Only 10%-20% of all cases of antibiotic-associated diarrhea (AAD) are caused by infection with Clostridium difficile. Other infectious organisms causing AAD include Clostridium perfringens, Staphylococcus aureus, Klebsiella oxytoca, Candida species, and Salmonella species. Most of the clinically mild AAD cases are due to functional disturbances of intestinal carbohydrate or bile acid metabolism, to allergic and toxic effects of antibiotics on intestinal mucosa, or to pharmacological effects on motility. Saccharomyces boulardii and Enterococcus SF68 can reduce the risk of developing AAD. Patients receiving antibiotic treatment should avoid food containing high amounts of poorly absorbable carbohydrates. Mild cases of AAD that may or may not be caused by C. difficile can be resolved by discontinuation of antibiotic therapy and by dietary carbohydrate reduction. Only severe AAD caused by C. difficile requires specific antibiotic treatment.

Dumping syndrome is a frequent complication of cancer and non-cancer oesophageal and gastric surgery, as well as bariatric surgery (also known as metabolic surgery). These interventions change gastric anatomy and innervation, which can enable a considerable amount of undigested food to reach the small intestine too rapidly 1-4. Dumping syndrome comprises a constellation of symptoms that can be subdivided into early and late dumping syndrome symptoms, which can occur jointly or separately 1-8. Typically, symptoms of early dumping syndrome occur within the first hour after a meal and include gastrointestinal symptoms (abdominal pain, bloating, borborygmi, nausea and diarrhoea) and vasomotor symptoms (flushing, palpitations, perspiration, tachycardia, hypotension, fatigue, desire to lie down and, rarely, syncope) 1,2. The underlying mechanisms might involve osmotic effects, peptide hormone release and autonomic neural responses 1. Symptoms of late dumping syndrome usually occur between 1 and 3 h after a meal and are primarily the manifestations of hypoglycaemia, which mainly results from an incretin-driven hyperinsulinaemic response after carbohydrate ingestion. Hypoglycaemia-related symptoms are attributable to neuroglycopenia (which is indicated by fatigue, weakness, confusion, hunger and syncope) and to vagal and sympathetic activation (indicated by perspiration, palpitations, tremor and irritability) 1,2. The literature has referred to late dumping syndrome as 'reactive hypoglycaemia' or, after bariatric surgery, as 'postbariatric hypoglycaemia'. However, on the basis of a common pathophysiology of rapid exposure of the small intestine to nutrients, which is also seen in early dumping syndrome (see subsequent discussion), we refer to this phenomenon as 'late dumping syndrome'. The prevalence of dumping syndrome depends on the type and extent of surgery, and on the criteria used to diagnose dumping syndrome. Dumping syndrome occurs in approximately 20% of patients undergoing

The purpose of these studies was to gain insight into the pathophysiology of pure osmotic diarrhea and the osmotic diarrhea caused by carbohydrate malabsorption.

The self-limited nature of reflux-associated laryngitis in non-smokers is largely underestimated. Laryngitis improves despite the persistence of reflux. Pantoprazole may be helpful especially in relieving acute symptoms, but the advantage of long-term treatment over placebo has been greatly overestimated.

Increasing interest is focusing on the role of intestinal tone, distensibility, and mechanosensation in the genesis of abdominal symptoms. Experimental approaches usually feature balloon distension of the bowel with measurements of perception, tone, and compliance and/or elastance; however, the methodologies are standardized incompletely. We examined the reproducibility of repeated assessments of sensory perception, basal tone, and compliance and/or elastance of the rectum during distension. We also evaluated the response to inflations that varied in regard to control of pressure or volume, pattern of distension, and rate of inflation. Five healthy volunteers were studied under two separate protocols. The first featured a series of experiments on each of 5 days; the other consisted of 2 separate days of study. Repeated distensions evoked reproducible responses of sensation and compliance and/or elastance on a single day, providing a conditioning distension preceded them. Day-to-day variability was also sufficiently small to allow valid comparisons to be made on different days in healthy persons. The configuration of the distension profile (phasic, staircase, or ramp) and the rate of inflation (from 1 to 40 ml/s) had little effect on distensibility or perception. Perceptions were sometimes transient and sometimes constant, but no relationship was found between these temporal features and the magnitude of the stimulus. These observations help provide a basis as to how the responses to rectal distension can be best studied.

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Background and aims: Chemonociception in the human small intestine has not been studied extensively. Although capsaicin can cause intestinal sensations, it is not known if this is due to stimulation of chemoreceptors or to motor changes. Our aims were to evaluate motor activity during capsaicin induced nociception and to compare qualities of jejunal nociception induced by capsaicin and mechanical distension. Methods: Twenty nine healthy subjects swallowed a tube with a perfusion site at the ligament of Treitz and, 7 cm distally, a barostat balloon. Phasic motor activity was measured around the perfusion site and the balloon. Capsaicin solutions (40, 200, and 400 mg/ml) 2.5 ml/min were perfused for 60 minutes or until severe discomfort occurred. A graded questionnaire for seven different sensations was completed every 10 minutes and after capsaicin perfusion was replaced by saline perfusion because of severe discomfort. Sensations arising from pressure controlled distensions were assessed before and after capsaicin perfusion when sensations had stopped (n = 19), or during capsaicin administration when no discomfort was reported (n = 5). Results: Capsaicin perfusion induced feelings of pressure, cramps, pain, and warmth. The quality and abdominal location of these sensations were similar to those induced by distension, except for warmth (p,0.01) and pressure (p,0.05). Seven of 12 subjects receiving 40 mg/ml capsaicin and all subjects receiving higher capsaicin concentrations developed discomfort. Perfusion had to be stopped after 55 (3.3), 15 (5.7), and 10 (2.2) minutes with 40, 200, and 400 mg/ml capsaicin, respectively, whereafter the sensations disappeared within 10 minutes. Repeated capsaicin (200 mg/ml) applications significantly reduced the time until discomfort occurred (p = 0.01). Jejunal tone was not altered by capsaicin but phasic activity proximal to the perfusion site was reduced during capsaicin induced discomfort (p,0.001). Pain thresholds during distensions were not different before and after capsaicin perfusion. Conclusion: Despite the similarities in abdominal localisation and perceptional quality of capsaicin and distension induced sensations, our results rule out the fact that abdominal discomfort evoked by capsaicin involves sensitisation of mechanoreceptors or an increase in phasic and tonic motor activity. Capsaicin evokes abdominal sensations by stimulation of chemoreceptors which proves the existence of chemonociception in the human small intestine.

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