H O Nielsen, K Lauritsen, M G Hansen, L A Christiansen
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引用次数: 0
摘要
15例患者在前切除术后3至35年进行了研究,其中8例为胃十二指肠(Billroth I (BI))吻合,7例为胃空肠(Billroth II (BII))吻合。研究包括胃酸分泌、饲粮对血清胃泌素的反应以及残胃粘膜活检中胃泌素产生细胞的免疫组织化学搜索。所有患者均出现低氯酸血症。胃泌素对喂食的反应最小。除了BI手术患者餐后3小时血清胃泌素值明显高于BII手术患者外,两组患者的胃泌素产生没有更大的差异。残胃中未发现产生胃泌素的细胞,甚至在假幽门化生的区域也未发现。结论:胃前切除术后胃泌素的产生是由胃外g细胞引起的;这些细胞很难受到食物的刺激,对低氯酸血症和高胃酸血症没有反应。
Gastrin production following antrectomy. A study on the occurrence of gastrin-producing cells and the serum gastrin response to feeding.
Fifteen patients were studied 3 to 35 years after antrectomy, with a gastroduodenal (Billroth I (BI)) anastomosis in 8, and a gastrojejunal (Billroth II (BII)) anastomosis in 7. The investigations included gastric acid secretion, serum gastrin response to feeding and immunohistochemical search for gastrin-producing cells in gastric remnant mucosal biopsies. All of the patients had hypochlorhydria. The gastrin response to feeding was minimal. Apart from a significantly higher value of serum gastrin 3 hours post-prandial in BI operated as compared to BII operated patients, no greater differences were found in the gastrin production between the two groups of patients. No gastrin-producing cells could be identified in the gastric remnant, not even in areas of pseudopyloric metaplasia. It is concluded that the gastrin production following antrectomy is caused by extragastric G-cells; these cells are poorly stimulated by food, and do not respond to hypochlorhydria with hypergastrinaemia.