THE LOW-DOSE DEXAMETHASONE SUPPRESSION TEST IN PATIENTS WITH ADRENAL INCIDENTALOMAS - COMPARISONS WITH CLINICALLY EUADRENAL SUBJECTS AND PATIENTS WITH CUSHINGS-SYNDROME
S. Tsagarakis et al., THE LOW-DOSE DEXAMETHASONE SUPPRESSION TEST IN PATIENTS WITH ADRENAL INCIDENTALOMAS - COMPARISONS WITH CLINICALLY EUADRENAL SUBJECTS AND PATIENTS WITH CUSHINGS-SYNDROME, Clinical endocrinology, 48(5), 1998, pp. 627-633
OBJECTIVE Increasing evidence favours subtle glucocorticoid excess in
many patients with adrenal incidentalomas. However, existing evidence
is based mainly on the overnight dexamethasone suppression test, a tes
t that is commonly abnormal even among clinically euadrenal subjects.
The aim of the present study was to evaluate patients with adrenal inc
identalomas for subtle glucocorticoid excess by the more specific low-
dose dexamethasone test (LDDST). moreover, since the criteria of what
constitutes an abnormal cortisol response following this test have bee
n largely anecdotal, we report our results in comparison with those ob
tained in clinically euadrenal subjects, and patients with Gushing's s
yndrome. DESIGN A prospective study of 57 patients with adrenal incide
ntalomas with CT characteristics highly suggestive of benign adrenocor
tical adenomas and 85 clinically euadrenal subjects consisting of 54 o
bese women with BMI>30 kg/m(2) (range 30-54.7), 13 women with BMI<30 k
g/m(2) (range 20.3-29.6) and 18 healthy volunteers (10 women and eight
men) over 40 years of age (mean age 51.7 +/- 9.9, range 40-74; mean B
MI 30 +/- 6.6, range 20.3-47.5 kg/m(2)). A retrospective analysis was
performed on 60 patients with a confirmed diagnosis of Gushing's syndr
ome. MEASUREMENTS All subjects were admitted to the endocrine ward and
underwent a standard LDDST, as follows: after a 48-h stabilization pe
riod, a 24-h urine collection for basal urinary free cortisol was perf
ormed. Basal serum cortisol and plasma ACTH were measured at 0800 h th
e following day, and subjects were started on dexamethasone 0.5 mg 6-h
ourly for 2 days. Post-dexamethasone cortisol and ACTH levels were mea
sured at 0800h, 6h after the last dose of dexamethasone. RESULTS Follo
wing dexamethasone suppression serum cortisol concentrations became un
detectable (<28 nmol/l) in all clinically euadrenal subjects. In patie
nts with incidentally discovered adrenal masses, post-LDDST cortisol c
oncentrations were undetectable in 12 (21%), between 28-140nmol/l in 3
8 (67%), and 140-216 nmol/l in seven (12%) patients; post-LDDST cortis
ol values correlated positively with the size of the adenoma (r=+0.482
, P<0.001). Post-LDDST cortisol concentrations in patients with Gushin
g's syndrome ranged from 85 to 1786 nmol/l; in 3/42 (7%) patients with
ACTH-dependent Gushing's syndrome cortisol concentrations were <140 n
mol/l. CONCLUSIONS On the basis of our data in a large group of clinic
ally euadrenal subjects, we suggest that following LDDST cortisol conc
entrations should become undetectable with the currently used radioimm
unoassays. In patients with adrenal incidentalomas, application of the
LDDST confirmed the presence of incomplete suppression of cortisol in
the majority of patients. We suggest that the LDDST is a sensitive in
dex of autonomous cortisol production in patients with adrenal inciden
talomas; following this test a grading of subtle glucocorticoid excess
may be obtained but future studies correlating biochemical, clinical
and epidemiological data are required, in order to develop widely agre
ed cut-off levels of clinically significant glucocorticoid excess in t
hese patients.