Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sphincter of Oddi (SO) dysfunction presents with vague abdominal pain and/or abnormal liver function tests, and is presumably due to SO stenosis or spasm. Clinical, laboratory, and imaging methods of diagnosis have been less than ideal. Initially, we determined normal quantitative hepatobiliary scintigraphy (QHBS) parameters both pre- and post-sincalide administration. Thirty-one "normals" were analyzed, and post-sincalide common bile duct (CBD) dynamics could be satisfactorily determined in 29 (94%) subjects. Normal values at sincalide-augmented QHBS are reported. Next, 10 patients suspected of having SO dysfunction were studied prospectively using SO manometry and QHBS. The two tests were in agreement in seven cases (4: normal CBD dynamics, 3: abnormal). In one case of advanced SO stenosis, QHBS was abnormal, but SO manometry could not be performed. In the two remaining cases, SO manometry and QHBS gave discordant results. Of greatest importance, no significant correlation existed between the quantitative parameters of these two tests. Sincalide-augmented QHBS is possible and may, in the future, be of value in the diagnosis of SO dysfunction and/or partial CBD obstruction.
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PMID:Sincalide-augmented quantitative hepatobiliary scintigraphy (QHBS): definition of normal parameters and preliminary relationship between QHBS and sphincter of Oddi (SO) manometry in patients suspected of having SO dysfunction. 239 13

Radionuclide hepatobiliary imaging was performed on a patient with a longstanding history of scleroderma who presented with abdominal pain suggestive of biliary disease. Cystic duct patency was documented after 10 min with tracer accumulation in the second portion of the duodenum which failed to progress consistent with the duodenal hypomotility of scleroderma. The patient was given intravenous Kinevac resulting in gastroesophageal reflux of radionuclide.
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PMID:Gastroesophageal reflux demonstrated by hepatobiliary imaging in scleroderma. 381 54

Sincalide, the C-terminal octapeptide fragment of the cholecystokinin, was used to contract the gallbladder during routine oral cholecystography in 18 patients. In 14 patients clinically important contraction occurred. The average reduction in gallbladder size for these patients was 32.7% of the preinjection size (range 15.1%-67.9%). Within 8-12 minutes cystic duct visualisation occurred in 8 and common bile duct visualisation in 3 patients. Spasm of the gallbladder neck was found in 2 cases. The blood pressure and heart rate did not change significantly during the study. Six patients felt slight nausea for 1-4 minutes and two vomited. We conclude that sincalide may be useful in biliary tract function studies in special clinical conditions (i.e. upper abdominal pain with unknown aetiology).
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PMID:The effect of intravenously administered sincalide on the human gallbladder during oral cholecystography. 630 54

The authors investigated whether parenteral nutrition-associated cholestasis (PNAC) in surgical neonates could be alleviated by the administration of cholecystokinin-octapeptide (CCK). Two groups of infants were studied, after major abdominal or cardiac surgery in the newborn period. The low-dose group consisted of three infants with PNAC who received cholecystokinin-octapeptide (Sincalide) at a dose of 0.02 micrograms/kg intravenously (IV), twice daily. The high-dose group comprised eight infants with PNAC who received an initial dose of 0.02 micrograms/kg IV or intramuscularly, three times daily on the first day, followed by a daily doubling of the dose up to as high as 0.32 micrograms/kg. In the low-dose group, direct bilirubin levels declined a mean of 50.2 +/- 14.5%. In the high-dose group, direct bilirubin levels declined a mean of 23.4 +/- 14.3%. In three patients in the high-dose group, no decline occurred. All three had clinical signs of overt liver failure and died of liver failure within 2 months after treatment with CCK. By excluding these patients from the high-dose group, the decline in bilirubin levels increased to 49.6 +/- 10.9%. Side effects from CCK occurred in two patients and consisted of abdominal pain and feeding intolerance. Treatment with CCK appears to be associated with a decline in direct bilirubin levels, provided overt liver failure has not developed.
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PMID:Treatment of parenteral nutrition-associated cholestasis with cholecystokinin-octapeptide. 747 37