Siegfried W. Yu

Systematic review: dietary fibre and FODMAP‐restricted diet in the management of constipation and irritable bowel syndrome

Dietary fibre supplements have been advocated for the management of chronic constipation (CC) and irritable bowel syndrome (IBS). Recently, a fermentable oligosaccharide, disaccharide, monosaccharide and polyol (FODMAP) restricted diet has been recommended for IBS.

Anorectal physiology and pathophysiology in the elderly.

Anorectal medical disorders facing the elderly include fecal incontinence, fecal impaction with overflow fecal incontinence, chronic constipation, dyssynergic defecation, hemorrhoids, anal fissure, and pelvic floor disorders. This article discusses the latest advances in age-related changes in morphology and function of anal sphincter, changes in cellular and molecular biology, alterations in neurotransmitters and reflexes, and their impact on functional changes of the anorectum in the elderly. These biophysiologic changes have implications for the pathophysiology of anorectal disorders. A clear understanding and working knowledge of the functional anatomy and pathophysiology will enable appropriate diagnosis and treatment of these disorders.

Advances in the management of constipation-predominant irritable bowel syndrome: the role of linaclotide

Constipation-predominant irritable bowel syndrome (IBS-C) is a commonly prevalent and clinically challenging disorder to treat. Until recently, most therapeutic agents had limited ability to address the complexity of symptoms inherent to the syndrome. The development of linaclotide provides a physiologically sound approach to treatment of the multiple symptoms of IBS-C. Clinical trials demonstrate the efficacy of linaclotide, and a platform to better understand the symptomatology of IBS-C. Based on recent clinical evidence, linaclotide should be considered for patients with IBS-C because it improves abdominal pain and bowel symptoms. In phase III trials, linaclotide met the US Food and Drug Administration responder endpoint with a number needed to treat (NNT) of 5.1–7.9, and European Medicines Agency coprimary endpoints at 12 weeks with a NNT of 4.39–7.69, and at 26 weeks with a NNT of 4.93–5.68. It is safe and effective, with diarrhea reported as the most common adverse effect, which leads to discontinuation of the medication in approximately 5% of patients.

Optimal Testing for Diagnosis of Fructose Intolerance: Over-dosage Leads to False Positive Intolerance Test

TO THE EDITOR: We read with interest the recent article by Goebel-Stengel et al1 and wish to express our appreciation and enthusiasm for their work on small intestinal bacterial overgrowth (SIBO) and carbohydrate intolerance in patients with irritable bowel syndrome (IBS). However, we have significant concerns regarding their methodology and basis for diagnosis of fructose intolerance.

Brain fogginess, gas and bloating: a link between SIBO, probiotics and metabolic acidosis

Background: D‐lactic acidosis is characterized by brain fogginess (BF) and elevated D‐lactate and occurs in short bowel syndrome. Whether it occurs in patients with an intact gut and unexplained gas and bloating is unknown. We aimed to determine if BF, gas and bloating is associated with D‐lactic acidosis and small intestinal bacterial overgrowth (SIBO). Methods: Patients with gas, bloating, BF, intact gut, and negative endoscopic and radiological tests, and those without BF were evaluated. SIBO was assessed with glucose breath test (GBT) and duodenal aspiration/culture. Metabolic assessments included urinary D‐lactic acid and rblood L‐lactic acid, and ammonia levels. Bowel symptoms, and gastrointestinal transit were assessed. Results: Thirty patients with BF and 8 without BF were evaluated. Abdominal bloating, pain, distension and gas were the most severe symptoms and their prevalence was similar between groups. In BF group, all consumed probiotics. SIBO was more prevalent in BF than non‐BF group (68 vs. 28%, p = 0.05). D‐lactic acidosis was more prevalent in BF compared to non‐BF group (77 vs. 25%, p = 0.006). BF was reproduced in 20/30 (66%) patients. Gastrointestinal transit was slow in 10/30 (33%) patients with BF and 2/8 (25%) without. Other metabolic tests were unremarkable. After discontinuation of probiotics and a course of antibiotics, BF resolved and gastrointestinal symptoms improved significantly (p = 0.005) in 23/30 (77%). Conclusions: We describe a syndrome of BF, gas and bloating, possibly related to probiotic use, SIBO, and D‐lactic acidosis in a cohort without short bowel. Patients with BF exhibited higher prevalence of SIBO and D‐lactic acidosis. Symptoms improved with antibiotics and stopping probiotics. Clinicians should recognize and treat this condition.

