Breath hydrogen excretion was measured in eight lactase (EC 3.2.1.108)-deficient volunteers ingesting 18 g lactose in the form of milk, yoghurt and heated yoghurt. Total excess hydrogen excretion (area under curve) was significantly lower after yoghurt and heated yoghurt, than after milk: 103 (SE 29), 191 (SE 32), and 439 (SE 69) respectively (P less than 0.001). The oro-caecal transit time of fermentable components from yoghurt and heated yoghurt (mainly lactose) was longer than that from milk: 165 (SE 17), 206 (SE 19), v. 103 (SE 19) min (P less than 0.01). An intestinal perfusion technique was used in the same subjects after ingestion on two consecutive days of 18 g lactose in yoghurt and heated yoghurt. Significantly less lactose was recovered from the terminal ileum after yoghurt than after heated yoghurt meals: 1740 (SE 260) v. 2825 (SE 461) mg (P less than 0.05), and approximately one-fifth of the lactase activity contained in yoghurt reached the terminal ileum. These findings indicate that more than 90% of the lactose in yoghurt is digested in the small intestine of lactase-deficient subjects and suggest that both the lactase activity contained in the viable starter culture and a slow oro-caecal transit time are responsible for this excellent absorption.

No abstract

Dehydration in severely malnourished children can safely be corrected within 6 hours. All study ORSs were equally efficient in correcting dehydration. Rice-ORS significantly reduced the stool output and ORS intake, confirming previous reports.

ABSTRACT. To establish if intestinal permeability to exogenous antigens is involved in cow's milk allergy (CMA) in infants, 33 children 1 to 24 months old (18 controls and 1 5 with CMA) were tested for intestinal permeability to the protein marker horseradish peroxidase (HRP). Jejunal biopsies were performed either during the initial period of diagnosis, at the mean (and SE) age of 3 f 1 months, and/or 1 yr later, at the age of 13 f 2 months, just before and after a milk challenge. A small fragment of the biopsy was studied for histology and the remainder was mounted in an Ussing chamber for simultaneous measurement of mucosal to serosal transport of H R P in its intact and degraded forms and electrical parameters including short-circuit current and conductance. No modification in H R P absorption was noted in control children aged from 2 months to 11 yr, indicating that gut closure probably occurred earlier in life. During the initial period of CMA, transepithelial H R P fluxes were significantly higher, about 8-fold, in children with CMA (intact H R P flux = 48.5 f 15.2, 95% confidence interval, 11.2 to 85.7 versus 5.9 + 1.2, 95% confidence interval 2.9 to 8.3, in control children) In addition, short-circuit current was increased but conductance was unchanged. After several months on a milkfree diet, H R P flux and short-circuit current returned to control values. Just after the milk challenge and independently of -the clinical issue, a slight rise in H R P permeability was observed but it was not significant and remained within control values. These results suggest that increased permeability to proteins is probably not the primary cause of CMA, and that the increase in protein endocytosis noted during the initial period of CMA seems rather to be a secondary effect of an abnormal immunological response leading to mucosal inflammation and impairment of the endocytic process. (Pediatr Res 24:197-202, 1988)