Caw. Evans et al., GASTRIC-ACID SECRETION AND ENTERIC INFECTION IN BANGLADESH, Transactions of the Royal Society of Tropical Medicine and Hygiene, 91(6), 1997, pp. 681-685
Citations number
34
Categorie Soggetti
Public, Environmental & Occupation Heath","Tropical Medicine
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.