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Normally only small numbers (<10>3 organisms/ml) of bacteria (lactobacilli, enterococci gram-positive aerobes, facultative anaerobes), are found in the proximal small bowel, and motility, particularly phase 3 of the migrating motor complex (MMC), is most important in preventing bacterial overgrowth. Important in maintaining the relatively sterile environment of the proximal small bowel are gastric acid (HCl), pancreatic and biliary secretions, mucosal immunity and a competent ileocecal valve (ICV). Conditions which cause stasis or recirculation of colonic contents into the small bowel result in overgrowth of bacteria, mainly coliforms and anaerobes.
The pathophysiology of small bowel bacterial overgrowth (SBBO):
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Overgrowth of anaerobic bacteria (bacteroides, clostridia) results in release of cholyl-amidases which deconjugate bile acids (BAs). Unconjugated BAs (UBAs) have a higher pKa than conjugated BAs (CBAs) and are predominantly protonated at the normal proximal small bowel pH of 6.0. Protonated UBAs are passively absorbed in the jejunum and are not available for micelle formation.
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Bacteria release proteases that can damage brush border disaccharidases, in particular lactase, resulting in CHO malabsorption.
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The effect of bacterial proteases on tight junctions or secondary intestinal inflammation may alter intestinal permeability.
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Anaerobic bacteria ingest cobalamin (vitamin B12) and synthesize folate.
Clinical manifestations of SBBO include watery diarrhea, steatorrhea, abdominal pain, bloating, and weight loss, and, over time, vitamin B12 and fat-soluble vitamin deficiencies. Serum folate levels remain normal or are elevated, due to bacterial synthesis of folate, and serve to distinguish SBBO from tropical sprue, in which both folate and B12 deficiencies are common. Diarrhea is due to stimulation of colonic secretion by unabsorbed FAs and the osmotic effect of unabsorbed CHOs and FAs.
Diagnosis of SBBO can be made by:
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Quantitative culture of small bowel aspirate (>105 colony-forming units (CFUs)/ml, the "gold standard."
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Growth of strict anaerobes.
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14C-xylose breath test.
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Schilling test pre- and post-antibiotic treatment.
Management includes:
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Antibiotics, often cycled.
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Screen for and treat nutritional deficiencies.
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Lactose-free diet.
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Medium-chain triglycerides (MCTs) which are not dependent upon micelles for absorption.
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Supplementation with vitamin B12, A, D, E, K when deficiencies are documented.
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Prokinetic agents to stimulate motility (e.g. metoclopramide, erythromycin, low dose octreotide (for scleroderma)
Category: Gastroenterology Notes
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