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Health condition · Clinically reviewed

Cushing’s syndrome, cortisol excess — diagnosis and modern treatment.

Excess cortisol from pituitary (Cushing’s disease), adrenal, ectopic or exogenous steroid source. Endocrinology-led diagnosis and cause-directed surgery / medication.

A radiographer guides a patient onto the bed of an advanced 3 Tesla MRI scanner in a London imaging suite

Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Every claim is checked against Society for Endocrinology, NICE and Endocrine Society sources you can see at the end.

  • 03

    Current for 2026

    Reflects UK guidance on cortisol screening, ACTH differentiation and modern medical therapy including osilodrostat.

Key facts

Cushing’s syndrome at a glance.

The essentials, in plain English — what it is, how it is screened, how the cause is worked out, and how it is safely treated in the UK today.

  • What it is

    Chronic glucocorticoid excess — sustained high cortisol from an endogenous or exogenous source, driving metabolic, cardiovascular and psychiatric harm.

  • ACTH-dependent

    Pituitary adenoma (Cushing’s disease) or ectopic ACTH secretion — cortisol excess driven by high circulating ACTH.

  • ACTH-independent

    Adrenal adenoma, carcinoma or bilateral hyperplasia — the adrenal itself over-produces cortisol with suppressed ACTH.

  • Most common cause

    Long-term exogenous glucocorticoids (oral, inhaled or topical steroids) are by far the commonest cause overall.

  • Diagnosis

    Screening with 24-hr urinary free cortisol, midnight salivary cortisol or the low-dose dexamethasone suppression test.

  • Prognosis

    Cardiovascular and metabolic complications drive outcome — early cause-directed treatment restores near-normal life expectancy.

Why this guide matters

A subtle diagnosis with far-reaching effects.

Cushing’s develops quietly, mimics common problems and drives serious cardiovascular and metabolic harm — early recognition changes the trajectory.

  • Screening tests come first

    Urinary, salivary and dexamethasone tests confirm cortisol excess before imaging.

  • ACTH tells you where to look

    Suppressed ACTH points to the adrenal; unsuppressed points to pituitary or ectopic.

  • Surgery is usually curative

    Cause-directed pituitary, adrenal or ectopic tumour surgery is first line.

How the diagnosis is made

From first suspicion to cause-directed treatment.

The seven steps a UK endocrine team will normally follow, in order — so you know what to expect and why.

  1. 01

    Recognising

    Clinical recognition

    Moon face, central weight gain, purple striae, proximal weakness, hypertension and new-onset diabetes prompt suspicion.

  2. 02

    Recognising

    Two screening tests

    24-hour urinary free cortisol, midnight salivary cortisol and/or the low-dose dexamethasone suppression test — two abnormal results are needed.

  3. 03

    Confirming

    ACTH level

    Plasma ACTH separates ACTH-dependent (pituitary or ectopic) from ACTH-independent (adrenal) causes.

  4. 04

    Confirming

    MRI pituitary

    Dedicated pituitary MRI if ACTH is not suppressed — most cases are a small microadenoma.

  5. 05

    Confirming

    CT adrenals

    Cross-sectional adrenal imaging when ACTH is suppressed — identifies adenoma, carcinoma or bilateral hyperplasia.

  6. 06

    Confirming

    Petrosal sinus sampling

    Specialist inferior petrosal sinus sampling in tertiary centres when pituitary vs ectopic origin remains unclear.

  7. 07

    Managing

    Endocrinology consultation

    Specialist review to plan surgery, medical therapy and lifelong follow-up for recurrence and comorbidity.

Typical pathway: several weeks from first screening test to a confirmed cause and a treatment plan.

Symptoms

What Cushing’s syndrome actually looks like.

Features build up gradually and overlap with common conditions — comparing recent photos with older ones often reveals the change.

  • Central weight gain

    Progressive truncal weight gain with sparing of the limbs — a hallmark distribution.

  • Moon face and buffalo hump

    Rounded facial fullness and a fat pad over the upper back from cortisol-driven fat redistribution.

  • Purple striae

    Wide, violaceous stretch marks on abdomen, thighs or arms — classic and highly suggestive.

  • Proximal muscle weakness

    Difficulty climbing stairs or rising from a chair as cortisol drives proximal myopathy.

  • Hypertension

    New or worsening hypertension, often difficult to control on standard therapy.

  • Diabetes

    New-onset type 2 diabetes or worsening glycaemic control from cortisol-induced insulin resistance.

  • Psychiatric symptoms

    Depression, anxiety, insomnia, irritability or, occasionally, frank psychosis from sustained hypercortisolism.

  • Red flag: severe hypokalaemia

    Low potassium with severe hypertension suggests ectopic ACTH — urgent specialist work-up.

Treatment

How Cushing’s syndrome is treated in the UK.

Cause-directed surgery is first line, with modern medical therapy and radiotherapy for persistent or refractory disease. Here is what each option does and why the details matter.

  • Transsphenoidal pituitary surgery

    First-line for Cushing’s disease — selective microadenomectomy through the nose by a specialist pituitary surgeon.

  • Adrenalectomy

    Surgical removal of the affected gland for unilateral adrenal adenoma or carcinoma — usually laparoscopic.

