On a number of occasions, there have been descriptions of epidemic achlorhydria in subjects undergoing repeated gastric secretory studies, typically as part of research protocols. We observed a case in a 37-yr-old healthy man undergoing weekly gastric analyses, along with endoscopy and gastric biopsy, as part of a research protocol studying gastric adaptation to aspirin. In the middle of the 2nd wk of aspirin administration, he developed severe nausea and epigastric discomfort. Aspirin administration was discontinued, but, as per protocol, gastric analyses, endoscopies, and biopsies were continued. Compared to the week preceding the acute illness, biochemical analyses showed a transient 7.4-fold increase in basal gastric acid, 3.6-fold increase in pepsin secretion, 8.8-fold increase in DNA loss, 5.6-fold increase in mucus secretion, and 12-fold increase in gastric bleeding. Basal acid secretion was zero, and pepsin secretion was one-third of control during the 2nd wk of the infection. Endoscopy at the time of symptoms showed erosions in the gastric body and antrum, as well as numerous mucosal hemorrhages and an acute ulcer in the antrum. Endoscopy 7 days later revealed that the gastric mucosa had almost completely recovered, with only a shallow erosion seen at the site of the previous ulcer. Gastric biopsies were normal before and during the first 2 wk of aspirin ingestion. Gastric biopsies taken at the time of the acute illness (associated with increased basal acid secretion) showed marked acute inflammation of the antrum with many Campylobacter pylori bacilli. At that time, neither acute inflammation nor C. pylori were found in biopsies from the body of the stomach. Biopsies obtained 1 wk later (zero basal acid) showed acute inflammation of both the gastric body and antrum. One week later, biopsies from the gastric body showed mild focal acute inflammation, moderate chronic inflammation, and an occasional lymphoid follicle; the gastric antrum showed chronic inflammation. Antral biopsies obtained 2 yr later showed persistent chronic gastritis with prominent lymphoid follicles and scattered foci of acute inflammatory cells; C. pylori bacilli were still present, but were less apparent. We believe that the syndrome of acute (epidemic) gastritis is often iatrogenic C. pylori infection. Our case shows that increased basal acid and pepsin secretion occur before onset of basal acid hypochlorhydria in the acute phase of C. pylori infection.