Background-Uncontrolled studies of lactose intolerant subjects have shown that symptom severity decreases after chronic lactose consumption. Adaptation of the colonic flora might explain this improvement. Aims-To compare the eVects of regular administration of either lactose or sucrose on clinical tolerance and bacterial adaptation to lactose. Methods-Forty six lactose intolerant subjects underwent two 50 g lactose challenges on days 1 and 15. Between these days they were given 34 g of lactose or sucrose per day, in a double blind protocol. Stool samples were obtained on days 0 and 14, to measure faecal -galactosidase and pH. Symptoms, breath H 2 excretion, faecal weight and electrolytes, and orofaecal transit time were assessed. Results-Except for faecal weight, symptoms were significantly milder during the second challenge in both groups, and covariance analysis showed no statistical difference between them. In the lactose group, but not in the sucrose group, faecal -galactosidase activity increased, pH dropped, and breath H 2 excretion decreased. Conclusion-Bacterial adaptation occurred when lactose intolerant subjects ingested lactose for 13 days, and all symptoms except diarrhoea regressed. Clinical improvement was also observed in the control group which displayed no signs of metabolic adaptation. This suggests that improved clinical tolerance may be just a placebo eVect. (Gut 1997; 41: 632-635)

13carbon urea breath test is sensitive and specific in children. Two samples collected at T0 and T40 provide the most discriminating procedure.

We studied seven healthy volunteers before and during acute (PD1) and chronic (PD2) ingestion of 30 g polydextrose (PD)/d. The energy value of PD was assessed after [U-14C]PD was added to the 10-g morning dose of PD during PD1 and at the end of PD2. Thirty-one +/- five percent (mean +/- SD) (PD1) and 29 +/- 4% (PD2) of the dose appeared in breath within 48 h. A small fraction of the ingested radioactivity was recovered in urine (4 +/- 1%) and excreted in flatus (< or = 1%) and in feces as volatile fatty acids (VFAs) (< 1%) and bacteria (3-4%); the remaining radioactivity in stools, 33 +/- 3% (PD1) and 32 +/- 4% (PD2), was assumed to be intact PD. Breath excretion of the label was 49 +/- 5% after intracolonic infusion of [U-14C] acetate. The energy value of PD, calculated by means of Miller and Wolin's stoichiometric equation of colonic fermentation, was similar during PD1 and PD2: 4.0 and 6.1 kJ/g, respectively, when breath 14CO2 and VFA production from PD were used for calculation.

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To compare the effects of digestible (pregelatinized) and partially indigestible (retrograded) cornstarches on some metabolic indexes, we studied eight healthy volunteers during two periods separated by 1 wk. In each period, fasting volunteers consumed at 0800 the test meal containing either the digestible or partially indigestible cornstarch; blood and breath were sampled in the absorptive period for 8 h. To study its late effects, the same test meal as that served at 0800 was given again at 2200, and blood and breath were sampled for 3 h in the postabsorptive period the next morning, i.e., 10 h after ingestion of the test meal. In the absorptive period, blood glucose and insulin were significantly higher after ingestion of digestible cornstarch than after partially indigestible cornstarch. In the postabsorptive period concentrations of blood glucose, insulin, and fatty acids were not significantly different, whereas concentrations of blood acetate, breath hydrogen, methane, and 13CO2, and the respiratory quotient and satiety were significantly higher (P < 0.05) and concentrations of blood glycerol significantly lower (P < 0.05) after ingestion of partially indigestible cornstarch than after digestible cornstarch. We conclude that in healthy humans, digestion of partially indigestible cornstarch is slow in the small intestine and its colonic fermentation continues 10-13 h after its ingestion. Compared with pregelatinized cornstarch, the shift in starch digestion induced by retrogradation leads to a reduction in glycemic and insulinemic responses in the absorptive period and in lipolysis in the postabsorptive.

Twelve healthy volunteers were studied for two test periods, at the beginning of which they ingested a diarrheogenic load (60 g) of lactulose in 350 mL water with 10 g polyethylene glycol 4000 (PEG); the two periods were separated by a lactulose feeding period of 8 d, during which a nondiarrheogenic load (20 g) of lactulose was taken twice daily. The transit time and flow rates of water and lactulose in the distal ileum of four subjects were not different before and after the lactulose feeding period. In the other eight subjects, stool weight and frequency, fecal pH, and fecal outputs of carbohydrates and osmotic moieties after the ingestion of 60 g lactulose dropped significantly (P < 0.05) after the lactulose feeding period, whereas the orofecal transit time and fecal concentrations of beta-galactosidase and lactic acid increased (P < 0.05). We conclude that changes in colonic function induced by prolonged exposure to a nondiarrheogenic amount of lactulose mitigate the severity of the diarrhea because of the larger dose of lactulose.

IntroductionPrevious studies have documented a high frequency of endotoxemia associated with cardiopulmonary bypass (CPB). Endotoxemia may be responsible for some of the complications associated with cardiac surgery. The purpose of the study was to examine the prevalence of endotoxemia during cardiopulmonary bypass supported aortocoronary bypass grafting surgery (ACB) using a new assay, the Endotoxin Activity Assay (EAA), and explore the association between endotoxemia and post-operative infection.MethodsThe study was a single center prospective observational study measuring EAA during the perioperative period for elective ACB. Blood samples were drawn at induction of anesthesia (T1), immediately prior to release of the aortic cross-clamp (T2), and on the first post-operative morning (T3). The primary outcome was the prevalence of endotoxemia. Secondary outcomes assessed included infection rates, intensive care unit (ICU) and hospital length of stay. An EAA of < 0.40 units was interpreted as "low", 0.41 to 0.59 units as "intermediate", and ≥0.60 units as "high".ResultsA total of 57 patients were enrolled and 54 patients were analyzable. The mean EAA at T1 was 0.38 +/- 0.14, at T2 0.39 +/- 0.18, and at T3 0.33 +/- 0.18. At T2 only 13.5% (7/52) of patients had an EAA in the high range. There was a positive correlation between EAA and duration of surgery (P = 0.02). In patients with EAA ≥0.40 at T2, 26.1% (6/23) of patients developed post-operative infections compared to 3.5% (1/29) of those that had a normal EAA (P = 0.0354). Maximum EAA over the first 24 hours was also strongly correlated with risk of post-operative infection (P = 0.0276).ConclusionsHigh levels of endotoxin occur less frequently during ACB than previously documented. However, endotoxemia is associated with a significantly increased risk of the development of post-operative infection. Measuring endotoxin levels during ACB may provide a mechanism to identify and target a high risk patient population.

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