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Background: Fiber and water-holding agents are used for the treatment of constipation. In what may appear to be a paradox, they are sometimes also used for the treatment of diarrhea; it has been proposed that they sequester water from liquid stools and/or increase the ratio of fecal solids to fecal water and thereby improve stool consistency. The purpose of the present study was to test the validity of this hypothesis in normal subjects in whom secretory diarrhea was induced by phenolphthalein. Methods: In random sequence, 9 subjects with phenolphthalein-induced diarrhea were treated with placebo, psyllium, calcium polycarbophil, or wheat bran. Results: Calcium polycarbophil and wheat bran had no effect on fecal consistency or on fecal viscosity. By contrast, psyllium made stools firmer and increased fecal viscosity. In a dose-response study in 6 subjects, doses of 9, 18, and 30 g of psyllium per day caused a near linear increase in fecal viscosity. Conclusion: Psyllium, but not calcium polycarbophil or wheat bran, improves fecal consistency and viscosity in subjects with experimentally-induced secretory diarrhea.

Although the osmotic gap of fecal fluid is often used to distinguish osmotic diarrhea from secretory diarrhea, there has never been a scientific evaluation of the validity of this concept. Similarly, although a low fecal fluid pH value is used to indicate that diarrhea is mediated by carbohydrate malabsorption, the validity of this method is unproven. Therefore, in the present study, diarrhea was induced in normal subjects by different mechanisms and fecal fluid osmotic gap (using an assumed fecal fluid osmolality of 290 mOsm/kg) and pH were measured. In secretory diarrhea caused by phenolphthalein, the osmotic gap was always less than 50 mOsm/kg, whereas in osmotic diarrhea caused by polyethylene glycol, magnesium hydroxide, lactulose, and sorbitol, the osmotic gap always exceeded 50 mOsm/kg. In osmotic diarrhea caused by sodium sulfate, the fecal fluid osmotic gap was less than 50 mOsm/kg, but phenolphthalein-induced secretory diarrhea could be distinguished from sodium sulfate-induced osmotic diarrhea by the fecal chloride concentration. When diarrhea was caused by carbohydrate malabsorption (lactulose or sorbitol), the fecal fluid pH was always less than 5.6 and usually less than 5.3; by contrast, other causes of diarrhea rarely caused a fecal pH as low as 5.6 and never caused a pH less than 5.3. It is concluded that measurement of fecal fluid osmotic gap and pH can distinguish various mechanisms of experimental diarrhea in normal subjects. The concepts on which these tests are based are therefore verified experimentally.

Neuropeptide Y is a neurotransmitter in enteric and postganglionic sympathetic neurons. In animal models of intestinal water and ion transport, neuropeptide Y decreases stimulated secretion but has no consistent effect on basal transport. In the present study, the effect of neuropeptide Y on jejunal water and electrolyte transport in healthy volunteers was investigated under basal conditions and during intestinal secretion induced by intraluminal administration of prostaglandin E 2 . The triple-lumen tube technique was used for perfusion of the small intestine with a plasmalike electrolyte solution containing polyethylene glycol as a nonabsorbable volume marker. After an initial control period (saline IV) neuropeptide Y was administered IV at a dose of 400 pmol · kg −1 · h −1 . Neuropeptide Y significantly increased net absorption of water, sodium, potassium, and chloride under basal conditions. The peptide significantly reduced the secretion of these electrolytes induced by an intraluminal prostaglandin E 2 concentration of 5 μmol/L and reduced net water secretion by 36%. The results of the current study suggest that neuropeptide Y can change intestinal water and ion transport from secretion toward absorption.

Effect of Pantoprazole on Reflux-Associated Laryngitis: A Placebo-Controlled Crossover Study Andreas J. Eherer, Dept of Internal Medicine, KarI-Franzens Univ, Graz Austria; Walter Habermann, Dept of Oto-Rhino-Laryngology, KarI-Franzens Univ, Graz Austria; Heinz F. Hammer, Dept of Internal Medicine, Kari-Franzens Univ, Graz Austria; Karl Klasler, Gerhard Friedrich, Dept of Oto-Rhino-Laryngology, KarI-Franzens Univ, Graz Austria; Guanter J. Krejs, Dept of Internal Medicine, KarI-Franzens Univ, Graz Austria