Take dexamethasone exactly as your clinician instructs—commonly 1 mg orally at 23:00 the night before. Have blood drawn for serum cortisol (often about 08:00) the next morning or give a late‑night salivary sample if directed. Continue usual medications only if told; stop systemic steroids and inform your clinician about drugs that affect dexamethasone metabolism (rifampicin, phenytoin, carbamazepine, oral oestrogens).

The overnight dexamethasone suppression test gives a single low dose (usually 1 mg orally at 11 pm) to suppress pituitary ACTH by negative feedback; morning serum cortisol is measured. In people with an intact hypothalamic–pituitary–adrenal axis cortisol is suppressed; failure to suppress indicates autonomous cortisol production (Cushing’s syndrome). Medications and stress can affect results.

The commonly used cutoff for the overnight low‑dose dexamethasone suppression test is an 8:00 AM serum cortisol of 50 nmol/L (1.8 µg/dL). Suppression below this value is considered normal; a cortisol ≥50 nmol/L (≥1.8 µg/dL) indicates inadequate suppression and warrants further evaluation for Cushing’s syndrome. Laboratories may use slightly different thresholds—interpret results with clinical context.

The dexamethasone suppression test (DST) evaluates hypothalamic–pituitary–adrenal (HPA) axis function in suspected depression. The patient takes a low dose of dexamethasone at night and morning cortisol is measured; failure to suppress cortisol (non‑suppression) suggests HPA dysregulation seen in some major depressive subtypes. Its diagnostic value is limited by medications and medical conditions and it’s mainly used in research.

The dexamethasone suppression test assesses how the body’s cortisol production responds to an artificial steroid (dexamethasone). It helps diagnose Cushing’s syndrome, distinguishes between pituitary, ectopic, or adrenal causes of cortisol excess, and guides further testing and treatment planning by measuring whether cortisol is appropriately suppressed after dexamethasone administration. It is a key tool in evaluating abnormal cortisol levels.

Addison’s disease is diagnosed by clinical suspicion (fatigue, weight loss, hyperpigmentation, low blood pressure) plus labs showing hyponatraemia, hyperkalaemia and low morning cortisol with elevated plasma ACTH. Definitive testing uses a short ACTH (cosyntropin) stimulation test; autoimmune antibody testing (e.g., 21‑hydroxylase), renin/aldosterone levels and adrenal imaging (CT) help identify the cause.