February, 2001

by Mary J. Shomon

According to the January 25th issue of the New England Journal of Medicine, malabsorption problems that develop in almost a fourth of all patients with autoimmune polyglandular syndrome type I may be due to a deficiency in cholecystokinin, also known as CKK.

Cholecystokinin (CCK) is a peptide, comprised of a number of amino acids, that is released into the bloodstream from endocrine cells that lining the small intestine. After eating, CCK stimulates pancreatic enzyme secretion and creates a feeling of fullness, by slowing down the process by which the stomach empties. Because cells in the intestines are actually part of the endocrine system, autoimmune endocrine failure may also involve the failure of these cells.

The investigators suggest that this mechanism may account for the malabsorption seen in other patients with this syndrome. "A deficiency of enteroendocrine cells should be considered in any patient in whom the usual tests fail to reveal an explanation for the malabsorption syndrome," they advise. (N Engl J Med 2001;344:270-274.)

Note from Mary Shomon: A question that this news also raises is whether autoimmune thyroid disease patients suffer from similar problems in CKK deficiency. Stimulation of CKK is the main purpose of a new dietary aid that some thyroid patients have been trying, called Satietrol. For more information on Satietrol, see: http://thyroid.about.com/library/weekly/aa020201a.htm