Loss of the gastric acid barrier may lead to recurrent enteric infecti
ons, small intestinal bacterial overgrowth, persistent diarrhoea, and
thus malnutrition. To investigate this possibility, a new, non-invasiv
e test of gastric acid secretion was developed ideal for field use in
the developing world, where chronic diarrhoea and undernutrition are c
ommon. The test relies on the capacity of the kidney to retain H+ duri
ng gastric acid secretion, leading to a postprandial urine 'alkaline t
ide'. Gastric intubation studies of seven healthy adult volunteers sho
wed a direct relation between changes in gastric acid secretion and ch
anges in urine acid output (measured as the H+/creatinine molar ratio
in spot urine samples). Subjects who secreted gastric acid in response
to stimulation with a sham feed showed a fall in urine acid output >0
.5 mmol H+/mmol creatinine (range -7.4 to -1.52 mean -1.12). The most
reproducible decrease in urine acid output in response to normal food
was observed around the time breakfast was usually eaten and was aboli
shed by 36 hours of treatment with ranitidine. Breakfast time reductio
ns in postprandial urine acid output in 22 healthy English children we
re comparable with those in healthy adults, and significantly differen
t from values in achlorhydric adults. They were much more variable, ho
wever, in 106 Gambian children in whom values spanned both normochlorh
ydric and achlorhydric ranges (-2.7 to +1.8). Measuring changes in uri
ne acid output at breakfast time provides a reliable indirect measure
of gastric acid secretion that can be used in field conditions, enabli
ng the relation between gastric acid output and the development of dia
rrhoeal diseases to be investigated.