Serum Group I Pepsinogens by Radioimmunoassay in Control Subjects and Patients With Peptic Ulcer

Serum pepsinogen I concentrations in peptic ulcer patients in relation to ulcer location and stage.

“…They indicted that all gastric ulcerations occurred in the region of the antral gland and that most of the ulcerations were adjacent to the border zone in resected specimens with gastric or duodenal ulcers. 9 They also reported that distances between the mucosal border and pyloric rings were variable, ranging over a wide area on the lesser curvature." From information obtained from multiple biopsy specimens in 570 Japanese patients, the fundic-pyloric border was found to transit proximally with advancing age and a proximal transition occurs extending more rapidly along the lesser curvature of the stomach.…”

Relationship among serum pepsinogens, serum gastrin, gastric mucosal histology andH. pylorivirulence factors in a paediatric population

“…The relationship among serum pepsinogen I (PGI), serum pepsinogen II (PGII) and gastric mucosal histology had already been recognized before identification of Helicobacter pylori [1] and appeared to reflect corresponding variations in gastric mucosal inflammation. Furthermore, a decrease in serum PGI has also been shown to occur in fundus atrophy, reflecting loss of zymogen-producing cells and thus resulting in a lowering of the serum PGI:PGII ratio (PGII, unlike PGI which is only produced by chief cells in the fundus and corpus, is uniformly produced by chief cells and mucous neck cells throughout the stomach and to some extent in the Brunner glands in the first section of the duodenum) [1]. Presently, low serum PGI levels and a low PGI:PGII ratio are considered good predictors of severe gastric atrophy [2,3]; in contrast, high levels of serum PGI are frequently observed in duodenal ulcer disease [4] recognized to be associated with chronic gastritis but without significant fundic atrophy [5].…”

Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells

“…5 Patients with duodenal ulcers have increased pepsinogen I levels, which was believed to be of genetic origin. 6 However, numerous studies have shown that both duodenal ulcer patients and healthy volunteers with H pylori infection have increased serum pepsinogen I levels which decrease after H pylori eradication. [7][8][9][10] Different studies have shown that H pylori sonicate and H pylori lipopolysaccharide stimulate pepsinogen release from either isolated rabbit gastric glands 11 or guinea pig gastric mucosa, 12 suggesting a direct stimulatory effect of H pylori on chief cells.…”