Hudson N, Balsitis M, Everitt S, Hawkey C J
Division of Gastroenterology, University Hospital, Nottingham.
Gut. 1995 Aug;37(2):191-4. doi: 10.1136/gut.37.2.191.
Non-steroidal anti-inflammatory drug (NSAID) therapy is associated with delayed gastroduodenal ulcer healing. In rats the degree of angiogenesis (new vessel formation) within the ulcer bed correlates strongly with the extent and speed of ulcer healing and may be inhibited by NSAIDs. This study therefore assessed the vascularity of 38 antral gastric ulcers immunohistochemically, 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 significant 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 < 0.05)), and maximum vessel diameter (29 (20.75-30.75) v 33.75 (24-45) (p < 0.05)) when compared with controls. In deep granulation tissue NSAID therapy was similarly associated with a significant 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 NSAID related delayed ulcer healing.
非甾体抗炎药（NSAID）治疗与胃十二指肠溃疡愈合延迟有关。在大鼠中，溃疡床内的血管生成（新血管形成）程度与溃疡愈合的程度和速度密切相关，且可能被NSAIDs抑制。因此，本研究采用血管内皮细胞标志物CD31，对17例服用NSAIDs的患者和19例对照患者的38个胃窦部溃疡进行免疫组织化学评估其血管分布情况。在浅表肉芽组织中，与对照组相比，NSAID治疗使毛细血管中位数显著减少（13.5（四分位间距：9.5 - 18）对23.5（14 - 31）（p < 0.005））、血管芽数量显著减少（6（4 - 12.5）对17（12 - 23）（p < 0.05））以及最大血管直径显著减小（29（20.75 - 30.75）对33.75（24 - 45）（p < 0.05））。在深部肉芽组织中，NSAID治疗同样使毛细血管数量显著减少（9（6.5 - 12）对14（9 - 19.25）（p < 0.04））、血管芽数量显著减少（5（3.5 - 8.5）对13（7 - 16.5）（p < 0.01））以及最大血管直径显著减小（23（18 - 20.5）对33（21.5 - 45）（p < 0.02））。相邻腺性黏膜的血管分布没有差异。血管生成受损可能是NSAID相关溃疡愈合延迟的重要机制。
