Lactose malabsorption was assessed by the hydrogen breath test in 40 Italian patients with irritable bowel syndrome and 42 controls without abdominal disturbances. Sixty-five percent of patients were "low milk consumers" (0-250 ml milk per day) compared with 38% of controls (P less than 0.02). Lactose loads of 25 and 50 g caused malabsorption in 82.5 and 87.5% patients and in 55 and 62% controls, respectively (patients vs controls P less than 0.02). Malabsorption was more frequent in the "low milk consumers" group (P less than 0.05). During a four-month lactose-free diet as the only treatment 7.5% of patients became symptom-free (and remained so for a further eight-month diet), 52.5% improved, and 40% showed no change.

SUMMARYThe effect of loperamide and naloxone on mouth-to-caecum transit time was evaluated by the lactulose hydrogen breath test in four men and four women. Each subject underwent tests during the administration of placebo, loperamide (12-16 mg po), naloxone (40 ,ug/kg/h by a three-hour intravenous infusion), and loperamide plus naloxone, carried out at intervals of one or two weeks. The transit time was significantly longer after loperamide, and this effect was antagonised by the concomitant administration of naloxone whereas naloxone administered alone had no effect on mean transit time. No clinically important side effects were reported.Morphine changes the motility pattern in the gastrointestinal tract,' decreases the propulsion of its contents,2 3 reduces gastric4 and intestinal secretions5 and increases water and ions absorption.6 7 Loperamide, an opioid agonist,

Orocecal transit time was assessed with lactulose hydrogen breath test in 12 obese patients during intravenous infusion of placebo or naloxone 40 micrograms/kg/hr given in randomized order and in double-blind conditions. Transit time was also evaluated in 22 healthy controls. Orocecal transit was significantly (P less than 0.01) longer in the obese patients, during placebo treatment (median 130, range 100-200 min) than in the healthy controls (median 75, range 40-170 min). Compared with placebo, transit time in the obese subjects was delayed (P less than 0.05) during naloxone treatment (median 150, range 100-230 min).

The within-subject repeatability of orocecal transit assessed with lactulose hydrogen breath test was evaluated in 15 healthy volunteers and 16 constipated or obese patients. The test was repeated twice in each subject. Mean (SD) transit time was 105 (63) and 103 (60) min in the first and second series of tests, respectively, showing that the first measurement did not affect the second. The within-subject repeatability of the test was related to the length of transit, the scatter of the differences between the first and second test being greater with the increase of the mean gastrointestinal transit time. The 95% coefficient of repeatability was 84 min for all measurements and 30 and 118 min, respectively, for transit times under and over 100 min. The lowest reproducibility of the test was found in constipated patients with prolonged orocecal transit.

Orocecal transit time was determined by the lactulose hydrogen breath test in nine healthy volunteers after administration of placebo, loperamide (16 mg per os), and loperamide (16 mg per os) followed by oral naloxone at doses of 16 and 32 mg. The four tests were performed in double-blind conditions and in random sequences. Transit time (mean, SD) after loperamide (128.8 min, 32.9) was significantly increased (P less than 0.05) compared with placebo (85.5 min, 35.7), loperamide followed by naloxone 16 mg (88.8 min, 46.2), and loperamide followed by naloxone 32 mg (84.4 min, 40.6). These results show that the peripheral opioid agonist loperamide delays orocecal transit in healthy subjects and that naloxone per os at adequate doses antagonizes this effect.