Bi. Hirschowitz et al., LONG-TERM TREATMENT WITH LANSOPRAZOLE FOR PATIENTS WITH ZOLLINGER-ELLISON SYNDROME, Alimentary pharmacology & therapeutics, 10(4), 1996, pp. 507-522
Background: Normalization of gastric secretion and cure of associated
upper gastrointestinal lesions by resection of gastrinoma is possible
in approximate to 20% of patients with Zollinger-Ellison syndrome, lea
ving approximate to 80% dependent on medical treatment with proton pum
p inhibitors for acid suppression. Methods: Lansoprazole was given for
3-48 months (median 28 months) to 26 Zollinger-Ellison syndrome patie
nts with peptic ulcer manifestations in all and oesophagitis in 13, St
arting with 60 mg/day, the dose was individualized to lower basal acid
output to less than 5 mmol/h for those with intact stomachs and less
than 1 mmol/h in those who had prior gastrectomy or with oesophagitis.
The patients were studied every 3 months for 1 year and then every 6
months with gastric analysis (basal and maximal acid and pepsin output
) and endoscopy with biopsy for enterochromaffin-like (ECL) cells. Res
ults: Lansoprazole inhibited basal acid output by 95%, pepsin output b
y 65% and remained effective at the initial mean (66+/-4.3 mg/day) or
smaller doses (56+/-12 mg/day) at 48 months. Mucosal lesions healed an
d symptoms (ulcer-type pain, diarrhoea, heartburn, weight loss) resolv
ed rapidly, usually within a few weeks. Serum gastrin and ECL cell pop
ulations, which were elevated before treatment, remained statistically
unchanged but one of the three multiple endocrine neoplasia I (MEN-I)
patients developed a small carcinoid. Of the three patients with meta
static gastrinoma at diagnosis one has died and one has progressed, wh
ile the third has had stable liver metastases for 26 years. Ulcer-type
relapses occurred in three of the ave post-gastrectomy patients, one
with fatal jejunal ulcer perforation despite adequate acid suppression
. No biochemical or clinical adverse events due to lansoprazole were e
ncountered, Conclusion: Lansoprazole effectively inhibits acid and pep
sin secretion in Zollinger-Ellison syndrome patients without any demon
strated side-effects. Despite strict acid control, post-gastrectomy Zo
llinger-Ellison syndrome patients were more liable to ulcer relapse, w
hile oesophagitis was not a marker for therapeutic difficulty.