Anorectal Manometry in Defecatory Disorders: A Comparative Analysis of High-resolution Pressure Topography and Waveform Manometry

Background/Aims Whether high-resolution anorectal pressure topography (HRPT), having better fidelity and spatio-temporal resolution is comparable to waveform manometry (WM) in the diagnosis and characterization of defecatory disorders (DD) is not known. Methods Patients with chronic constipation (Rome III) were evaluated for DD with HRPT and WM during bearing-down “on-bed” without inflated rectal balloon and “on-commode (toilet)” with 60-mL inflated rectal balloon. Eleven healthy volunteers were also evaluated. Results Ninety-three of 117 screened participants (F/M = 77/16) were included. Balloon expulsion time was abnormal (> 60 seconds) in 56% (mean 214.4 seconds). A modest correlation between HRPT and WM was observed for sphincter length (R = 0.4) and likewise agreement between dyssynergic subtypes (κ = 0.4). During bearing down, 2 or more anal pressure-segments (distal and proximal) could be appreciated and their expansion measured with HRPT but not WM. In constipated vs healthy participants, the proximal segment was more expanded (2.0 cm vs 1.0 cm, P = 0.003) and of greater pressure (94.8 mmHg vs 54.0 mmHg, P = 0.010) during bearing down on-commode but not on-bed. Conclusions Because of its better resolution, HRPT may identify more structural and functional abnormalities including puborectal dysfunction (proximal expansion) than WM. Bearing down on-commode with an inflated rectal balloon may provide additional dimension in characterizing DD.

Response to Sachdeva et al: Brain Fogginess and SIBO Is Not a Mirage

We thank Prof. Sachdeva and colleagues for their useful comments, and pleased that they found this article “fascinating” and “thought provoking”, and happy to respond to their concerns. (1) Is Brain Fogginess a center-point to SIBO? We believe that BF is a feature in a select group of SIBO patients in whom the small bowel is colonized with Dlactic acid producing organisms, particularly lactobacillus species, contained in probiotics. We emphasize that not all SIBO patients have BF or colonization with these organisms. Also, with only seven publications on BF, Sachdeva et al. have accepted that BF occurs in POTS, fibromyalgia, etc.; but are suspicious of this in SIBO; it is time that gastroenterologists recognize that BF can be a manifestation of SIBO. (2) Objective test for BF? There is no definition or validated questionnaire or objective test for BF according to neurologists we have discussed, and hence could not perform any tests. We are currently validating a questionnaire. (3) Is BF and SIBO linked? Absolutely, and was the essence of our study. BF was reproduced in 66% of subjects during the breath test, and most of them had evidence of SIBO (GBT or culture). The lower yield (sensitivity) of GBT and duodenal aspirate is consistent with multiple other studies, as they only measure proximal SIBO and miss distal SIBO. (4) BF not related to lactic acidosis? Our patients did not report BF 24 h a day. It would wax and wane, but a majority experienced this postprandially. Hence, we tested them with a GBT; both to assess whether BF can be reproduced in the lab, and to validate that it was not an imaginary or supratentorial (functional) symptom, as well as to identify its association with SIBO. The fact that in almost all in whom the urinary D-Lactic acid increased did occur after a glucose meal and was associated with BF proves the link between BF and D-lactic acidosis. (5) Lack of reproducibility of BF on breath testing challenges link with SIBO? As discussed above and by Rezai et al. in North American Consensus, current modalities for SIBO testing are imperfect. The small bowel is 19 ft long, and can be colonized anywhere. In contrast, glucose when administered orally is absorbed within the first 3–6 ft of small bowel, and duodenal aspirates are typically from the proximal 2 ft of small bowel. Hence, to rely on glucose breath testing alone to make a diagnosis of SIBO will provide a low yield of about 33% and miss many other patients. This was a reason why we used two tests, both GBT and duodenal aspirates to maximize the detection of SIBO in our patients. Therefore, the author’s contention that many patients with a negative GBT had D-lactic acidosis and/or BF makes it unlikely that they had SIBO, is inaccurate. Finally, we would encourage them to use our protocol and identify this syndrome in their patient population, and relieve their suffering, and yes we are now performing a post-treatment study.

