Effect of Helicobacter pylori on Serum Pepsinogen I and Plasma Gastrin in Duodenal Ulcer Patients

Abstract

Duodenal ulcer patients have increased serum pepsinogen I (PGI) concentrations and an increased prevalence of Helicobacter pylori infection. We have examined the effect of eradicating the infection on PGI. In 12 duodenal ulcer patients in whom H. pylori was successfully eradicated, the median basal PGI was 90 ng/ml (range, 37-252) before treatment and fell to 74 ng/ml (28-197) 1 month after treatment (p less than 0.01). In 12 patients in whom therapy failed to eradicate the infection, the PGI was 87 ng/ml (35-128) before treatment and remained unchanged at 83 ng/ml (36-119) 1 month after treatment. In the group with successful eradication the median basal plasma gastrin was 43 ng/l (15-95) before treatment and fell to 30 ng/l (17-75) 1 month after treatment (p less than 0.003), but there was no change in the corresponding values in the group without eradication (55 ng/l; range, 25-120, and 45 ng/l; range, 5-175; p = 0.9). In conclusion, eradication of H. pylori results in a fall in PGI and plasma gastrin, and these changes are not due merely to the anti-H. pylori drugs themselves or to discontinuation of previous ulcer therapy.

Alteration of correlation between serum pepsinogen concentrations and gastric acid secretion after H. pylori eradication

“…Then, the relative decrease in PG I caused by H. pylori eradication was smaller than that in PG II (32 vs. 59%), resulting in an increase in the PG I/II ratio from 3.4 ± 1.4 pretreatment to 5.2 ± 1.6 at 1 month after eradication (P \ 0.01). These alterations in serum PGs caused by H. pylori eradication are consistent with findings in a number of previous reports [27][28][29]. Between 1 and 7 months after eradication, there were no significant changes in serum PGs, except for a slight decrease in PG I in this period (P \ 0.05).…”

“…Meanwhile, both PG I and II are invariably decreased by the eradication and, due to the relatively larger decrease in PG II than PG I, the resultant PG I/II ratio is usually elevated after eradication [27][28][29]. Thus, since alterations in gastric acid secretion and serum PG following H. pylori eradication do not always occur in parallel, the posttreatment correlation between these two parameters could be different from the pretreatment one.…”

Usefulness of Serum Pepsinogens in Helicobacter pylori Chronic Gastritis: Relationship With Inflammation, Activity, and Density of the Bacterium

“…There are two possible reasons in order to explicate these reports. First, an alteration of gastric glands functions, caused directly by a stimulation of H. pylori, could increase the secretion of sPGI, as shown in in vitro studies [22,23]. Second, when inflammation is localized in the antrum, the alterations of the gastric secretion (i.e., exaggerated meal-stimulated gastrin release) stimulate corpus glands to secrete chloride acid and pepsinogens [24][25][26].…”

A study of the pathogenesis of Helicobacter pylori negative chronic duodenal ulceration.

“…The values in the patients with idiopathic DU (5 9 (1-20) (16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29), p<OOS) (Fig 4). The patients with idiopathic DU had peak acid output values (37 ) that were similar to those of the H pylori positive patients with DU.…”

“…The liquid emptying rate in the patients with idiopathic DU was significantly faster than in the H pylori negative healthy volunteers (median 60 minute percentage retentions 23 (range [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33] and 34 (30-53) respectively (p<0 01) (Fig 5)). (Fig 5).…”