Breath testing prior to SIBO treatment? No.

This is half of a two-part debate — read the opposing argument.

My problem with current concepts of small intestinal bacterial overgrowth (SIBO) and the use of breath tests in their diagnosis, is that I have been around too long. Long enough, unfortunately, to remember the origins of this entity as a cause of maldigestion and malabsorption. Fascinated, as always, by pathophysiology, I was captivated by how the “contamination” of the small intestine by colonic bacteria led to the premature deconjugation of bile acids, consumption of vitamin B12, production of folic acid and competition with the host for ingested nutrients.1,2 An inevitable clinical picture dominated by diarrhea and malnutrition ensued, and the work-up revolved around defining and resultant nutritional deficiencies and uncovering any possible causative factors. Receding white hair also means that I recollect the original use of the lactulose breath hydrogen test that we now routinely use to diagnose SIBO — to measure mouth-to-cecum transit.3

Fast forward to today and we find SIBO incriminated as a major contributor to irritable bowel syndrome (IBS), largely based on the use of the lactulose breath hydrogen test. It is among those who present with “typical” IBS symptoms and, I suspect, bloating, in particular, that hydrogen breath tests are performed and SIBO diagnosed. Yes, we do see individuals with “classical” SIBO — those with non-responsive celiac disease (a pretty rare phenomenon), complicated Crohn’s disease and disorders, such as scleroderma (where motility is compromised and stasis results). These, however, represent a minority of those who are asked to ingest glucose or lactulose and exhale into a tube over a few hours.

So the issue is: Do breath tests reliably detect SIBO in those in whom they are most commonly employed, and do their results enhance therapy? Before we can even attempt to address these questions, we must surely agree on a definition of the entity we seek to diagnose — SIBO. For me, the edifice so carefully built all those years ago has crumbled and SIBO, as it is currently viewed, has all the permanence and structural integrity of a mirage. It is what you want it to be; indeed, it is, in most instances, what the tests tell you.4 What then of tests for SIBO? The much-maligned approach of jejunal aspiration and culture is dismissed as invasive and inadequate in the microbiome era, while others point to the many shortcomings of breath tests and of the lactulose breath test, in particular. What is fascinating and almost amusing to me about our “modern” concerns surrounding the lactulose breath test is that they focus on a confounder that relates to its original proposed use — the measurement of small bowel (or, more correctly, oro-cecal) transit. How quickly we forget! Specifically, rapid small-intestinal transit, as occurs in some with IBS and other diarrheal illnesses, will lead to the premature (within 80 to 90 minutes) peak in breath hydrogen now regarded as diagnostic of SIBO.5 Even the glucose breath test, long regarded as more accurate, has come under suspicion with the recognition that glucose loads are not completely absorbed in the small intestine and some unabsorbed glucose reaches the colon with a resultant breath hydrogen peak.6 Before we can make any progress on how we test for SIBO we have to agree on what it is. We cannot rely on unreliable tests to tell us what it is; to do so results in an unending circular argument. Our hope is that new technologies to sample the small intestine,6 allied to high-throughput sequencing or metagenomics to define the microbial composition of the small bowel and metabolomics to detect the potentially harmful metabolites that they produce, will provide a new definition of SIBO, and one that brings us back to where I started: pathophysiology.

Before we can even attempt to address these questions, we must surely agree on a definition of the entity we seek to diagnose — SIBO.

Do breath tests guide therapy? Here there is a remarkable lack of data. There are little or no data on any antibiotic regimen in any indication. Indeed, what antibiotic one chooses, as well as its dose and duration, owes more to habit than science and few, if any, studies of SIBO have involved long-term (especially relevant to a chronic condition such as IBS), longitudinal assessments of symptoms and breath tests in response to any antibiotic. In the IBS-type patient with diarrhea or without constipation (not necessarily the same thing), rifaximin does work, but we await data to tell us that breath testing helps predict responders. In the meantime, I can counter that the modulation of the colonic microbiome or the small intestinal metabolome or an anti-inflammatory effect might provide alternate explanations for the benefits of rifaximin. Until we resolve these fascinating questions there is no reason not to try an empiric course of rifaximin in the appropriate patient, and when simpler and cheaper remedies have failed. Just don’t wait for a breath test to tell you what to do.

