Acid secretion and acid suppression in pathogenesis and healing of peptic ulcer disease

Numerous environmental and genetic factors have been implicated in the pathogenesis of peptic ulcer disease. Although the cause of this disorder has not been established, acid pepsin has been acknowledged at least as a permissive factor in its development. More important, inhibition of nocturnal or 24-hour intragastric acidity is predictably associated with ulcer healing. Famotidine 40 mg at bedtime maintains approximately one-third of pH readings at or above 3.5, reduces pepsin activity, and has no adverse effect on mean total serum gastric concentrations after one week of therapy. In addition, the effect of this dose of famotidine is comparable to ranitidine 300 mg at bedtime and predicts comparable rates of ulcer healing. Thus, monitoring of intragastric pH levels may be useful in identifying potent healers of peptic ulcer disease and in selecting optimal doses or timing of drug administration. Studies of famotidine using such measurements have suggested that this new H2-receptor antagonist is comparable to ranitidine in the healing of duodenal ulcers.