Levi S, Goodlad R A, Lee C Y, Stamp G, Walport M J, Wright N A, Hodgson H J
Department of Medicine, Royal Postgraduate Medical School, London, UK.
Digestion. 1992;53(3-4):129-33. doi: 10.1159/000200987.
We demonstrate that, in patients taking non-steroidal anti-inflammatory drugs (NSAIDs), there is inhibition of the proliferation of mucosal cells that normally leads to healing of duodenal ulcers. A microdissection technique was used to quantitate mitosis in duodenal crypts at the ulcer edge, giving a regeneration index of mitotic rate at that site, as compared to nearby mucosa. In patients with duodenal ulcers occurring in the absence of NSAID therapy, there was a brisk regenerative response (median index 2.48, range 1.55-9.81, n = 8), significantly greater than in patients taking NSAIDs (median index 1.10, range 0.73-2.16, n = 10, p = 0.014). Inhibition of the process of epithelial cell division normally involved in duodenal ulcer healing could contribute to the delay in ulcer healing which may explain the higher complication rate for duodenal ulcer during NSAID therapy.
我们证明，在服用非甾体抗炎药（NSAIDs）的患者中，正常情况下会导致十二指肠溃疡愈合的黏膜细胞增殖受到抑制。采用显微切割技术对溃疡边缘十二指肠隐窝中的有丝分裂进行定量，得出该部位有丝分裂率的再生指数，并与附近黏膜进行比较。在未接受NSAID治疗而发生十二指肠溃疡的患者中，存在活跃的再生反应（中位指数2.48，范围1.55 - 9.81，n = 8），显著高于服用NSAIDs的患者（中位指数1.10，范围0.73 - 2.16，n = 10，p = 0.014）。通常参与十二指肠溃疡愈合的上皮细胞分裂过程受到抑制，可能会导致溃疡愈合延迟，这或许可以解释NSAID治疗期间十二指肠溃疡并发症发生率较高的原因。
