Small Intestinal Transit, Bacterial Growth, and Bowel Habits in Diabetes Mellitus

Role of small intestinal bacterial overgrowth and delayed gastrointestinal transit time in cirrhotic patients with minimal hepatic encephalopathy

“…Finally, it should be recognized that many patients with chronic liver disease are diabetic, or receiving b-adrenoreceptor blockers. While diabetes mellitus may contribute to the pathogenesis of SIBO by prolonging intestinal transit [29,30], b-adrenoreceptor blockers may decrease the rates of SIBO by accelerating the intestinal transit [27,28]. In this study use of propranolol or prevalence of diabetes mellitus was not significantly different in patients who had SIBO from those without; hence they are unlikely to contribute to the pathogenesis of MHE or SIBO.…”

“…This method is invasive, requires intubation of the small bowel and laboratory skill in isolating anaerobes. We used GHBT, which is simple, inexpensive, noninvasive, easily applicable with no chance of contamination [44] and has remained the most commonly used non-invasive test to diagnose SIBO in most previous studies [29,46,48]. Second, the present study is cross-sectional and patients with and without SIBO were not prospectively followed-up to show the effect of SIBO on natural history of MHE.…”

“…Administration of non-selective b-adrenergic antagonist propranolol [27,28] and presence of diabetes mellitus [29,30] have been demonstrated to influence gastrointestinal motility; hence both parameters have been included in the analysis. PHES was not included as it was a diagnostic parameter for diagnosing MHE.…”

Fatal Enteritis Necroticans (Pigbel) in a Diabetic Adult

“…A well-recognized complication of diabetes is reduced gastric and small intestinal motility, caused by autonomic dysfunction in which there is a delay in small-intestinal transit time (21)(22)(23)(24). This reduced gastrointestinal motility is associated with overgrowth of bacteria that are normally present in the proximal small bowel (22). Our patient had also self-administered the antidiarrheal agent Imodium (loperamide), which inhibits gastrointestinal peristaltic activity and potentially contributed to clostridial overgrowth and an accumulation of toxin in the gut.…”

“…The metabolic condition of the previously reported child with poorly controlled Type 1 diabetes might be reflective of a state of malnutrition (15), but this cannot be said of the patient in our case, whose glucose was thought to be adequately controlled. A well-recognized complication of diabetes is reduced gastric and small intestinal motility, caused by autonomic dysfunction in which there is a delay in small-intestinal transit time (21)(22)(23)(24). This reduced gastrointestinal motility is associated with overgrowth of bacteria that are normally present in the proximal small bowel (22).…”