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Intravenous amino acids stimulate gastric acid secretion by an unknown mechanism. In patients on parenteral nutrition, this amino acid-induced gastric acid secretion might contribute to the failure of H2-receptor antagonists to raise intragastric pH above 4.0, a level thought to be needed to prevent stress ulceration. Therefore we studied the effect of single and repeated doses of the H+/K+-ATPase blocker omeprazole on the intragastric pH during a 3-hr infusion of amino acids in 10 healthy volunteers; 5% glucose was used as a control infusion. Amino acids significantly decreased intragastric pH when compared to glucose infusion (P <0.05). After intravenous administration of 40 mg, 80 mg and 2 × 40 mg omeprazole, this amino acid-induced fall in pH was significantly inhibited (P < 0.01). No advantage of the 80-mg dose over the 40-mg dose could be demonstrated. The repeated dose of 40 mg showed a tendency to higher pH values compared to the single-dose experiments, which reached significance in the amino acid experiments only (P <0.05). Neither during the infusion of amino acids nor the glucose infusion omeprazole was able to continuously raise intragastric pH above 4.0. In conclusion, this study shows that intravenous omeprazole prevents gastric acid stimulation by intravenous amino acids but fails to continuously raise intragastric pH above 4.

Enprostil, a synthetic prostaglandin E2analog, has been shown to decrease gastric acid secretion and plasma gastrin levels during short-term treatment. However, effects of prolonged treatment with enprostil on these parameters in humans are unknown. We have studied the effects of 35 µg enprostil twice daily on 24-hour intragastric pH, basal gastrin, and meal-stimulated gastrin release in 10 healthy volunteers. Enprostil, 35 µg, was ingested twice daily for 4 weeks. Subjects were studied on day 0 (preentry) and days 1 and 29, when enprostil was taken 30 minutes before the first and third standard test meals at 9 AM and 5 PM. Enprostil significantly increased 24-hour median pH (p < 0.02) on day 1 but not on day 29. Enprostil had no significant effect on basal gastrin levels compared with placebo. However, on day 1, but not on day 29, postprandial gastrin levels were significantly lower compared with preentry (p < 0.05). On day 29 postprandial gastrin levels after the second standard test meal were significantly higher compared with preentry data (p < 0.05). In conclusion, 35 µg enprostil twice daily reduced gastric acidity and serum gastrin levels on the first day of treatment, but this effect attenuated and even transiently reversed during a 4-week treatment period.

Pancreatitis is the most common complication of endoscopic retrograde cholangiopancreatography (ERCP). Prophylactic rectal administration of non-steroidal anti-inflammatory drugs (NSAIDs) is considered as standard of care to reduce the risk of post-ERCP pancreatitis. It has been suggested that aggressive hydration might further reduce this risk. Guidelines already recommend aggressive hydration in patients who are unable to receive rectal NSAIDs, although it is laborious and time consuming. We aimed to evaluate the added value of aggressive hydration in patients receiving prophylactic rectal NSAIDs.