Walsh J H, Nair P K, Kleibeuker J, Passaro E P, Deventer G V, Strom E, Rotter J I, Kauffman G L, Samloff I M, Lewin K J
Scand J Gastroenterol Suppl. 1983;82:45-58.
There are few detailed studies of patients with pathological hypergastrinaemia of antral origin. We have identified four patients with severe acid hypersecretion associated with peptic ulcer disease and in whom no evidence for gastrinoma or isolated retained antrum could be found. Three of these patients also had hypergastrinaemia. In two patients, one with gastric ulcers and one with duodenal ulcer disease, the hypergastrinaemia appeared to be due to antral gastrin cell hyperfunction and there was also evidence for mild antral gastrin cell hyperplasia. In the other hypergastrinaemic patient, a primary intestinal gastrin cell hyperfunction syndrome was suspected, but a hidden gastrinoma could not be excluded. The remaining patient had nearly fatal hypersecretory ulcer disease and cimetidine failed to control the hypersecretory state. In this patient the hypersecretion responded to a more potent H2 antagonist with resolution of a metabolic encephalopathy. No general pathophysiological mechanism could be identified in these patients or in larger groups of patients with gastric or duodenal ulcer disease.
关于起源于胃窦的病理性高胃泌素血症患者的详细研究较少。我们发现了4例与消化性溃疡病相关的严重胃酸分泌过多患者,且未发现胃泌素瘤或孤立性胃窦残留的证据。其中3例患者也有高胃泌素血症。在2例患者中,1例患有胃溃疡,1例患有十二指肠溃疡病,高胃泌素血症似乎是由于胃窦胃泌素细胞功能亢进所致,并且也有轻度胃窦胃泌素细胞增生的证据。在另1例高胃泌素血症患者中,怀疑为原发性肠道胃泌素细胞功能亢进综合征,但不能排除隐匿性胃泌素瘤。其余1例患者患有几乎致命的分泌过多性溃疡病,西咪替丁未能控制分泌过多状态。在该患者中,分泌过多对一种更强效的H2拮抗剂有反应,同时代谢性脑病得到缓解。在这些患者或更多的胃溃疡或十二指肠溃疡病患者群体中,未发现普遍的病理生理机制。