Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment

Citation
A. Cats et al., Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment, HUMAN PATH, 31(6), 2000, pp. 684-690
Citations number
37
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
HUMAN PATHOLOGY
ISSN journal
00468177 → ACNP
Volume
31
Issue
6
Year of publication
2000
Pages
684 - 690
Database
ISI
SICI code
0046-8177(200006)31:6<684:PCPAFG>2.0.ZU;2-0
Abstract
Parietal cell protrusion (PCP), swelling and bulging of parietal cells, has been observed in the oxyntic mucosa of patients receiving omeprazole. The frequency of this event and the underlying mechanisms remain to be clarifie d. As such, it is unknown whether there is a relation with either serum gas trin or Helicobacter pylori infection, and whether PCP predisposes to the d evelopment of fundic gland cysts (FGC). We therefore investigated the devel opment of PCP and FGC in gastroesophageal reflux disease (GERD) patients tr eated with omeprazole and correlated findings to duration of therapy, gastr in, and H pylori infection. In a randomized, double-blinded study, GERD pat ients were evaluated by endoscopy with biopsy sampling for histology and cu lture at baseline, and after 3 and 12 months' therapy with omeprazole 40 mg daily. H pylori-positive patients were randomized to additional eradicatio n therapy or placebo antibiotics at baseline. All histological slides were scored blinded for time and outcome of culture for the presence of PCP and FGC. Fasting serum samples from all visits were used for gastrin measuremen ts. The prevalence of PCP increased during omeprazole therapy from 18% at b aseline to 79% and 86% at 3 and 12 months (P < .001, baseline v both 3 and 12 months). The prevalence of PGC increased from 8% to 17% and 35% (P < .05 , baseline v 12 months). The prevalence of PCP and FGC did not differ among the H pylori-positive and H pylori-negative patients at baseline (PCP 16% v 20% and FGC 7% v 8%, respectively). Whereas H pylori eradication did not significantly affect development of PCP (P = .7), FGC developed significant ly more often in the H pylori-eradicated patients when compared with persis tent H pylori-positive patients (P < .05). PCP development was related to s erum gastrin rise during therapy. In conclusion, PCP occurs in most patient s within the first months of omeprazole treatment and is related to increas ed gastrin levels. FGC develops more gradually and is enhanced by H pylori eradication. HUM PATHOL 31:684-690. Copyright (C) 2000 by W.B. Saunders Com pany.