Can Physiologic FDG Uptake by the Bowel Be Reduced?

Hossein Jadvar, MD, PhD, MPH, MBA


June 12, 2009


Normal bowel accumulates variable amounts of 2-[fluorine 18]fluoro-2-deoxy-D-glucose (FDG). The exact etiology for the physiologic FDG uptake in the bowel remains unknown, but may be related to a variety of factors including the smooth muscle, mucosa, normal bacterial flora, bowel lumen material, and other factors. Reduction of FDG accumulation in the bowel is desirable because variable high uptake can either confound lesion detection in the abdomen and pelvis or be a source of false-positive results during positron-emission tomographic (PET) scintigraphy.[1] In this regard, the anatomic information that is provided by co-registered computed tomography (CT) with the new hybrid PET-CT imaging systems can be helpful, but it remains inadequate. Recently, investigators from the Mayo Clinic determined whether the normal FDG accumulation in the bowel can be reduced with oral 5 mg diphenoxylate hydrochloride/0.05 mg atropine sulfate (Lomotil® [Pfizer]), which is known to decrease smooth muscle peristalsis.

Pretreatment with Diphenoxylate Hydrochloride/Atropine Sulfate (Lomotil) Does Not Decrease Physiologic Bowel FDG Activity on PET/CT Scans of the Abdomen and Pelvis

Murphy R, Doerger KM, Nathan MA, Lowe VJ
Mol Imaging Biol. 2009;11:114-117


A prospective, randomized, double-blinded study was performed in 69 patients undergoing FDG PET-CT scans for imaging evaluation of lymphoma.[1] Nearly half of the patients were randomized to a control (placebo) group and received 10 mL of water. The intervention group received a 10-mL oral dose of diphenoxylate hydrochloride/atropine sulfate. Both groups received an intravenous administration of 20 mCi of FDG 30-60 minutes later. PET-CT scans were reviewed independently by 2 experienced readers blinded to the grouping of patients. The uptake in the bowel on each scan was scored according to the following scheme: 0 (no uptake), 1 (uptake less than that in liver), 2 (uptake equivalent to that in liver), 3 (uptake greater than that in liver). The scores of the 2 groups were compared using an extension of the Fisher's Exact test for ordered contingency tables. The results of the study showed that (1) pretreatment with diphenoxylate hydrochloride/atropine sulfate did not reduce bowel FDG activity, and (2) there was greater lower gastrointestinal tract FDG uptake in the diphenoxylate hydrochloride/atropine sulfate group compared to the placebo group. The authors concluded that pretreatment with diphenoxylate hydrochloride/atropine sulfate prior to FDG PET-CT scanning does not reduce bowel FDG uptake.


The findings of this study corroborates the negative findings of an earlier study that evaluated whether intravenous pharmacologic manipulation of the bowel smooth muscle peristalsis with either sincalide (increases peristalsis) or atropine (decreases peristalsis) can affect the level of FDG uptake in the bowel.[1] These results are in contrast to the findings of another study with 20-mg intravenous N-butylscopolamine, which demonstrated that there was a statistically significant reduction in bowel FDG uptake.[2] These disparate results may be due to differing modes of action on the bowel peristalsis by diphenoxylate hydrochloride/atropine sulfate (based on stimulation of opiate receptors) and N-butylscopolamine (based on anticholinergic effect). The differing routes of drug administration may have also been contributory.

The authors did not control for the potential confounding effects of differing blood glucose level and background hepatic activity (which was used as the reference for scoring scheme) across scans. It is noted also that the intraclass correlations for inter-reader reliability between the 2 readers was only fair. Use of semiquantitative measures such standardized uptake value could have helped in increasing intrareader and inter-reader agreement. In addition, the potential reasons for the curious finding of statistically significant higher FDG uptake in the lower gastrointestinal bowel after diphenoxylate hydrochloride/atropine sulfate was not discussed. Nevertheless, further research is needed to determine the exact source(s) of physiologic FDG accumulation to design appropriate methods for reducing the FDG uptake in normal bowel.