Evidence of Altered Copper Metabolism in Patients with Chronic Pancreatitis

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Abstract
1. The copper content of duodenal juice obtained during secretin-pancreozymin tests has been compared in 12 healthy volunteers and 12 patients with chronic pancreatitis in whom normal gall-bladder function was confirmed by oral cholecystography. Of the 12 chronic pancreatitis patients 10 had not received any pancreatic supplement, one was on supplements for 10 years and one for 2 years. 2. In the control subjects the output of copper secretion into the duodenum displayed two phases: a sharp increase in the first 10 min after secretin [intravenous injection of 2 Crick-Harper-Raper units/kg of secretin (Boots)] and a second sharp rise in the first 10 min after pancreozymin [intravenous injection of 2 Crick-Harper-Raper units/kg of pancreozymin (Boots)]. 3. In patients with chronic pancreatitis the pattern of copper secretion was similar to that of control subjects, but in the first 10 min after secretin the output of copper was significantly higher (P < 0.001). The post-secretin output of bilirubin was also higher in chronic pancreatitis (P < 0.02), but the volume of duodenal juice (P < 0.01), the outputs of bicarbonate (P < 0.001) and trypsin (0.05 < P < 0.1) were reduced compared with those of control subjects. The parallel increases in outputs of bilirubin and copper suggested that bile was the source of the increased copper in this group. 4. In the two chronic pancreatitis patients who received pancreatic supplements the post-secretin copper outputs were within normal limits. In a further group of five chronic pancreatitis patients who had been taking pancreatic supplements for many years the post-secretin copper output was not only less than in untreated chronic pancreatitis patients (P < 0.001), but less than in control subjects (P < 0.005). The output of bilirubin was similarly reduced (P < 0.01 and < 0.02 respectively). 5. Since bile is the major route for disposal of absorbed copper and since, under normal steady-state conditions, biliary copper excretion provides an index of copper absorption, our data suggest differences in long-term copper absorption between untreated and treated chronic pancreatitis patients. A component in pancreatic juice may therefore limit copper absorption under normal circumstances. Untreated chronic pancreatitis patients (who lack this factor) would absorb more copper, producing, over many years, an increase in hepatic and whole-body copper content. Long-term feeding of pancreatic supplements, by reducing copper absorption, would gradually deplete whole-body copper content.