Small Intestinal Bacterial Overgrowth: What It Is and Isn't
Purpose of review To critically review recent literature on small intestinal bacterial overgrowth (SIBO).
Recent findings When originally described, SIBO was added to the list of causes of the malabsorption syndrome and the pathophysiology of its consequences for the digestion and absorption of various nutrients was gradually revealed. More recently, SIBO was incriminated as a cause of diarrhea, especially in the elderly. However, the suggestion that SIBO may be a causative factor in irritable bowel syndrome and of its constituent symptoms has sparked debate and controversy on the very definition of SIBO. This debate revolves around the tests employed and the diagnostic cut-off values (for bacterial numbers) used to diagnose SIBO in clinical practice.
Summary A fundamental problem with SIBO, and one that allows controversy to simmer, is the lack of a universally accepted and applied gold standard for the diagnosis of SIBO. Hopefully, the application of molecular microbiological methods to the characterization of the small intestinal microbiome will tell us, once and for all, what is normal and when 'abnormality' is truly responsible for symptoms and disease. Meanwhile, therapy remains, for the most part, empirical and is based on the correction, wherever possible, of any underlying cause, attention to nutritional deficiencies, and the use of antibiotics.
When originally described in a series of classical clinical and pathophysiological studies performed toward the middle of the last century, small intestinal bacterial overgrowth (SIBO) could be succinctly defined as 'clinical and/or laboratory evidence of maldigestion/malabsorption related to qualitative and/or quantitative alterations in the small intestinal microbiota'. In these elegant studies, the consequences of SIBO in terms of B12 absorption, bile salt deconjugation, protein, carbohydrate and fat assimilation, and intestinal injury were delineated and a number of underlying disorders (e.g., achlorhydria, dysmotility, fistulae, and strictures) revealed. Diagnosis rested largely on the aspiration and quantitative culture of jejunal contents and therapy was based on the empiric use of broad-spectrum antibiotics.
Much has changed since then. First, breath tests and the analysis of duodenal fluid obtained through an endoscope replaced jejunal aspirates. Second, the clinical context wherein the diagnosis of SIBO is entertained shifted dramatically from those aforementioned situations in which a plausible basis for the development of SIBO was evident and its clinical consequences (steatorrhea, B12 deficiency, protein-losing enteropathy) visible, to a situation in which SIBO is incriminated as the cause of a broad spectrum of intestinal and extraintestinal ills. A good example of this seismic shift in our concept of SIBO is the much publicized proposal that SIBO is associated with irritable bowel syndrome (IBS), a suggestion that has generated considerable controversy and thrown the definition of SIBO into sharp relief. In these instances, SIBO is linked to symptoms or clinical entities in the absence of evidence of maldigestion/malabsorption and in a context in which the pathophysiological relationship with SIBO is far from clearly defined. Consequently, and critically, these associations then become totally reliant on two factors: the definition of SIBO and the performance characteristics of the test used to define it and, specifically, on the ability of that test to distinguish health from disease. Typically, correlations between original test results and the clinical responses to SIBO eradication have not been reported or, if they have, their interpretation remains rather murky. Absent such evidence and lacking biochemical and/or pathological findings that can be plausibly linked to SIBO, it has often been unclear in these situations whether SIBO is a cause, a consequence, or an epiphenomenon in relation to the other supposedly associated disorder.
Abstract and Introduction
Abstract
Purpose of review To critically review recent literature on small intestinal bacterial overgrowth (SIBO).
Recent findings When originally described, SIBO was added to the list of causes of the malabsorption syndrome and the pathophysiology of its consequences for the digestion and absorption of various nutrients was gradually revealed. More recently, SIBO was incriminated as a cause of diarrhea, especially in the elderly. However, the suggestion that SIBO may be a causative factor in irritable bowel syndrome and of its constituent symptoms has sparked debate and controversy on the very definition of SIBO. This debate revolves around the tests employed and the diagnostic cut-off values (for bacterial numbers) used to diagnose SIBO in clinical practice.
Summary A fundamental problem with SIBO, and one that allows controversy to simmer, is the lack of a universally accepted and applied gold standard for the diagnosis of SIBO. Hopefully, the application of molecular microbiological methods to the characterization of the small intestinal microbiome will tell us, once and for all, what is normal and when 'abnormality' is truly responsible for symptoms and disease. Meanwhile, therapy remains, for the most part, empirical and is based on the correction, wherever possible, of any underlying cause, attention to nutritional deficiencies, and the use of antibiotics.
Introduction
When originally described in a series of classical clinical and pathophysiological studies performed toward the middle of the last century, small intestinal bacterial overgrowth (SIBO) could be succinctly defined as 'clinical and/or laboratory evidence of maldigestion/malabsorption related to qualitative and/or quantitative alterations in the small intestinal microbiota'. In these elegant studies, the consequences of SIBO in terms of B12 absorption, bile salt deconjugation, protein, carbohydrate and fat assimilation, and intestinal injury were delineated and a number of underlying disorders (e.g., achlorhydria, dysmotility, fistulae, and strictures) revealed. Diagnosis rested largely on the aspiration and quantitative culture of jejunal contents and therapy was based on the empiric use of broad-spectrum antibiotics.
Much has changed since then. First, breath tests and the analysis of duodenal fluid obtained through an endoscope replaced jejunal aspirates. Second, the clinical context wherein the diagnosis of SIBO is entertained shifted dramatically from those aforementioned situations in which a plausible basis for the development of SIBO was evident and its clinical consequences (steatorrhea, B12 deficiency, protein-losing enteropathy) visible, to a situation in which SIBO is incriminated as the cause of a broad spectrum of intestinal and extraintestinal ills. A good example of this seismic shift in our concept of SIBO is the much publicized proposal that SIBO is associated with irritable bowel syndrome (IBS), a suggestion that has generated considerable controversy and thrown the definition of SIBO into sharp relief. In these instances, SIBO is linked to symptoms or clinical entities in the absence of evidence of maldigestion/malabsorption and in a context in which the pathophysiological relationship with SIBO is far from clearly defined. Consequently, and critically, these associations then become totally reliant on two factors: the definition of SIBO and the performance characteristics of the test used to define it and, specifically, on the ability of that test to distinguish health from disease. Typically, correlations between original test results and the clinical responses to SIBO eradication have not been reported or, if they have, their interpretation remains rather murky. Absent such evidence and lacking biochemical and/or pathological findings that can be plausibly linked to SIBO, it has often been unclear in these situations whether SIBO is a cause, a consequence, or an epiphenomenon in relation to the other supposedly associated disorder.
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