Abstract
The aim of the present study was to develop a new pharmacologic method during hepatobiliary scintigraphy by which patients with functional and organic forms of gallbladder (GB) dysfunction can be differentiated. Quantitative hepatobiliary scintigraphy (QHBS) was performed on 31 patients with impaired GB motility selected by cerulein-augmented ultrasonography. Nineteen patients had acalculous biliary pain (ABP) and suspected GB dyskinesia, 6 patients had celiac disease, and 6 patients had type II diabetes mellitus. Sixty minutes after the isotope administration, 1 ng/bwkg/min cerulein (CCK10) was infused for 10 minutes, and then from the 90th minute, an equivalent dose of CCK10 was infused in the presence of 0.5 mg sublingual glyceryl trinitrate (GTN) in 12 or placebo in 7 consecutive patients. The GB ejection fraction (GBEF) was calculated repeatedly in time periods from 60 to 90 and from 90 to 120 minutes. In the majority of patients with ABP and suspected GB dyskinesia, CCK10 and GTN coadministration normalized the previously impaired GB-emptying. When the cumulative results of all 12 patients were calculated, we demonstrated significant differences (P=0.003) in the GBEF between the first (CCK10) versus the second (CCK10 plus GTN) stimuli: 19+/-11% versus 40+/-17%, respectively. In contrast, in 12 patients with celiac sprue and diabetes mellitus, no differences in the GBEF were detected when the first (CCK10 alone) versus the second (CCK10 plus GTN) stimuli was compared: 21+/-10% versus 22+/-13%, respectively. Finally, placebo and CCK10 coadministration in 7 consecutive patients with ABP and suspected GB dyskinesia did not influence the GBEF as compared with CCK10 alone: 13+/-9% versus 15+/-10%, respectively. GTN and CCK10 coadministration induces a significant improvement of the GBEF in patients with GB dyskinesia. The application of this new pharmacologic test during QHBS permitted the noninvasive separation of those patients with secondary impaired GB-emptying as a result of GB dyskinesia from those with primary forms of GB hypokinesia.
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