Wp. Geus et al., Post-prandial intragastric and duodenal acidity are increased in patients with chronic pancreatitis, ALIM PHARM, 13(7), 1999, pp. 937-943
Objectives: Patients with chronic pancreatitis and exocrine insufficiency h
ave lower intraduodenal pH compared to controls, It has been assumed that a
bnormal low intraduodenal pH in these patients not only results from impair
ed pancreatic bicarbonate secretion but also from an increased gastric acid
load to the duodenum.
Methods: We have tested this hypothesis by combined intragastric and intrad
uodenal 24 h pH monitoring in nine chronic pancreatitis patients with exocr
ine pancreatic insufficiency and nine healthy control subjects during stand
ardized test conditions. Postprandial gastrin and cholecystokinin release w
ere also determined.
Results: Median 24-h intraduodenal pH (5.90 vs. 6.00) and intragastric pH (
1.60 vs. 1.70) were not significantly different between patients and contro
ls. However, in the 2-h postprandial periods intraduodenal pH was below fiv
e for a significantly higher percentage of time in chronic pancreatitis pat
ients compared to controls (lunch: 14.5% vs. 0.17%, P = 0.011; dinner: 24.1
% vs, 5.75%, P = 0.05). The post-dinner intragastric pH was below three for
a significantly higher percentage of time in chronic pancreatitis patients
vs. controls (72.2 vs, 48.9%, P = 0.04). Postprandial gastrin release was
not significantly different between the two groups. Postprandial secretion
of cholecystokinin (CCK), as enterogastrone, was significantly (P < 0.01) r
educed in chronic pancreatitis patients (78 +/- 13 pmol/L, 120 min) compare
d to controls (155 +/- 14 pmol/L, 120 min).
Conclusions: Median intraduodenal and intragastric pH are not significantly
decreased in patients with chronic pancreatitis and exocrine insufficiency
but the postprandial time with an acidic pH in the duodenum (pH < 5) and i
n the stomach (pH < 3) is significantly (P I 0.05) increased.