Decreased acid secretion, due to therapy or disease, predisposes to in
creased bacterial counts in gastric juice. As bacterial numbers increa
se, the number of nitrate-reducing strains and the concentration of lu
minal nitrite usually also increase. However, there is controversy (ma
inly because of assay problems) about whether decreased acid increases
generation of N-nitroso compounds: these may be produced by acid or b
y bacterial catalysis, and the relative contributions of each are stil
l uncertain. Other potentially important factors include ascorbate sec
retion (can prevent nitrite conversion to nitroso compounds) and the p
articular spectrum of nitroso compounds produced. Nitrosation of sever
al histamine H-2-receptor antagonists has been demonstrated experiment
ally, but under conditions that are very unlikely to be encountered cl
inically. Some acid suppressant therapies have been claimed to aid era
dication of Helicobacter pylori, but more work is needed to evaluate t
his. If ulcer treatment regimens do not also address eradication of H.
pylori (when present), gastritis will progress, and the recently docu
mented association between H. pylori and gastric carcinoma needs to be
considered. Enteric flora probably also increase if acid secretion is
markedly reduced: this does not appear to have nutritional consequenc
es but probably reduces the resistance to occasional infections, of wh
ich cholera is the best documented.