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Overt steatorrhoea remains a problem for some patients with cystic fibrosis (CF) despite supraphysiological dosages of pancreatic enzymes. As pancreatin release and enzyme function is influenced by duodenal pH, we have used 24-h ambulatory pH measurements to assess the extent and duration of postprandial hyperacidity. Readings were obtained from the stomach and proximal duodenum in 16 CF patients (aged 6 months to 12 years) using a dual-channel antimony electrode. The fasting gastric and duodenal pH values were normal in all patients (mean pH values of 1.3, and 6.8, respectively). There was, however, a marked drop in duodenal pH in the first postprandial hour, which became more pronounced with successive meals. The total time that duodenal pH was < 5 varied from 15 to 90% of the recording (mean 57%). Overnight the duodenal pH returned to normal levels. A subgroup of five patients were studied before and after treatment with omeprazole, a potent inhibitor of gastric acid secretion. There were significant improvements in both weight gain and fat absorption. This study supports the hypothesis that the postprandial duodenal pH is excessively acid in patients with CF and may be an important element in the continuing fat malabsorption experienced by some patients. This malabsorption may limit the efficacy of the newer high-lipase pancreatic enzyme supplements and lead to delayed enzyme release, a possible factor in the recent reports of proximal colonic strictures.

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The rise in short-circuit current associated with the active transport ofglucose and alanine was measured in intestinal biopsy samples from children with cystic fibrosis. The glucose-induced increase in the short-circuit current was greater in the cystic fibrosis tissues than in control samples over the whole range of concentrations tested (2.5-35 mM), a reflection of an increased maximum rate of transport. Similar results were obtained with alanine. These findings suggest that active Na+-linked nutrient transport is enhanced in cystic fibrosis.