Acid and pepsin secretion in patients with esophagitis refractory to treatment with H2 antagonists.

The basis for treatment of esophagitis is suppression of gastric acid secretion. To determine whether lack of healing with standard treatment with H2 antagonists might be due to abnormal gastric secretion, 30 patients who remained unhealed after 12 weeks' therapy with histamine H2 antagonists were compared with 20 patients who healed after 6 or 12 weeks' therapy. The groups were matched with regard to age, weight, sex, and presence of hiatal hernia or duodenal ulcer. There were no significant differences in fasting gastric juice volume, pH, or acid or pepsin concentrations. All 30 refractory patients had basal acid output (BAO) less than 10 meq/h, and 16 of 30 had BAO less than 2 meq/h--that is, there was no evidence of hypersecretion in any refractory patients. Moreover, basal and maximal acid and pepsin outputs were not higher in non-healing patients. Refractory patients had a higher prevalence of initial severe (grade 3 or 4) esophagitis (80% versus 35% in those who healed, p less than 0.01) and of strictures (73 versus 15%, p less than 0.001), both of which serve as markers for refractoriness to treatment. Thus 77% of patients who presented with severe esophagitis failed to heal versus 32% of those with mild or moderate esophagitis (p less than 0.01). Refractoriness of esophagitis is not related to gastric acid or pepsin hypersecretion but represents a constitutional susceptibility to esophagitis and requires both short- and long-term treatment strategies that are not yet well defined.