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Three months of octreotide treatment decreases gastric acid secretion and argyrophil cell density in patients with Zollinger‐Ellison syndrome and antral G‐cell hyperfunction
Author(s) -
ANNIBALE B.,
FAVE G. DELLE,
AZZONI C.,
CORLETO V.,
CAMBONI G.,
D'AMBRA G.,
PILATO F. P.,
BORDI C.
Publication year - 1994
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.1994.tb00165.x
Subject(s) - medicine , gastrin , gastric acid , endocrinology , octreotide , zollinger ellison syndrome , pentagastrin , basal (medicine) , secretion , antrum , somatostatin , gastrinoma , enterochromaffin like cell , gastroenterology , stomach , insulin
SUMMARY Methods : The effects of three months of treatment with octreotide on gastric acid hypersecretion induced by hypergastrinaemia were investigated in patients with Zollinger‐Ellison syndrome ( n = 5) or antral G‐cell hyperfunction ( n = 4). Gastric acid secretion, fasting plasma gastrin concentrations and clinical findings were examined, and a morphometrical analysis of oxyntic endocrine cells was performed. Results : Administration of octreotide 100 meg b.d. subcutaneously significantly decreased the volume density of argyrophil cells (P < 0.05) as well as basal and pentagastrin‐stimulated acid secretion (P < 0.05). Although partial or complete loss of inhibition was found in most patients after 3 months, gastrin levels were decreased during the first 2 months of treatment (P < 0.05). Fundic D‐cells were not affected by treatment. Positive correlations were observed between volume density of argyrophil cells and basal acid output ( r = 0.65); plasma gastrin and basal acid output ( r = 0.74); plasma gastrin concentrations and volume density of argyrophil cells ( r = 0.80). Conclusion : These results support the important role of the enterochromamn‐like cell in maintaining acid secretion, and indicate a specific role for octreotide in the therapy of gastric acid hypersecretion associated with hypergastrinaemic diseases.