The early postprandial dumping syndrome: clinical manifestations and pathogenesis

Abstract

Our present concept of the pathogenesis of the early postprandial dumping syndrome is well summarized by Jesseph. Resection, division or bypass of the sphincter mechanism at the gastric outlet permits rapid passage of hyperosmolar material into the upper small intestine. This provides direct stimulation of the enterochromaffin (argentaffin) cells in the mucosa, which are highly concentrated here. The hyperosmolarity pulls fluid into the intestine resulting in a fall in plasma volume and distention of the intestine, further stimulating secretion by the argentaffin tissue. The plasma volume per se probably has little, if anything, to do with the symptoms produced although the outpouring of intravascular fluid into the intestinal lumen probably contributes to intestinal hyperperistalsis and the resultant symptoms of intestinal hurry. Although other sources are possible, studies to date would indicate that the argentaffin cells are the major source of humoral agents. In addition to serotonin, at least one vasoactive polypeptide, bradykinin, has been identified. It is likely that others are present and pharmacologic therapy will probably not be successful until these are more completely identified and characterized. The known biologic effects of serotonin and the kinins can certainly account for all the vasomotor and gastrointestinal symptoms characterizing the early postprandial dumping syndrome.