Digestive Diseases and Sciences, Vol. 32, No. 1l (November 1987), pp. 1255-1260 Persistence of Campylobacter pyloridis Despite Healing of Duodenal Ulcer and Improvement of Accompanying Duodenitis and Gastritis WAI-MO HUI, SHIU-KUM LAM, PAT-YIM CHAU, JOANA HO, IRENE LUI, CHING-LUNG LAI, ANNA SUK-FONG LOK and MATTHEW MA-TAI NG Campylobacter pyloridis has been associated with antral gastritis and duodenal ulcer. To study the pathogenetic role of these organisms in duodenal ulcer, endoscopic biopsies, two from the first part of duodenum, four from antrum, and four from body and fundus, were taken before and after four weeks of cimetidine treatment (1.2 g/day)from 67 patients with active duodenal ulcer. The biopsies were examined for the presence and severity of any inflammation by two independent pathologists in the absence of any clinical information and for the occurrence and density of Campylobacter pyloridis by culture and. Warthin-Starry stain. Before treatment, inflammation was present in 71.1, 100, and 25.8%, while the organisms were present in 34.3, 91.0, and 79.1% of the duodenal, antral, and fundal biopsies, respectively. With complete healing of duodenal ulcer, inflammation was present in 48.9, 98.2, and 30.2%, while the organisms were present in 25, 76.7, and 63.3% of the respective mucosae. With ulcer healing, duodenitis became significantly milder (P < 0.05). With improvement of gastritis and duodenitis, there was no significant change in the occurrence and density of Campylobacter pyloridis. These findings indicate that healing of duodenal ulcer is not influenced by the presence ofCampylobacter pyloridis, which is frequently found in the gas troduodenal mucosa of patients with duodenal ulcer, but does not appear tO be associated with mucosat inflammation except in the antrum. KEY WORDS: duodenal ulcer; campylobacter; duodenitiS; gastritis. The reports on the association of Campylobacter pyloridis with antral gastritis and peptic ulcer (1, 2) have aroused great interest on the bacterial etiology of peptic ulcer disease. Attention has been focused Manuscript received August 14, 1986; revised manuscript received January 5, 1987; accepted March 20, 1987. From the University Departments of Medicine, Pathology, and Microbiology, University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong. Supported by the Peptic Ulcer Research Fund (311/041/0372), and University Grants (311/030/8009/31, 311/030/8010/12, 311/ 030/8010/69, 335/041/0006) of the University of Hong Kong. Address for reprint requests: Prof. S.K. Lam, Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong K0ng. on cross-sectional studies on the correlation be- tween gastritis and bacteria in peptic Ulcer disease and antibody response to Campylobacter pyloridis (3-5). Studies on the changes in the occurrence of the bacteria with duodenal ulcer healing have been few (6, 7). We have demonstrated, using Warthin- Starry staining of biopsies from gastric antrum for Campylobacter pyloridis, that no change in bacte- rial density occurs in the antrum with the healing of the duodenal ulcer (7). Since duodenal ulcer occurs in the duodenum, and if Campylobacter pyloridis has any etiological role, we would expect changes in the bacterial density in the duodenum. This study Digestive Diseases and Sciences, VoL 32, No. 11 (November 1987) 0163-2116/87/1100-1255505.00/0 9 1987 Plenum Publishing Corporation 1255