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We read with interest the article by Craig and colleagues (Gut 2003;52:352–7) who reported disappointing results on the value of quantitative hepatobiliary scintigraphy (QHBS) in patients with a suspected sphincter of Oddi dysfunction (SOD). As our paper documenting contrary results was referred to,1 we must add a few words of comment.
Firstly, it should be emphasised that in patients with SOD there is an up to fivefold risk of post-endoscopic retrograde cholangiopancreatography and post-manometry pancreatitis, and therefore there is a strong need for any objective non-invasive method. Hence it is crucial to known whether QHBS can be applied to predict abnormal manometric results. Two European groups recently published concordant results1,2 which clearly showed abnormal results of QHBS and endoscopic sphincter of Oddi manometry (ESOM). These findings and those of Craig et al are so different that there must be some explanation. We believe this may be due to differences in study design and cholecystokinin (CCK) administration in particular.
In fact, the Australian group changed the CCK augmentation method during QHBS, as originally suggested by Sostre and colleagues3: whereas Sostre’s group injected a short three minute bolus of 20 ng/kg/body weight of CCK octapeptide (CCK-OP), completed 12 minutes before initiation of QHBS, Craig et al infused 20 ng/kg/body weight CCK-OP over 45 minutes, starting 15 minutes before QHBS, and continued the infusion during the first 30 minutes of the QHBS study. The authors believe that the modification had no effect on the scan. We disagree, as from a scintigraphic methodological aspect, the first 30 minutes of QHBS after radiotracer administration is critical. In cholecystectomised subjects, most of the radiotracer has been emptied from the biliary tree into the duodenum after 30 minutes.4 Once the tracer is in the duodenum, no further information is available on SO function and resistance. Manometry clearly reveals that CCK-OP has a relaxing effect on the SO.5 In scintigraphic terms, transient SO relaxation means rapid tracer emptying. Moreover, a paradoxical SO response after CCK-OP is a rare phenomenon, occurring in less than 25% of all SOD patients.6
Therefore, in most SOD patients with an elevated SO basal pressure, CCK-OP induces a significant pressure drop, as demonstrated by Hogan and Geenen.7 CCK-OP administration during QHBS must therefore be regarded as a relaxation test of the SO.7
We administered CCK during QHBS, 60 minutes after radiotracer administration, to demonstrate the reversibility of SO obstruction and to visualise baseline SO function before CCK-OP.1,8 We thereby proved significant acceleration of transpapillary bile flow by QHBS after CCK-OP as compared with the baseline study in 37 patients with suspected SOD, as demonstrated in table 1.8
In common with the study of Craig et al, we recently compared our scintigraphic (without CCK-OP) and manometric results.9 Comparison of our results with those of Craig et al reveals that a continuous CCK-OP infusion during QHBS might uniformly accelerate transpapillary bile flow, thus masking basal bile flow differences in SOD patients. As a net result, Craig et al achieved very high specificity at a cost of a low sensitivity as compared with our levels (table 2). Therefore, instead of continued debate in this field with results of small studies in different centres with different study designs, we suggest initiation of a large multicentre study for the non-invasive diagnosis of SOD as compared with manometry.
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