To describe the differences in presentation, biochemistry, and radiological evaluation of various etiologies of adrenal Cushing’s syndrome (CS) from a single center. To emphasize caution for interpretation of plasma adrenocorticotropic hormone (ACTH), as a spuriously unsuppressed ACTH level by immunometric assay may lead to therapeutic misadventures in adrenal CS. Design: Retrospective, single-center, observational study. Methods: Fifty-eight adrenal 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 between January 2006 to March 2020 were included. Data on demography, clinical evaluation, biochemistry, imaging, management, histopathology, and outcome were recorded in a standard format and analyzed. Results: Cortisol secreting ACC presented at 38(1–50) years with abdominal mass in 26/30 (86.7 %) and 16/30 (53.3 %) had metastases at presentation. ACA with autonomous cortisol excess presented at 25(4.9–40) years with discriminating features of CS in 14/15 (93.3 %), sex steroid production in 2/15, unenhanced HU <10 in only one, and relative washout >40% in 8/11 (72.7 %). One ACA and eight ACC patients had plasma ACTH (by Siemens Immulite assay) > 20 pg/ml, despite hypercortisolemic state. Conclusions: Cortisol-secreting ACC and ACA most often present with mass effects and florid CS, respectively. Baseline HU has low sensitivity to differentiate cortisol-secreting ACA from ACC. Plasma ACTH measured by Seimens Immulite is often unsuppressed, especially in ACC patients, which can be addressed by measuring ACTH by more accurate assays.