Duodenal Epithelial Thymidine Uptake in Patients with Duodenal Ulcer or Endoscopic Duodenitis FRED S. GORELICK, VINCENT A. DELUCA, DANIEL G. SHEAHAN, PIERLUIGI MARIGNANI, ROBERT S. GOLDBLATT, JERRY WlNNAN, and ELLIOT M. LIVSTONE To evaluate the relationship between duodenal ulcer disease and duodenitis, duodenal epithelial cell renewal was measured in mucosal biopsies by the incorporation of [3H]thymidine. When 14 patients with duodenal ulcer were compared to 13 control subjects or 7 with endoscopic duodenitis alone, the crypt size was the same in all groups. Similar to other inflammatory processes of the gastrointestinal tract, patients with endoscopic duodenitis showed increased proliferative indices including a greater number of cells incorporating [3H]thymidine. In contrast, the proliferative indices from the duodenal mucosa of patients with duodenal ulcers did not differ from a control group. In a group of 6 patients with both endoscopic duodenitis and duodenal ulcer, the [3H]thymi- dine incorporation was intermediate between control subjects or patients with duodenal ulcer alone and those with endoscopic duodenitis alone. When subjects were divided according to the histologic appearance of the duodenal mucosa, those having chronic duodenitis demonstrated enhanced [3H]thymidine incorporation in comparison to a control group or patients with chronic active duodenitis (polymorphonuclear leukocytes present). Although there are many possible explanations of these findings, one may speculate that duodenal ulceration does not stimulate duodenal epithelial proliferation. The relationship between inflammation of the duodenum and duodenal ulcer is a subject of con- troversy. While some consider duodenitis to be part of the spectrum of duodenal ulcer disease (1-3). Manuscript received December 17. 1981: revised manuscript received August 10. 1982: accepted December 13. 1982. From the Departments of Medicine and Pathology, Yale University School of Medicine. New Haven. Connecticut: and the Griffin Hospital, Derby, Connecticut. This project was supported by the Yale Digestive Cancer Research Fund. Dr. Gorelick was supported by a Research Fellowship Award from the National Foundation for Ileitis and Colitis during a portion of this study and is currently a recipient of a Clinical Investigator Award (KO8-AM-006591 from the National Institute of Arthritis, Metabolism and Digestive Diseases. Address for reprint requests: Dr. Fred S. Gorelick. Depart- ment of Internal Medicine, 92 LMP. Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510. others view it as a separate process (4. 5) or question its existence as a symptomatic entity (6). Some inflammatory disorders of the gastrointestinal tract including esophagitis (7), some forms of gastri- tis (8.9), celiac disease (10), and ulcerative colitis (11) characteristically have shown increased indices of epithelial renewal. A recent study also found enhanced mucosal proliferation in subjects with duodenal ulcer or duodenitis (12). In contrast, ani- mal models of duodenal ulcer disease (13) and sti-ess-induced gastritis (14) have demonstrated de- pressed indices of epithelial renewal. We examined mucosal proliferation in the duodenal bulb of pa- tients with duodenal ulcer or with duodenitis by measuring the in vitro incorporation of [3H]thymi- dine into duodenal mucosa obtained by endoscopic biopsy. 392 Digestive Diseases and Sciences, Vol. 28, No. 5 (May 1983) 0163-2116/83/0500-0392503.00/1 r 1983Digestive DiseaseSystems, Inc.