With either technique, any coliforms or anaerobes grown are highly likely to be significant. Academic purists advocate aspirating pure duodenal secretions via a catheter, but others prefer to “wash” the duodenum with 50–100 mL sterile saline and then aspirate back 10 mL fluid. SIBO can be diagnosed after culture of small bowel aspirate obtained by endoscopy. More significant indices of malabsorption, very low fat-soluble vitamin levels, or macrocytic anaemia are rare. Personal experience suggests that SIBO is sometimes also associated have very slightly increased levels of C-reactive protein (<15 mg/L). Faecal calprotectin levels might be mildly raised. Raised folate levels may also be seen because of increased synthesis and subsequent absorption by small intestinal bacteria. A clue to the presence of SIBO might be low serum levels of vitamin B12, which is often affected by competitive uptake, especially when the small intestine is colonised by aerobic bacteria. Diagnostic Testsĭiagnosis is not necessarily straightforward. Eradication of SIBO leads to significant improvement in symptoms, although the number of high-quality studies of treatment is limited. A systematic review suggested that the pooled prevalence of SIBO is 38% (95% CI 32–44) higher among individuals with irritable bowel syndrome than among controls (odds ratio 4.7, 95% CI 3.1–7.2). The British Society of Gastroenterology guidelines on investigations of chronic diarrhoea in adults recommended that SIBO should be routinely considered as a possible cause of gastrointestinal symptoms. SIBO can cause any gastrointestinal symptom, including those defined by the ROME IV criteria for irritable bowel syndrome.
Convincing data are emerging that in animals and humans, Toll-like receptor pathways are crucial to this interaction. Several studies suggest that small-intestinal bacterial overgrowth (SIBO) can promote or worsen extraintestinal disorders, such as non-alcoholic fatty liver disease, obesity, rosacea, and various neurological conditions – that is, diseases without gastrointestinal symptoms. Increased numbers of bacteria in the small intestine have been described as the cause of gastrointestinal symptoms after gastric surgery, in patients with exocrine pancreatic insufficiency, after treatment with long-term corticosteroids or chemotherapy for cancer, in patients with poorly controlled diabetes mellitus, chronic renal failure, small bowel diverticular disease, or a motility disorder, and after surgery to the ileocaecal valve. Maintaining the relative sterility of the small bowel relies on gastric acid and pancreatic enzyme production, gut motility, systemic and local immunity, and an intact ileal valve. Excessive numbers of bacteria, changes in the species of bacteria (in the small bowel), the site of colonisation, or altered bacterial function can lead to clinical disorders. The small bowel is predominantly colonised by Gram-positive and aerobic bacteria, whereas the large bowel contains mainly Gram-negative and anaerobic bacteria.
Introductionīacterial colonisation of the small intestine in a healthy individual is low relative to that of large bowel (109–1012 colony forming units/mL). A 7-day course of rifaximin was started, after which her symptoms resolved and her bowel function returned to normal. She complained that ongoing symptoms were significantly affecting her quality of life. A diagnosis of diarrhoea-predominant irritable bowel syndrome was made and she was prescribed loperamide and trialled with a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) but she reported no benefit. Blood tests, faecal calprotectin, colonoscopy to neo-terminal ileum, including random colonic biopsies, and a SeHCAT (23-seleno-25-homotaurocholic acid, selenium homocholic acid taurine) scan were normal. Her medical history included ileocaecal resection for Crohn’s disease. A 34-year-old woman presented with a long history of abdominal bloating and diarrhoea.
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