Our method was shown to be feasible and safe. The success of the intralesional injection of the sclerosing agent may be predicted when changes in the mucosal surface are observed: (a) immediately after the injection sufficient sclerosant is deemed to have been injected and to the proper depth in the bowel wall, if the mucosa bulges while the solution is being injected; and (b) if a shallow ulceration is seen in an early subsequent reexamination where the treated lesion was located, allowing scar tissue produced by the healing process of the ulcer to replace the former vascular lesion.

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Cytogenetic preparations were obtained by brushing the rectal mucosa during proctoscopy. of 61 individuals examined, 33 provided reliable material for chromosomal analysis: 10 normal controls, 5 with Crohn's disease involving the colon, 10 with chronic ulcerative colitis, 4 with ulcerative colitis complicated by cancer of the colon in whom special care was taken to obtain separated samples from both colitic and cancerous tissue, and 4 with cancer of the colon alone. Chromosome count and karyotypes were normal in all controls and patients with Crohn's disease. In chronic ulcerative colitis the modal chromosome number remained in the diploidy range. But aneuploid cells, or possible broken polyploid were seen in 2 patients, and in the inflamed mucosa of 2 other patients with cancer of the colon associated with ulcerative colitis. All these cells were in the hypotetraploidy range. No chromatid breaks were found in the controls and in patients with Crohn's disease, but patients with ulcerative colitis and colon cancer demonstrated a variable number of breaks. Profound abnormalities were demonstrated in patients with carcinoma, characterized by aneuploidy, chromatid breaks and marker chromosomes. This study documents significant chromosomal abnormalities in chronic ulcerative colitis, both in patients with and without colonic cancer.

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