LACK OF EFFECT OF H-2-RECEPTOR ANTAGONISTS AND ANTACIDS ON THE GASTRIC AND DUODENAL GASTRIN-PRODUCING, SOMATOSTATIN-PRODUCING AND SEROTONIN-PRODUCING CELLS IN PATIENTS WITH ACID PEPTIC DISORDERS
Wr. Yacoub et al., LACK OF EFFECT OF H-2-RECEPTOR ANTAGONISTS AND ANTACIDS ON THE GASTRIC AND DUODENAL GASTRIN-PRODUCING, SOMATOSTATIN-PRODUCING AND SEROTONIN-PRODUCING CELLS IN PATIENTS WITH ACID PEPTIC DISORDERS, Canadian journal of gastroenterology, 10(4), 1996, pp. 255-259
Standard therapeutic approaches to acid peptic disorders have dealt wi
th neutralizing or inhibiting aggressive factors and/or bolstering def
ensive factors. Gastric and duodenal mucosal biopsies were examined fr
om 90 patients with various acid peptic disorders, as follows: reflux
esophagitis (n=24), gastric ulcer (n=13), duodenal ulcer (n=47) and no
nulcer dyspepsia (n=6). Seven patients with minimal dyspeptic symptoms
and an endoscopically and histologically normal stomach and duodenum
served as controls. Immunoperoxidase staining for gastrin-producing G
cells, somatostatin-producing D cells and serotonin-producing EC cells
was carried out on fundic, antral and duodenal biopsies, and quantita
ted using a Zeiss MOP videoplan. no significant effects secondary to t
reatment with antacid, ranitidine or cimetidine were observed on endoc
rine cell densities and ratios. Biopsies obtained on different occasio
ns over time indicated that in patients on enprostil (a synthetic E(2)
prostaglandin), there was a trend towards increasing cell counts, sug
gesting that the serum gastrin-lowering effect of this drug may result
from inhibition of gastrin release. Thus, H-2 receptor antagonists an
d antacids do not alter gastric or duodenal mucosal G, D or EC cells i
n patients with acid peptic disorders.