Background: Omeprazole maintenance therapy for gastro-oesophageal reflux di
sease (GERD) has been associated with an increased incidence of atrophic ga
stritis in H. pylori-infected patients and with a decreased absorption of p
rotein-bound. but not of unbound cobalamin.
Aim: To test the hypothesis that the combination of decreased cobalamin abs
orption and atrophic gastritis decreases serum cobalamin levels during omep
razole therapy.
Methods: Forty-nine H. pylori-positive GERD patients were treated with omep
razole for a mean (+/- s.d.) period of 61 (25) months. At the start of omep
razole treatment (T-0) and at the latest follow-up visit (T-1), serum was o
btained for measurement of cobalamin. Corpus biopsy specimens were obtained
at entry and follow-up for histopathological scoring according to the upda
ted Sydney classification.
Results: At inclusion, none of the 49 patients had signs of atrophic gastri
tis. During follow-up, 15 patients (33%) developed atrophic gastritis, nine
of whom had moderate to severe atrophy. These 15 patients did not differ f
rom the other 34 patients with respect to age, serum cobalamin at To or the
duration of follow-up. During follow-up, no change was observed in the med
ian serum cobalamin level in the 34 patients without atrophy; (T-0) 312 (13
6-716) vs. (T-1) 341 (136-839) pmol/L (P = 0.1). In the 15 patients who dev
eloped atrophy, a decrease in cobalamin was seen from 340 (171 to 787) at b
aseline to 285 (156-716) at latest follow-up (P < 0.01).
Conclusions: The development of atrophic gastritis during omeprazole treatm
ent in H. pylori-positive GERD patients is associated with a decrease of se
rum Vitamin B-12 levels.