Regan P T, Malagelada J R, DiMagno E P
Gut. 1980 Jul;21(7):614-8. doi: 10.1136/gut.21.7.614.
To investigate the relationship between the duodenal outputs of calcium and diseases of the pancreas, we measured calcium secretion into the duodenum (during saline perfusion and after stimulation with an intravenous infusion of cholecystokinin (CCK) or secretin) in healthy controls, patients with chronic alcoholic or idiopathic pancreatitis, and patients with pancreatic cancer. The effects of acute and chronic hypercalcaemia and previous cholecystectomy were also studied. Our results indicate a characteristic increase in duodenal calcium outputs in response to CCK in chronic pancreatitis which is unaffected by the level of serum calcium, aetiology of the pancreatitis, previous cholecystectomy, and the presence or absence of radiological pancreatic calcifications. Although unproven, indirect observations support a pancreatic source for the increased calcium secretion. As we measured the outputs of calcium into the duodenum, previously described increases in calcium concentration are not merely a reflection of reduced volume secretion in chronic pancreatitis. Duodenal calcium outputs were significantly reduced in patients with cancer of the pancreas.
为了研究十二指肠钙输出量与胰腺疾病之间的关系，我们测量了健康对照组、慢性酒精性或特发性胰腺炎患者以及胰腺癌患者十二指肠内的钙分泌情况（在生理盐水灌注期间以及静脉输注胆囊收缩素（CCK）或促胰液素刺激后）。还研究了急性和慢性高钙血症以及既往胆囊切除术的影响。我们的结果表明，慢性胰腺炎患者十二指肠钙输出量对CCK的反应有特征性增加，这不受血清钙水平、胰腺炎病因、既往胆囊切除术以及是否存在胰腺放射学钙化的影响。尽管未经证实，但间接观察结果支持钙分泌增加源于胰腺。由于我们测量的是十二指肠内的钙输出量，因此先前描述的钙浓度增加不仅仅是慢性胰腺炎时分泌量减少的反映。胰腺癌患者的十二指肠钙输出量显著降低。