The clinical dilemma right now is that we are using poorly performing tests to diagnose a condition that we cannot define, and we are choosing a treatment whose mode of action is unclear. Not exactly an ideal situation! There is much to do. In the meantime, while definitions are refined and diagnostic tests honed, what do we do? Yes, use breath tests in the aforementioned situations where SIBO is a real possibility, but be resistant to their use elsewhere. Treat their results with a healthy dose of skepticism.

Dr. Pimentel says breath testing is an important part of the workup of patients.

Key takeaways

  1. With the exception of the setting of maldigestion and malabsorption, the role of SIBO in the pathogenesis of gastrointestinal symptoms is far from clear.
  2. The true spectrum of SIBO needs to be revisited using new technologies and modern molecular microbiology.
  3. Breath tests suffer from limitations in accuracy and their ability to predict responses to antibiotics has not been well defined.
  4. Meanwhile, the treatment of suspected SIBO remains empiric.

Disclosures: Dr. Quigley is a consultant for Alimentary Health, Axon Pharma, Biocodex, Salix and Vibrant, and has shares in Alimentary Health. Dr. Quigley is on the AGA Research Awards Panel and on the Clinical Gastroenterology and Hepatology editorial board. He is also on the board of directors for the International Scientific Association for Prebiotics and Probiotics.

References

1. Tabaqchali S., Booth C.C. Jejunal bacteriology and bile-salt metabolism in patients with intestinal malabsorption. Lancet. 1966;2:12-15.
2. Roberts S.H., James O., Jarvis E.H. Bacterial overgrowth syndrome without “blind loop”: A cause for malnutrition in the elderly. Lancet. 1977;2;1193-1195.
3. Bond J.H., Levitt M.D. Use of breath hydrogen (H2) to quantitate small bowel transit time following partial gastrectomy. J Lab Clin Med. 1977;90:30-36.
4. Quigley E.M.M. The spectrum of small intestinal bacterial overgrowth (SIBO). Curr Gastroenterol Rep. 2019;21:3.
5. Rezaie A., Buresi M., Lembo A., Lin H., McCallum R., Rao S., Schmulson M., Valdovinos M., Zakko S., Pimentel M. Hydrogen and methane-based breath testing in gastrointestinal disorders: The North American consensus. Am J Gasterenterol. 2017;112(5):775-784.

2 comments

  • Why has no one done the obvious study of comparing duodenal/jejunal aspirate culture with the results of breath tests in the same patient? My guess is that SIBO will turn out to be a vanishingly small cause of IBS in this context and that the breath tests will more likely reflect rapid transit to the colon than anything else.

  • I believe Dr Quigley has brought out 2 very important questions: 1. Is SIBO a common cause of IBS?, and therefore is it reasonable to want to work up every patient who presents with bloating for SIBO? and 2. Is the hydrogen breath test diagnostic for a poorly defined syndrome like SIBO?
    I for one don’t even know if SIBO exists outside of the post surgical blind loops we used to see 35 years ago( but have not seen for decades in community clinical practice), or in the classical cases Dr Quigley outlined above. I do see quite a bit of IBS on a daily basis for the past 36 years , and I am certain that SIBO is not a major contributor to its etiology, since I do not require antibiotics, including rifaxamin to treat them. Bloating is a common symptom but postprandial bloating is most likely due to IBS, or less likely gastroparesis.IBS is most likely due to stress and anxiety in a persons life, and is overwhelmingly controlled with anticholinergics in judicious doses and anxiolytics if needed. This along with spending time talking to the patient, seeing them frequently until you actually know something about them, and they trust you, and you helping them reduce the stressors in their lives, is what is needed to get excellent results in 85 % of patients and fair to good results in another 10%. Perhaps it is the 5% that do not respond who I should be evaluating for SIBO?
    THe other important question that Dr Quigley insinuates is that none of Koch’s postulates have been fulfilled for this entity called SIBO.
    Despite the lack of academic papers on the anticholinergics as valuable tools in treating IBS, one cannot ignore the mountain of excellent results that good clinicians have produced over the past 4-5 decades in their own practices. Then again it may all boil down to the magic of how one presents themselves to the patient and how much confidence the patient has, and how much they believe in the power of the doctor treating them, that dictates the outcome. That is more likely in my opinion then the chance that SIBO is an important etiology of IBS, no matter how it is to be defined.

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