Impaired increase of prostaglandin E₂ in gastric juice during steroid therapy in children

Abstract

To investigate the aetiology of steroid-induced peptic ulcers in children, prostaglandin E2 (PGE2) release and acid secretion into gastric juice was evaluated in 10 children receiving a corticosteroid before and after injection of pentagastrin. The concentration of luminal PGE2 was measured by radio-immunoassay. The basal levels of PGE2 concentration and acid secretion in gastric juice did not differ significantly between the steroid therapy group and control group. After stimulation with pentagastrin, acid secretion increased significantly (P < 0.01) in both groups and PGE2 concentration increased significantly (P < 0.01) only in the control group. Prostaglandin E2 concentration was significantly lower in the steroid therapy group than in the control group 20-40 and 40-60 min after pentagastrin stimulation (P < 0.01 and P < 0.05, respectively). Since PGE2 has a cytoprotective effect on the gastric mucosa, the results of impaired increase of PGE2 in response to increased acid secretion during steroid therapy may indicate causality with the development of steroid-induced peptic ulcers.

Early Development of Human Gastric H,K‐Adenosine Triphosphatase

“…These include an adherent mucus gel layer, bicarbonate secretion, surface epithelial cells, and an intact mucosal blood flow (26,27). Prostaglandin E 2 , involved in these protective actions, increases parallel to the decrease in gastric pH (28). However, the mechanisms for mucosal protection are not fully understood.…”

Arachidonic Acid-Derived Bioactive Lipids: Their Role and the Role for Their Inhibitors in Dermatology

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