Phenylbutazone induces equine glandular gastric disease without decreasing prostaglandin E2 concentrations

In equids, phenylbutazone at high doses induces gastric disease, primarily in the glandular portion of the stomach. However, the mechanism of nonsteroidal anti‐inflammatory drug (NSAID)‐induced gastric disease in horses has yet to be determined. While phenylbutazone‐associated ulceration is often attributed to a decrease in basal gastric prostaglandins, this has not been demonstrated in the horse. Twelve horses were randomly assigned to treatment (n = 6; 4.4 mg/kg phenylbutazone PO in 20 ml molasses q 12 hr for 7 days) or placebo (n = 6; 20 ml molasses PO q 12 hr for 7 days) groups. Before treatment and 3 and 7 days after initiation of treatment, gastroscopy was performed and glandular gastric biopsies were collected and frozen at −80°C. Glandular disease was assessed on a scale of 0–4. Prostaglandin E2 concentrations in biopsies were measured using a commercially available enzyme‐linked immunosorbent assay. All phenylbutazone‐treated horses developed grade ≥2 glandular disease. Prostaglandin concentrations increased over time (p = .0017), but there was no effect of treatment (p = .49). These findings indicate that despite induction of glandular disease grade ≥2, phenylbutazone did not decrease basal glandular gastric prostaglandin E2 concentration.