论文部分内容阅读
一个世纪以来,人们对阿米巴性结肠炎并发病的发病机理进行过许多研究。一般认为,阿米巴可以分泌一种溶组织酶,能够破坏并溶化附近组织,引起粘膜形成阿米巴溃疡。随着阿米巴局部移动和继发细菌感染,结肠粘膜形成的阿米巴性溃疡可进一步发展为壁层坏死,导致结肠穿孔。本文则对阿米巴性结肠炎透壁病变的病理做了进一步研究,并对其发病机理重新作出评价。本研究提示阿米巴性结肠炎从表浅溃疡向透壁坏死进展是由于阿米巴侵入了该结肠的供血动脉,随后使该动脉发生血栓性闭塞和缺血性坏死所致。作者从1978年6月至1982年12月对50例阿米巴性结肠炎疑有透壁性病变者作了剖腹探查。其中44
For more than a century, there have been many studies on the pathogenesis of concurrent amoebic colitis. It is generally believed that amebic secretes a lysozyme that destroys and solubilizes nearby tissues, causing mucosal amoebiasis. With the local movement of amoeba and secondary bacterial infections, amoebic ulcers forming colonic mucosa can further develop into parietal necrosis, leading to colon perforation. This article is a further study of the pathology of transmural lesions of amoebic colitis, and to re-evaluate the pathogenesis. This study suggests that progression of amoebic colitis from superficial ulceration to transmural necrosis is due to amoebic invasion of the donor arteries of the colon followed by thrombotic occlusion and ischemic necrosis of the artery. The author from June 1978 to December 1982 50 cases of amoebic colitis suspected transmural lesions were exploratory laparotomy. 44 of them