Fiddian-Green R G
Lancet. 1977 Jan 8;1(8002):74-7. doi: 10.1016/s0140-6736(77)91084-4.
The pathogenesis of peptic ulceration cannot be explained by an abnormal capacity to secrete acid, for ulcers develop in patients who secrete acid normally. Duodenal and gastric ulcers have a common cause. The location of an ulcer in each individual is primarily determined by his capacity to secrete acid at that time. There is a difference between the mechanisms which heal an ulcer and cure a patient of his disease. Procedures that reduce an individual's capacity to secrete acid, heal an ulcer by moving the focus of the ulcerogenic forces to a more proximal site. It is necessary to remove an antral factor if in addition the patient is to be cured of his disease. It is postulated that this antral factor is the gastrin (G17) which is released in abnormal amounts into gastric juice in patients with ulcers and with gastrinomas. The abnormal amount of G17 in gastric juice may be responsible for releasing abnormal amounts of G34 into the circulation from the duodenum and from gastrinomas. The abnormal release of gastrin develops as a result of an impaired response to duodenal acidification manifest in part by an impaired release of secretin. It is postulated that the abnormal stimulation of antral gastrin release may on occasions give rise to antral G-cell hyperplasia, and that the abnormal secretion of gastrin into gastric juice may on occasions give rise to gastrinomas. These abnormalities may cause ulcers by producing an uncontrolled secretion of acid and an abnormal exposure to bile.
消化性溃疡的发病机制不能用分泌酸的能力异常来解释，因为溃疡也会在酸分泌正常的患者中发生。十二指肠溃疡和胃溃疡有共同的病因。每个个体中溃疡的位置主要取决于其当时分泌酸的能力。溃疡愈合机制和治愈患者疾病的机制有所不同。降低个体分泌酸能力的程序，通过将致溃疡因素的作用部位转移到更近端的位置来愈合溃疡。如果要治愈患者的疾病，还必须去除胃窦因素。据推测，这种胃窦因素就是胃泌素（G17），在溃疡患者和胃泌素瘤患者中，它会以异常量释放到胃液中。胃液中异常量的G17可能导致十二指肠和胃泌素瘤将异常量的G34释放到循环中。胃泌素的异常释放是由于对十二指肠酸化反应受损所致，部分表现为促胰液素释放受损。据推测，胃窦胃泌素释放的异常刺激有时可能导致胃窦G细胞增生，而胃泌素向胃液中的异常分泌有时可能导致胃泌素瘤。这些异常可能通过产生不受控制的酸分泌和异常暴露于胆汁而导致溃疡。
