Precursor lesions of gastric polyps during Ppi therapy.

Issn Print: 0954-691X

Publication Date: 2001/12/01

Precursor lesions of gastric polyps during PPI therapy.


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Gastric polyps are common during omeprazole maintenance therapy (OMT). Their etiology is unknown, but a sequence of parietal cell protrusions (PCP), i.e. cellular budding due to expansion of secretory canaliculi, and fundic gland cysts (FGC) leading to fundic gland polyps (FGP) is suggested. Development of both PCP and hyperplastic polyps (HPP) has been related to increased serum gastrin, that of FGP to H. pylori eradication. Our aim was to show that PCP, FGC and FGP are sequential lesions developing during OMT and to study their relation with H. pylori. In a prospective study, GERD patients were annually seen for endoscopy before and during OMT. From this cohort, patients developing gastric polyps were matched with patients without polyps according to age, duration of OMT and H. pylori status. Biopsy specimens from antrum and corpus were obtained for histology and culture, and scored for the presence of PCP, FGC and gastritis according to the updated Sydney system (gastritis, atrophy, intestinal metaplasia). 20 patients (mean ± SD age 67 ± 17 yrs, mean ± SD OMT duration 45 ± 31 months) developed polyps (15 FGP, 5 HPP) during follow-up. The control group contained 20 patients (mean ± SD age 64 ± 15 yrs, mean ± SD OMT duration 44 ± 30 months). H. pylori was present in 1/15 (7%) FGP and in 3/5 (60%) HPP patients [P = 0.03]. PCP was present in all FGP and HPP patients and in 18 (90%) controls. FGC was present in 17 (85%) polyp patients (14 FGP, 3 HPP) and in 9 (45%) controls [P = 0.02; OR (95% CI) = 6.9 (1.5–31.4)]. Mean ± SD antral atrophy scores were slightly lower in polyp patients than in controls, respectively 0 ± 1 versus 1 ± 1 (P = 0.05). The other gastritis scores did not differ between both groups. In conclusion, this study shows for the first time that FGC is the histologic precursor of FGP. PCP occurs in nearly all patients during OMT. This precludes the determination of a sequential relation between PCP on the one hand and FGC and FGP on the other hand. FGC and FGP predominantly occur in H. pylori-negative subjects, possibly because bacterial proteolytic enzymes prevent glandular outlet obstruction despite narrowing of the glandular isthmus by PCP. Another explanation may be that reduced glandular secretion due to H. pylori-induced gastritis prevents FGC and FGP formation.
A Cats, BE Schenk, E Bloemena, EC Klinkenberg-Knol, SGM Meuwissen, EJ Kuipers. Depts of Gastroenterology and Pathology, Free University Hospital Amsterdam; Dept of Gastroenterology and Hepatology, Academic Hospital Rotterdam.


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