TY - JOUR
T1 - Impaired transit of chyme in chronic intestinal pseudoobstruction. Correction by cisapride
AU - Camilleri, Michael
AU - Brown, Manuel L.
AU - Malagelada, Juan R.
N1 - Funding Information:
Received October 7, 1985. Accepted March 3, 1986. Address requests for reprints to: Juan-R. Malagelada, M.D., Gastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota 55905. This work was supported in part by grants AM 26428, AM 34988, and RR 00585 from the National Institutes of Health, and by Janssen Pharmaceutics Inc., New Jersey. This work was presented in part at the annual meeting of the American Gastroenterological Association, New York, New York, May 1985, and has appeared in abstract form (Gastroenterology 1985;88:1340). The authors acknowledge the advice of Dr. A. R. Zinsmeister, Section of Medical Research Statistics, Mayo Foundation, and the technical support of G. M. Thomforde and A. Omdahl. They thank the nursing staff of the Clinical Research Center, St. Marys Hospital; V. Woyczik for typing and preparing the manuscript; and P. Haase, Pharm.D., for assistance in the execution of the double-blind drug protocol. 0 1986 by the American Gastroenterological Association 0016-5085/86/$3,50
PY - 1986/9
Y1 - 1986/9
N2 - Chronic intestinal pseudoobstruction is a clinical syndrome whose pathophysiology, objective diagnosis, and treatment are poorly understood. We investigated 8 patients with this syndrome in whom intestinal dysmotility was established manometrically by two or more of the following criteria: abnormal configuration or propagation of interdigestive motor complexes, sustained incoordinate pressure activity, nonpropagated bursts of phasic pressure activity, and failure of a solid-liquid meal to induce a fed pattern. To establish the functional impairment and region of the gut primarily affected by the disease, we quantified radioscintigraphically the gastrointestinal transit of the solid (131I-fiber) and liquid (99mTc-DTPA) components of a meal. Our techniques allowed us to quantify separately gastric emptying and pylorus-to-cecum transit. Furthermore, we evaluated the effects of a new prokinetic agent, cisapride. Gastric emptying times in pseudoobstruction were not significantly delayed; however, transit times through the small bowel (t 1 2) were markedly prolonged [solids, 235 ± 43 min (mean ± SEM) vs. 138 ± 25 controls, p < 0.05; liquids, 310 ± 67 vs. 181 ± 28 controls, p = 0.07]. Cisapride was effective in reducing the delayed intestinal transit time to within the normal range (Δ solids = -115 ± 25 min; Δ liquids = -146 ± 71 min; p < 0.05 for both). These studies suggest that intestinal dysmotility in this group of patients with pseudoobstruction was associated with delayed small bowel transit of radiolabeled solid and liquid components of chyme. Cisapride can restore to normal the delayed transit, indicating that it may potentially correct the impaired propulsive activity in the small bowel of these patients.
AB - Chronic intestinal pseudoobstruction is a clinical syndrome whose pathophysiology, objective diagnosis, and treatment are poorly understood. We investigated 8 patients with this syndrome in whom intestinal dysmotility was established manometrically by two or more of the following criteria: abnormal configuration or propagation of interdigestive motor complexes, sustained incoordinate pressure activity, nonpropagated bursts of phasic pressure activity, and failure of a solid-liquid meal to induce a fed pattern. To establish the functional impairment and region of the gut primarily affected by the disease, we quantified radioscintigraphically the gastrointestinal transit of the solid (131I-fiber) and liquid (99mTc-DTPA) components of a meal. Our techniques allowed us to quantify separately gastric emptying and pylorus-to-cecum transit. Furthermore, we evaluated the effects of a new prokinetic agent, cisapride. Gastric emptying times in pseudoobstruction were not significantly delayed; however, transit times through the small bowel (t 1 2) were markedly prolonged [solids, 235 ± 43 min (mean ± SEM) vs. 138 ± 25 controls, p < 0.05; liquids, 310 ± 67 vs. 181 ± 28 controls, p = 0.07]. Cisapride was effective in reducing the delayed intestinal transit time to within the normal range (Δ solids = -115 ± 25 min; Δ liquids = -146 ± 71 min; p < 0.05 for both). These studies suggest that intestinal dysmotility in this group of patients with pseudoobstruction was associated with delayed small bowel transit of radiolabeled solid and liquid components of chyme. Cisapride can restore to normal the delayed transit, indicating that it may potentially correct the impaired propulsive activity in the small bowel of these patients.
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U2 - 10.1016/0016-5085(86)90631-1
DO - 10.1016/0016-5085(86)90631-1
M3 - Article
C2 - 3525315
AN - SCOPUS:0022505102
SN - 0016-5085
VL - 91
SP - 619
EP - 626
JO - Gastroenterology
JF - Gastroenterology
IS - 3
ER -