Omeprazole is the first of a new class of drugs, the acid pump inhibitors, which control gastric acid secretion at the final stage of the acid secretory pathway and thus reduce basal and stimulated acid secretion irrespective of the stimulus. In patients with duodenal or gastric ulcers, omeprazole as a single 20mg daily dose provides more rapid and complete healing compared with ranitidine 150mg twice daily or 300mg at night-time, or cimetidine 800 or 1000 mg/day. Patients poorly responsive to treatment with histamine H-2-receptor antagonists respond well to omeprazole - most ulcers healed within 4 to 8 weeks of omeprazole 40 mg/day therapy. Omeprazole 20 or 40 mg/day has been administered as maintenance therapy for peptic ulcer disease for up to 5.5 years with very few ulcer recurrences. In patients with erosive or ulcerative oesophagitis, omeprazole 20 or 40 mg/day produces healing in about 80% of patients after 4 weeks, and is superior to ranitidine with respect to both healing and symptom relief. Healing rates of > 80% are achieved after 8 weeks in patients with severe reflux oesophagitis unresponsive to H-2-receptor antagonists. Maintenance therapy with a daily 20mg dose prevents relapse in about 80% of patients over a 12-month period. Omeprazole is considered to be the best pharmacological option for controlling gastric acid secretion in patients with Zollinger-Ellison syndrome. Daily dosages of 20 to 360 (median 60 to 70mg successfully reduce basal acid output to target levels (< 10 mmol/h or < 5 mmol/h in patients with severe oesophagitis or partial gastrectomy) during treatment for up to 4 years. Omeprazole is well tolerated in short term studies (up to 12 weeks); the reported incidence of serious side effects (about 1%) being similar to that seen in patients treated with an histamine H-2-receptor antagonist. The longer term tolerability of omeprazole has been investigated in patients treated for up to 5.5 years. Slight hyperplasia, but no evidence of enterochromaffin-like (ECL) cell dysplasia or neoplasia or ECL cell carcinoids has been reported. ECL cell carcinoids have been observed in rats after life-long treatment with high doses of omeprazole or ranitidine, or in rats with partial corpectomy; the weight of experimental evidence indicates that this is a result of prolonged hypergastrinaemia. Thus, omeprazole is a highly effective alternative to other treatments available for reflux oesophagitis, and duodenal and gastric ulcers - including those conditions poorly responsive to histamine H-2-receptor antagonists. The potential of omeprazole as prophylaxis for peptic ulcer and reflux oesophagitis is promising and awaits further confirmation of its long term safety. Nevertheless, omeprazole has now reached a stage of its development where it should receive careful consideration by prescribing clinicians as a first-line agent.