  • Ectopic tumour resection

    Curative resection of the ACTH-secreting source (commonly a bronchial carcinoid or neuroendocrine tumour) when it can be localised.

  • Steroid taper (iatrogenic)

    Slow, supervised reduction of exogenous glucocorticoids with cover for the recovering HPA axis — never stop abruptly.

  • Medical therapy

    Steroidogenesis inhibitors — ketoconazole, metyrapone, mitotane or osilodrostat — used before surgery or when surgery is not curative.

  • Pituitary radiotherapy

    Stereotactic or conventional radiotherapy for persistent or recurrent Cushing’s disease after surgery.

  • Cabergoline

    Dopamine agonist used in selected patients with residual Cushing’s disease when other options are unsuitable.

  • Bilateral adrenalectomy

    Definitive option for refractory disease — cures hypercortisolism but requires lifelong steroid replacement and Nelson-syndrome surveillance.

What this guide is based on

The sources behind every number on this page.

UK national guidance and specialist society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your endocrinologist knows your history and can tell you which parts apply to you. Never stop or change steroid or steroidogenesis-inhibitor therapy without specialist review.

  • Society for Endocrinology. Clinical guidelines on Cushing’s syndrome.

  • NICE CKS. Cushing’s syndrome.

  • Endocrine Society. Clinical practice guideline on the treatment of Cushing’s syndrome.

  • The Pituitary Foundation. Patient information on Cushing’s.

Red flags

When Cushing’s becomes an emergency.

Most of Cushing’s is managed in outpatients — these are the situations that need urgent specialist input.

  • Severe hypokalaemia

    Potassium below 3.0 mmol/L, especially with alkalosis and hypertension — urgent ectopic ACTH work-up.

  • Uncontrolled hyperglycaemia

    Persistently high glucose despite treatment — needs urgent endocrine and diabetes review.

  • Diabetic ketoacidosis

    DKA in a patient with active Cushing’s — emergency admission and IV insulin protocol.

  • Osteoporotic fracture

    Low-trauma vertebral or hip fracture — assess bone density and start bone-protective therapy.

  • Severe depression or suicidality

    Cortisol-driven mood disturbance can be profound — arrange urgent mental-health support.

  • Post-surgical adrenal insufficiency

    Predictable after curative surgery — needs hydrocortisone replacement and sick-day rules until recovery.

  • Nelson syndrome

    Pituitary tumour enlargement after bilateral adrenalectomy — requires MRI surveillance and specialist review.

  • Cushing’s in pregnancy

    Rare and high-risk — needs joint endocrine and maternal-medicine care in a specialist centre.

  • Ectopic ACTH malignancy

    Rapid onset with severe metabolic disturbance suggests aggressive tumour — urgent oncology work-up.

Living with it

After treatment, a steady road back.

Recovery from Cushing’s is gradual — four small things make the biggest difference to how you feel week by week.

A quiet reminder

Recovery is measured in months.

Even after curative surgery, muscle strength, mood and metabolic control take time to rebuild — steady progress is the norm.

  1. 01 Routine

    Stay on top of your medication

    Take steroidogenesis inhibitors exactly as prescribed and never adjust doses without endocrine advice.

  2. 02 Preparedness

    Know your post-surgical steroid plan

    After curative surgery you will need hydrocortisone until your own axis recovers — carry a steroid emergency card.

  3. 03 Recovery

    Give your body time

    Muscle strength, mood and metabolic control improve over months — expect a gradual recovery, not an overnight one.

  4. 04 Reviews

    Annual endocrine follow-up

    Yearly review of cortisol status, cardiovascular risk, bone health and psychological wellbeing.

Frequently asked

Everything we get asked about Cushing’s syndrome.

Quick answers on syndrome vs disease, screening tests, treatment choices, post-surgical recovery and when to worry.

  • What is the difference between Cushing’s syndrome and Cushing’s disease?

    Cushing’s syndrome is any cause of chronic cortisol excess. Cushing’s disease is the specific subtype driven by an ACTH-secreting pituitary adenoma — the commonest endogenous cause.

  • How is Cushing’s syndrome diagnosed?

    Two independent screening tests are used: 24-hour urinary free cortisol, midnight salivary cortisol and the low-dose dexamethasone suppression test. Plasma ACTH then separates pituitary or ectopic causes from adrenal causes, followed by targeted imaging.

  • What is the most common cause?

    Long-term exogenous glucocorticoids — oral, injected, inhaled or topical steroids — are the commonest cause overall. The commonest endogenous cause is a pituitary microadenoma (Cushing’s disease).

  • What treatments are used?

    Cause-directed surgery is first line: transsphenoidal pituitary surgery for Cushing’s disease, adrenalectomy for an adrenal source, or resection of an ectopic ACTH tumour. Medical therapy (ketoconazole, metyrapone, osilodrostat, mitotane) is used before surgery or when surgery is not curative.

  • Will I need steroid replacement after surgery?

    Yes — after successful curative surgery your own HPA axis is temporarily suppressed and hydrocortisone replacement is essential until it recovers, sometimes for many months.

  • When should I seek urgent help?

    Severe hypokalaemia, uncontrolled hyperglycaemia, a fragility fracture, severe depression or symptoms of adrenal insufficiency after surgery all warrant urgent endocrine review.

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