Samloff I M, Taggart R T
Clin Invest Med. 1987 May;10(3):215-21.
The role of pepsin in the pathogenesis of peptic ulcer has been the subject of intense study and debate for many years. Two difficulties inherent in distinguishing between the role of acid alone vs acid and pepsin are that a) acid-containing gastric juice always contains pepsin, and, b) that hydrogen ion concentration (pH) is a major determinant of the activity of pepsin. However, studies in animal models of peptic ulcer indicate clearly that pepsin, in combination with acid, produces much more severe and more extensive mucosal damage than acid alone. Recent interest in pepsin and its precursor, pepsinogen, has stemmed from the finding that each is remarkably heterogeneous, and that the heterogeneity has a genetic basis. Results of studies using radioimmunoassays specific for the 2 major forms of pepsinogen, pepsinogen I and pepsinogen II, have shown that serum levels of pepsinogen I and pepsinogen II, and the ratio of pepsinogen I to pepsinogen II, can be used as noninvasive probes of gastric mucosal structure and function, indicators of the genetics and heterogeneity of duodenal ulcer, and as markers of increased risk for duodenal ulcer and gastric ulcer.
多年来,胃蛋白酶在消化性溃疡发病机制中的作用一直是深入研究和争论的主题。区分单纯酸的作用与酸和胃蛋白酶的作用存在两个内在困难:一是含酸的胃液总是含有胃蛋白酶;二是氢离子浓度(pH值)是胃蛋白酶活性的主要决定因素。然而,消化性溃疡动物模型的研究清楚地表明,胃蛋白酶与酸共同作用时,会比单纯酸造成更严重、更广泛的黏膜损伤。最近对胃蛋白酶及其前体胃蛋白酶原的关注源于这样一个发现,即它们各自都具有显著的异质性,且这种异质性有遗传基础。使用针对两种主要胃蛋白酶原形式(胃蛋白酶原I和胃蛋白酶原II)的放射免疫测定法进行的研究结果表明,胃蛋白酶原I和胃蛋白酶原II的血清水平以及胃蛋白酶原I与胃蛋白酶原II的比率,可作为胃黏膜结构和功能的非侵入性检测指标、十二指肠溃疡遗传和异质性的指标,以及十二指肠溃疡和胃溃疡风险增加的标志物。