Fp. Lopasso et al., Acid secretory response in the late follow-up of proximal gastric vagotomyfor duodenal ulcer without Helicobacter pylori eradication, HEP-GASTRO, 46(25), 1999, pp. 240-244
BACKGROUND/AIMS: The profile of acid secretory responses was studied in 20
patients who had had proximal gastric vagotomy (PGV) surgery performed 11-2
2 years previously in order to treat duodenal ulcers (DU). The presence of
Helicobacter pylori was detected in all of the patients.
METHODOLOGY: The recurrence of DU was diagnosed in 10 patients and the othe
r 10 remained without recurrence during the follow-up period. The control g
roups included 10 DU patients with refractory responses to H2 receptor anta
gonists and 10 "normal" subjects. Both control groups had untreated Helicob
acter pylori infection. Measures of I) basal acid output, 2) acid output fo
r 30min under continuous IV infusion of 0.2 ug/kg/h of pentagastrin acid, a
nd 3) the response for 30 and 60min after starting a sham feeding, modified
by the "chew and spit" technique under simultaneous IV infusion of 0.2 ug/
kg/h of pentagastrin were performed. Serum gastrin was measured during fast
ing and at sham feeding. The densities of the gastrin cells of antrum and d
uodenum were estimated by morphometric counting.
RESULTS: Both basal output and acid response to sham feeding plus pentagast
rin infusion were higher in the DU controls and DU recurrence patients. The
response to pentagastrin infusion did not show any discriminant value. Fas
ting serum gastrin values increased after PGV, either with or without DU re
currence. Gastrin cell hyperplasia was not demonstrated in any of these gro
ups.
CONCLUSIONS: The secretory profile of patients with both late DU recurrence
after PGV and Helicobacter pylori infection lies between DU patients refra
ctory to the H2 receptor antagonist approach and those free of DU recurrenc
e after PGV-both of them with current Helicobacter pylori infection. The ch
aracteristic pattern of late DU recurrence after PGV and untreated Helicoba
cter infection is that of increased basal acid output and higher acid secre
tion responsiveness to sham feeding plus pentagastrin in the presence of hi
gher serum levels of gastrin.