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PET Imaging of Adrenal Cortical Tumors with the 11 ß-Hydroxylase Tracer ¹¹C-Metomidate

Subfemtomole Biorecognition Project, Uppsala University PET Centre, Uppsala
Departments of Surgery and Diagnostic Radiology, University Hospital, Uppsala, Sweden

Correspondence: For correspondence or reprints contact: Mats Bergström, PhD, Uppsala University PET Centre, University Hospital, S-751 85 Uppsala, Sweden.

ABSTRACT

The purpose of the study was to evaluate PET with the tracer ¹¹C-metomidate as a method to identify adrenal cortical lesions. Methods: PET with ¹¹C-metomidate was performed in 15 patients with unilateral adrenal mass confirmed by CT. All patients subsequently underwent surgery, except 2 who underwent biopsy only. The lesions were histopathologically examined and diagnosed as adrenal cortical adenoma (n = 6; 3 nonfunctioning), adrenocortical carcinoma (n = 2), and nodular hyperplasia (n = 1). The remaining were noncortical lesions, including 1 pheochromocytoma, 1 myelolipoma, 2 adrenal cysts, and 2 metastases. Results: All cortical lesions were easily identified because of exceedingly high uptake of ¹¹C-metomidate, whereas the noncortical lesions showed very low uptake. High uptake was also seen in normal adrenal glands and in the stomach. The uptake was intermediate in the liver and low in other abdominal organs. Images obtained immediately after tracer injection displayed high uptake in the renal cortex and spleen. The tracer uptake in the cortical lesions increased throughout the examination. For quantitative evaluation of tracer binding in individual lesions, a model with the splenic radioactivity concentration assigned to represent nonspecific uptake was applied. Values derived with this method, however, did show the same specificity as the simpler standardized uptake value concept, with similar difference observed for cortical versus noncortical lesions. Conclusion: PET with ¹¹C-metomidate has the potential to be an attractive method for the characterization of adrenal masses with the ability to discriminate lesions of adrenal cortical origin from noncortical lesions.

Key Words: PET • adrenal cortex • adrenal tumors • steroid synthesis • etomidate • 11ß-hydroxylase

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