Positron emission tomography imaging of adrenal masses: (18)F-fluorodeoxyglucose and the 11beta-hydroxylase tracer (11)C-metomidate.
OBJECTIVE
(11)C-metomidate (MTO), a marker of 11beta-hydroxylase, has been suggested as a novel positron emission tomography (PET) tracer for adrenocortical imaging. Up to now, experience with this very new tracer is limited. The aims of this study were (1) to evaluate this novel tracer, (2) to point out possible advantages in comparison with( 18)F-fluorodeoxyglucose (FDG) and (3) to investigate in vivo the expression of 11beta-hydroxylase in patients with primary aldosteronism.


METHODS
Sixteen patients with adrenal masses were investigated using both MTO and FDG PET imaging. All patients except one were operated on. Five patients had non-functioning adrenal masses, while 11 had functioning tumours(Cushing's syndrome, n=4; Conn's syndrome, n=5; phaeochromocytoma, n=2). Thirteen patients had benign disease, whereas in three cases the adrenal mass was malignant (adrenocortical cancer, n=1; malignant phaeochromocytoma, n=1; adrenal metastasis of renal cancer, n=1).


RESULTS
MTO imaging clearly distinguished cortical from non-cortical adrenal masses (median standardised uptake values of 18.6 and 1.9, respectively, p<0.01). MTO uptake was slightly lower in patients with Cushing's syndrome than in those with Conn's syndrome, but the difference did not reach statistical significance. The expression of 11beta-hydroxylase was not suppressed in the contralateral gland of patients with Conn's syndrome, whereas in Cushing's syndrome this was clearly the case. The single patient with adrenocortical carcinoma had MTO uptake in the lower range.


CONCLUSIONS
MTO could not definitely distinguish between benign and malignant disease. FDG PET, however, identified clearly all three study patients with malignant adrenal lesions. We conclude: (1) MTO is an excellent imaging tool to distinguish adrenocortical and non-cortical lesions; (2) the in vivo expression of 11beta-hydroxylase is lower in Cushing's syndrome than in Conn's syndrome, and there is no suppression of the contralateral gland in primary aldosteronism; (3) for the purpose of discriminating between benign and malignant lesions, FDG is the tracer of choice.
Zettinig
Georg
G
Department of Nuclear Medicine, University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria, georg.zettinig@meduniwien.ac.at
Mitterhauser
Markus
M
Wadsak
Wolfgang
W
Becherer
Alexander
A
Pirich
Christian
C
Vierhapper
Heinrich
H
Niederle
Bruno
B
Dudczak
Robert
R
Kletter
Kurt
K
D000236:Adenoma / Q000000981:diagnostic imaging / Q000378:metabolism; D000310:Adrenal Gland Neoplasms / Q000000981:diagnostic imaging* / Q000378:metabolism*; D000328:Adult; D000368:Aged; D002250:Carbon Radioisotopes; D005045:Etomidate / Q000031:analogs & derivatives* / Q000493:pharmacokinetics*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D013252:Steroid 11-beta-Hydroxylase / Q000378:metabolism*; D014018:Tissue Distribution
D002250:Carbon Radioisotopes; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D013252:Steroid 11-beta-Hydroxylase; C084586:metomidate; D005045:Etomidate