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To describe the differences in presentation, biochemistry, and radiologicalevaluation of various etiologies of adrenal Cushing’s syndrome (CS) froma single center. To emphasize caution for interpretation of plasmaadrenocorticotropic hormone (ACTH), as a spuriously unsuppressed ACTH level byimmunometric assay may lead to therapeutic misadventures in adrenal CS.Design: Retrospective, single-center, observational study. Methods:  Fifty-eightadrenal CS patients [Adrenocortical carcinoma (ACC), n=30; Adenoma(ACA), n=15; Primary pigmented nodular adrenocortical disease (PPNAD),n=10; ACTH independent macronodular adrenal hyperplasia (AIMAH),n=3) evaluated at a tertiary care center in western India betweenJanuary 2006 to March 2020 were included. Data on demography, clinicalevaluation, biochemistry, imaging, management, histopathology, and outcome wererecorded in a standard format and analyzed. Results:  Cortisol secreting ACCpresented at 38(1–50) years with abdominal mass in 26/30(86.7%) and 16/30 (53.3%) had metastases atpresentation. ACA with autonomous cortisol excess presented at25(4.9–40) years with discriminating features of CS in 14/15(93.3%), sex steroid production in 2/15, unenhanced HU40% in8/11 (72.7%). One ACA and eight ACC patients had plasma ACTH (bySiemens Immulite assay) &gt; 20 pg/ml, despitehypercortisolemic state. Conclusions:  Cortisol-secreting ACC and ACA most oftenpresent with mass effects and florid CS, respectively. Baseline HU has lowsensitivity to differentiate cortisol-secreting ACA from ACC. Plasma ACTHmeasured by Seimens Immulite is often unsuppressed, especially in ACC patients,which can be addressed by measuring ACTH by more accurate assays.

Clinical Spectrum of Adrenal Cushing’s Syndrome and the Caution for Interpretation of Adrenocorticotrophic Hormone: A Single-Center Experience