ANGIOGENESIS IN GASTRIC-ULCERS - IMPAIRED IN PATIENTS TAKING NONSTEROIDAL ANTIINFLAMMATORY DRUGS

Non-steroidal anti-inflammatory drug (NSAID) therapy is associated wit h delayed gastroduodenal ulcer healing. In rats the degree of angiogen esis (new vessel formation) within the ulcer bed correlates strongly w ith the extent and speed of ulcer healing and may be inhibited by NSAI Ds. This study therefore assessed the vascularity of 38 antral gastric ulcers immuno-histochemically, using CD31 a vascular endothelial cell marker, in 17 patients taking NSAIDs and 19 control patients. In the superficial granulation tissue NSAID therapy was associated with a sig nificant reduction in the median number of capillaries (13.5 (IQR: 9.5 -18) v 23.5 (14-31) (p < 0.005)), number of vessel buds (6 (4-12.5) v 17 (12-23) (p < 0.005)), and maximum vessel diameter (29 (20.75-30.75) v 33.75 (24-45) (p < 0.05)) when compared with controls. In deep gran ulation tissue NSAID therapy was similarly associated with a significa nt reduction in the number of capillaries (9 (6.5-12) v 14 (9-19.25) ( p < 0.04)), number of vessel buds (5 (3.5-8.5) v 13 (7-16.5) (p < 0.01 )), and maximum vessel diameter (23 (18-20.5) v 33 (21.5-45) (p < 0.02 )). There were no differences in vascularity in the adjacent glandular mucosa. Impairment of angiogenesis may be an important mechanism of N SAID related delayed ulcer healing.