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Kallikrein-Kinin System in Postgastrectomy Dumping Syndrome

PATRICK Y. WONG, M.D.; RICHARD C. TALAMO, M.D.; BERNARD M. BABIOR, M.D., Ph.D.; GUY G. RAYMOND, B.A.; and ROBERT W. COLMAN, M.D., F.A.C.P.
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Grant support: grants HL-13206, HE-14479, AM-09115, and AM-05413 and career development awards HE-4807 (Dr. Colman), AM-19950 (Dr. Babior), and AI-31937 (Dr. Talamo); National Institutes of Health.

Presented in part in April 1973 at the American Federation for Clinical Research Meeting, Atlantic City, New Jersey.

▸Requests for reprints should be addressed to Patrick Y. Wong, M.D., Thorndike Memorial Laboratory, Harvard Medical Service, Boston City Hospital, Boston, MA 02118.


Boston, Massachusetts


Ann Intern Med. 1974;80(5):577-581. doi:10.7326/0003-4819-80-5-577
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The kallikrein-kinin system was studied in 10 postgastrectomy patients, 5 with the dumping syndrome and 5 patients without symptoms. After drinking 220 ml of 45% glucose, none of the asymptomatic patients developed symptoms of the dumping syndrome, elevated levels of bradykinin, or prekallikrein activation; the mean blood pressure fall was not significant. The symptomatic group had headaches, lightheadedness, diarrhea, and a significantly decreased mean blood pressure of 19.4%. A rise in plasma bradykinin levels to above normal occurred in all patients. Two had activation of plasma kallikrein, manifested by a drop in prekallikrein and complete disappearance of kallikrein inhibitor; one of these two also had increased free kallikrein, shown by kinin release from kininogen. The mechanism of kinin release in the other three patients is unknown. Our findings suggest that kinins may mediate some features of the dumping syndrome. In some patients kinin release seemed to result from the formation of plasma kallikrein. In others the exact mechanism of kinin release is unclear.

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