GASTRIC-ACID SECRETION AND ENTERIC INFECTION IN BANGLADESH

In developing countries many enteric infections are caused by acid-sen sitive pathogens. Failure of the gas tric acid barrier to infection ha s been reported in cholera but gastric acid secretion has been little studied in other enteric infections. We therefore studied basal and st imulated gastric acid in 185 Bangladeshi men admitted to hospital for the treatment of enteric infection. Patients with dysentery (amoebiasi s,n=24 and shigellosis, n=19) and culture-negative diarrhoea (n=69) ha d similar mean gastric acid levels (basal, 3-5 mmol/h; stimulated, 11- 17 mmol/h), which remained stable in those patients studied throughout 12 weeks of convalescence. In contrast, patients with secretory diarr hoea caused by cholera or enterotoxigenic Escherichia coli (ETEC) had low gastric acid levels (P<0.05 compared with other groups) (cholera, n=34: basal mean 1.8 mmol/h [SD=2.2], stimulated mean 7.9 mmol/h [SD=6 .4]; ETEC, n=39: basal mean 2.7 mmol/h [SD=2.8], stimulated mean 9.4 m mol/h [SD=7.5]). Cholera patients' gastric acid level rose during conv alescence to similar levels to the dysentery patients'. Low gastric ac id level was associated with severe disease in patients with cholera ( P<0.02) or ETEC (P<0.05). Gastric acid level fell with increasing age (P<0.007) but this did not account for the differences between groups. Gastric acid levels were not associated with Giardia duodenalis or St rongyloides stercoralis co-infection, fever, use of tobacco, or chewin g betel nut. Cholera and secretory diarrhoea caused by ETEC may, there fore, partly result from a reduction in gastric acid level which does not occur during dysentery. Factors which impair gastric acid secretio n may predispose to diarrhoeal disease in developing countries.