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for peptic ulcer, and the three patients in our study who had undergone vagotomy and drainage or gastric resection all needed frequent dilatations during both placebo and cimetidine treatment periods. Since our results show that cimetidine benefits oesophagitis, however, it seems reasonable to hope that a longer period of treatment might lessen the need for dilatation.

In animal models of intestinal hypersensitivity, lymphocyte-mediated damage to the small-bowel mucosa produces a characteristic pattern of morphologic abnormalities. Similar findings in human jejunal biopsy specimens may also indicate that T cells are involved in a disease process. To test the hypothesis that there is a generalized activation of mucosal T cells throughout the small-intestinal mucosa in Crohn's disease, measurements of the lengths of crypts and villi and intraepithelial lymphocyte (IEL) counts were made on jejunal specimens from 33 patients with this condition, and the results compared with the established reference values and with results of specimen measurements in a group of normal subjects. Taken as a group, the specimens from Crohn's patients had abnormal villus length, crypt length, and IEL counts. Focal histologic abnormalities such as ulcers, fissures, or granulomas were present in 10 of the specimens. When specimens with and without a focal abnormality were compared, the former showed shorter villi (median, 249.6 versus 331 microns, p less than 0.01), longer crypts (median, 330.4 versus 108.2 microns, p less than 0.01) and higher IEL counts (60.5 versus 32 IEL/100 enterocytes, p less than 0.01). These findings suggest that there is a mucosal cell-mediated immune response in the jejunum in Crohn's disease and that this is pronounced in the vicinity of microscopic, focal lesions.