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R. F. HARVEY, MD, MRCP
Bristol, England

AMA Arch Surg. 1974;108(3):381.

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To the Editor.—I have been following with interest the correspondence in the ARCHIVES between Dr. Silen (106:239, 1973) and Dr. Basso et al (106:364, 1973), following their paper on the mechanism of gastric hypersecretion in pancreatic exocrine deficiency (105:611-614, 1972). Recent studies in our laboratory suggest another possible explanation for their findings. Using a radioimmunoassay for cholecystokinin-pancreozymin (CCK-PZ),¹ we have shown that pancreatic exocrine deficiency in man is associated with very high fasting levels of CCK-PZ in the serum,² perhaps as a result of failure of the normal feedback inhibition of CCK-PZ secretion by a factor in pancreatic juice. Cholecystokinin-pancreozymin is structurally identical with gastrin in the C-terminal pentapeptide amide sequence, and therefore shows cross-reaction in gastrin immunoassay systems that employ antibodies directed toward this portion of the gastrin molecule. Basso and colleagues give no details of the antibody used in their gastrin assay, but if it . . . [Full Text PDF of this Article]

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