection.
• H. pylori stool PCR has showed sensitivity and specificity comparable to HpSA.
• Natural treatments have been used alone or in conjunction with standard treatments for the eradication of H. pylori.

~ Cass Nelson-Dooley, MS

Links

Am Family Physician “Update on Helicobacter pylori Treatments”[3]

References 

1. Booka M, Okuda M, Shin K, et al. Polymerase chain reaction--restriction fragment length polymorphism analysis of clarithromycin-resistant Helicobacter pylori infection in children using stool sample. Helicobacter. Jun 2005;10(3):205-213.
2. Sinha SK, Martin B, Gold BD, Song Q, Sargent M, Bernstein CN. The incidence of Helicobacter pylori acquisition in children of a Canadian First Nations community and the potential for parent-to-child transmission. Helicobacter. Feb 2004;9(1):59-68.
3. Ables AZ, Simon I, Melson ER. Update on Helicobacter pylori Treatment. American Family Physician. 2007;75(3):351-358.Lacy BE, Rosemore J. Helicobacter pylori: ulcers and more: the beginning of an era. J Nutr. Oct 2001;131(10):2789S-2793S.
4. Lacy BE, Rosemore J. Helicobacter pylori: ulcers and more: the beginning of an era. J Nutr. Oct 2001;131(10);2789S-2793S.
5. Allaker RP, Young KA, Hardie JM, Domizio P, Meadows NJ. Prevalence of helicobacter pylori at oral and gastrointestinal sites in children: evidence for possible oral-to-oral transmission. Journal of medical microbiology. Apr 2002;51(4):312-317.
6. Westblom TU. Molecular diagnosis of Helicobacter pylori. Immunological investigations. Jan-Feb 1997;26(1-2):163-174.
7. Morris C, Nelson-Dooley C. Prevalence and quantity of stool H. pylori DNA in 5,669 outpatients of all ages. Metametrix Institute Datamining. Duluth: Metametrix Clinical Laboratory; 2011.
8. Morris C, Nelson-Dooley C. Prevalence and quantity of stool H. pylori DNA in 15,090 outpatients of all ages. Metametrix Institute Datamining. Duluth: Metametrix Clinical Laboratory; 2009-2010.
9. De Korwin JD. [Advantages and limitations of diagnostic methods for H. pylori infection]. Gastroenterologie clinique et biologique. Mar 2003;27(3 Pt 2):380-390.
10. Schabereiter-Gurtner C, Hirschl AM, Dragosics B, et al. Novel real-time PCR assay for detection of Helicobacter pylori infection and simultaneous clarithromycin susceptibility testing of stool and biopsy specimens. Journal of clinical microbiology. Oct 2004;42(10):4512-4518.
11. Falsafi T, Favaedi R, Mahjoub F, Najafi M. Application of stool-PCR test for diagnosis of Helicobacter pylori infection in children. World J Gastroenterol. Jan 28 2009;15(4):484-488.
12. Yan WH, Chen J, Yu JD, Li ZY, Huang XL, Zhang XP. [Rapid detection of clarithromycin resistant Helicobacter pylori from children's gastric biopsy specimens by polymerase chain reaction-restriction fragment length polymorphism]. Zhonghua er ke za zhi. Nov 2009;47(11):848-851.
13. Weiss J, Tsang TK, Meng X, et al. Detection of Helicobacter pylori gastritis by PCR: correlation with inflammation scores and immunohistochemical and CLOtest findings. Am J Clin Pathol. Jan 2008;129(1):89-96.
14. Mishra S, Singh V, Rao GR, et al. Detection of Helicobacter pylori in stool specimens: comparative evaluation of nested PCR and antigen detection. Journal of infection in developing countries. 2008;2(3):206-210.
15. Medina M, Medina M, Martin G, et al. [Presence of Helicobacter pylori in gastric biopsies and feces of pediatric patients with celiac disease.]. Revista de gastroenterologia de Mexico. Apr-Jun 2009;74(2):94-98.
16. Makristathis A, Pasching E, Schutze K, Wimmer M, Rotter ML, Hirschl AM. Detection of Helicobacter pylori in stool specimens by PCR and antigen enzyme immunoassay. Journal of clinical microbiology. Sep 1998;36(9):2772-2774.
17. Stenstrom B, Mendis A, Marshall B. Helicobacter pylori--the latest in diagnosis and treatment. Australian family physician. Aug 2008;37(8):608-612.
18. Thrift AP, Pandeya N, Smith KJ, et al. Helicobacter pylori infection and the risks of Barrett's oesophagus: A population-based case-control study. Int J Cancer. Jun 16 2011.
19. Jarosz M, Dzieniszewski J, Dabrowska-Ufniarz E, Wartanowicz M, Ziemlanski S, Reed PI. Effects of high dose vitamin C treatment on Helicobacter pylori infection and total vitamin C concentration in gastric juice. Eur J Cancer Prev. Dec 1998;7(6):449-454.