Does colectomy predispose to small intestinal bacterial (SIBO) and fungal overgrowth (SIFO)

Objectives: After subtotal colectomy, 40% of patients report chronic gastrointestinal symptoms and poor quality of life. Its etiology is unknown. We determined whether small intestinal bacterial overgrowth (SIBO) or small intestinal fungal overgrowth (SIFO) cause gastrointestinal symptoms after colectomy. Methods: Consecutive patients with unexplained abdominal pain, gas, bloating and diarrhea (>1 year), and without colectomy (controls), and with colectomy were evaluated with symptom questionnaires, glucose breath test (GBT) and/or duodenal aspiration/culture. Baseline symptoms, prevalence of SIBO/SIFO, and response to treatment were compared between groups. Results: Fifty patients with colectomy and 50 controls were evaluated. A significantly higher (p = 0.005) proportion of patients with colectomy, 31/50 (62%) had SIBO compared to controls 16/50 (32%). Patients with colectomy had significantly higher (p = 0.017) prevalence of mixed SIBO/SIFO 12/50 (24%) compared to controls 4/50 (8%). SIFO prevalence was higher in colectomy but not significant (p = 0.08). There was higher prevalence of aerobic organisms together with decreased anaerobic and mixed organisms in the colectomy group compared to controls (p = 0.008). Patients with colectomy reported significantly greater severity of diarrhea (p = 0.029), vomiting (p < 0.001), and abdominal pain (p = 0.05) compared to controls, at baseline. After antibiotics, 74% of patients with SIBO/SIFO in the colectomy and 69% in the control group improved (p = 0.69). Conclusion: Patients with colectomy demonstrate significantly higher prevalence of SIBO/SIFO and greater severity of gastrointestinal symptoms. Colectomy is a risk factor for SIBO/SIFO.

Dietary fiber and risk of inflammatory bowel disease: fact or hype?

Dear Sir: We read with interest, as well as some alarm, the article by Ananthakrishnan and its accompanying editorial by Kaplan in the November 2013 issue of Gastroenterology. These authors suggest that increased dietary fiber intake, specifically from fruits, may have a protective effect on development of Crohn’s disease (CD) but not ulcerative colitis. They postulate 2 potential mechanism, including changes in the composition of the microbiota and increased fermentation of fiber from fruit into short chain fatty acids leading to decreased proinflammatory mediators, as well as increased activation of the aryl hydrocarbon receptor leading to improved protection against environmental insults. Although we do not dispute this interesting hypothesis, we do question the author’s conclusion that there is no “reverse causation,” where decreased fiber consumption is caused by symptoms related to undiagnosed CD. The article does not include gastrointestinal symptoms as part of their analysis, and as such, we are not able to assess how long patients were symptomatic before diagnosis. A study from Manitoba suggests that patients have a prolonged duration of symptoms before diagnosis of CD, with the lag time of symptom onset to diagnosis increasing at older ages of diagnosis. With this cohort, the median age at diagnosis of CD was 52 years with 1 patient diagnosed at age 85! The authors did perform a lag analysis utilizing fiber data from 2 to 4 years before the diagnosis of CD, which did show fiber derived from fruit remained a significant predictor of CD, and the overall dietary fiber was only “weakly attenuated.” This is the time period where symptoms are most likely develop, so it is not surprising that fiber was a significant predictor of CD diagnosis, given that increasing fiber may lead to worsening gastrointestinal symptoms in a patient with undiagnosed CD. This goes along with analysis of disease location showed the strongest effect of fiber intake with any ileal disease compared to any colonic disease. Logically, one would think that patients with ileal disease would be more symptomatically sensitive to dietary fiber than patients with colonic disease. Concerning us most is the notion inferred from the research manuscript and explicitly stated in the accompanying editorial “advocating for a high-fiber diet” to reduce the incidence of CD. High-fiber diets are to be avoided in patients with CD, specifically ileal disease, where dietary intake of items high in fiber can lead to bowel obstructions. It is highly likely that the nurses in the study who were silently slowly developing their Crohn’s strictures were unconsciously (or purposefully) decreasing fiber intake owing to symptoms that resulted when eating these foods. This would also explain why the same association was not seen in ulcerative colitis; these patients typically do not form strictures. Misunderstanding the potential benefits of high fiber intake can be disastrous for patients with stricturing CD. We readily agree with the conclusion that further studies are warranted to explore how dietary fiber may modulate inflammation seen in CD. However, we caution against advocating high fiber intake in patients who are at risk for, or already have, suspected or diagnosed CD.