Roediger W E
Department of Surgery, University of Adelaide at The Queen Elizabeth Hospital, Australia.
Dis Colon Rectum. 1988 Jun;31(6):482-7. doi: 10.1007/BF02552623.
The etiology of ulcerative colitis remains unresolved despite new immunologic, biochemical, and microbiologic observations made in this disease. A sequence of pathogenetic events has been adduced from abnormalities reported from human and experimental colitis with the express purpose of establishing priority of factors that may lead to an attack of acute ulcerative colitis. The presence of undefined bacterial metabolites in the colonic lumen causing specific breakdown of fatty acid oxidation in colonic epithelial cells is proposed to be the initiating event of the disease process that leads to an immune response and eicosanoid response perpetuating epithelial cell damage. The proposals embody the thesis that primary metabolic damage to colonocytes determines the clinical and pathologic manifestations of ulcerative colitis.
尽管在溃疡性结肠炎方面有了新的免疫学、生物化学和微生物学发现,但其病因仍未明确。从人类和实验性结肠炎报告的异常情况中归纳出了一系列致病事件,其明确目的是确定可能导致急性溃疡性结肠炎发作的因素的先后顺序。有人提出,结肠腔内存在未定义的细菌代谢产物,导致结肠上皮细胞中脂肪酸氧化的特定分解,这是疾病过程的起始事件,会引发免疫反应和类花生酸反应,使上皮细胞损伤持续存在。这些观点体现了这样一种论点,即结肠细胞的原发性代谢损伤决定了溃疡性结肠炎的临床和病理表现。