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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
Key points
- Caused by GH-secreting pituitary adenoma in >95% of cases. Gigantism if onset before epiphyseal fusion
- Insidious onset — average delay to diagnosis ~7–10 years. Compare old photos for facial change
- Clinical: coarsened facial features, enlarged hands/feet, prognathism, macroglossia, OSA, carpal tunnel, arthralgia
- Diagnosis: raised IGF-1 → confirm with OGTT (GH fails to suppress <1 mcg/L after 75 g glucose)
- First-line: transsphenoidal surgery. Medical: somatostatin analogues (octreotide LAR, lanreotide), pegvisomant
- Screen for complications: diabetes, hypertension, cardiomyopathy, colorectal polyps (colonoscopy), OSA
Overview
Acromegaly is a condition of chronic growth hormone (GH) excess in adults, almost always (>95%) caused by a benign GH-secreting pituitary adenoma (somatotroph adenoma). Excess GH stimulates hepatic IGF-1 production, which mediates most of the tissue effects. The condition causes progressive acral enlargement (hands, feet, jaw), soft tissue overgrowth, and widespread metabolic, cardiovascular, and musculoskeletal complications. When GH excess occurs before epiphyseal closure in childhood, it causes gigantism. Acromegaly is associated with MEN1 (multiple endocrine neoplasia type 1) and Carney complex. Rarely, GH excess results from ectopic GHRH-secreting tumours (carcinoid, pancreatic neuroendocrine tumours).
Epidemiology
Acromegaly has an incidence of approximately 3–5 per million per year and a prevalence of 40–130 per million. Equal sex distribution. Mean age at diagnosis is 40–50 years. The average delay from symptom onset to diagnosis is 7–10 years due to the insidious nature of changes. Most adenomas are macroadenomas (>10 mm) at diagnosis. Untreated acromegaly reduces life expectancy by approximately 10 years, primarily due to cardiovascular and cerebrovascular disease.
Clinical Features
Symptoms
Enlarged hands (increased ring/glove size) and feet (increased shoe size)
Coarsened facial features: prominent brow ridge, widened nose, thickened lips
Headache (from pituitary tumour mass effect)
Visual field defects (bitemporal hemianopia — optic chiasm compression)
Excessive sweating and oily skin
Arthralgias and joint stiffness
Snoring and sleep apnoea (macroglossia + soft tissue thickening)
Paraesthesiae (carpal tunnel syndrome — ~50%)
Menstrual irregularity, erectile dysfunction (co-secretion of prolactin or mass effect)
Signs
Enlarged spade-like hands with doughy thickened skin
Prognathism (protruding jaw), widened interdental spaces
Macroglossia (enlarged tongue)
Frontal bossing (prominent supraorbital ridges)
Skin tags (associated with colonic polyps)
Bitemporal hemianopia on visual field testing
Hypertension
Organomegaly (heart, liver, thyroid, kidneys)
Investigations
First-line
Serum IGF-1Best screening test — elevated for age and sex-matched reference range. Stable marker (unlike GH which fluctuates)
Second-line
Oral glucose tolerance test (OGTT) with GHConfirmatory test: 75 g glucose load. In acromegaly, GH fails to suppress <1 mcg/L (normally suppresses to <0.4). May paradoxically rise
MRI pituitary with gadoliniumLocalise and characterise adenoma — >70% are macroadenomas (>10 mm) at diagnosis
Visual field testing (Goldmann/Humphrey perimetry)If macroadenoma — assess for chiasmal compression
Pituitary function testsAssess for hypopituitarism (prolactin, TFTs, cortisol, gonadotrophins, IGF-1) — mass effect may compress normal pituitary
Specialist
EchocardiogramAcromegalic cardiomyopathy — LVH, diastolic dysfunction, valvular disease
ColonoscopyIncreased colorectal polyp and cancer risk. At diagnosis and then surveillance every 3–5 years
Sleep studyIf symptomatic — obstructive sleep apnoea is common (up to 80%)
HbA1c / fasting glucoseScreen for diabetes (GH is counter-regulatory — insulin resistance)
1
First-line: transsphenoidal surgery
- Endoscopic transsphenoidal adenomectomy by experienced pituitary surgeon
- Cure rates: ~80–90% for microadenomas, ~40–60% for macroadenomas (especially if invasive)
- Post-operative assessment: IGF-1 and OGTT at 12 weeks. Normal IGF-1 + GH suppression <1 mcg/L on OGTT = biochemical cure
- If not cured: consider second surgery, medical therapy, or radiotherapy
2
Medical therapy
- Somatostatin receptor ligands (SRLs): octreotide LAR 20–30 mg IM monthly or lanreotide 60–120 mg SC monthly
- SRLs normalise IGF-1 in ~50–60% and reduce tumour volume in ~30–70%
- Pegvisomant (GH receptor antagonist): normalises IGF-1 in >90% but does not shrink tumour. Monitor LFTs
- Cabergoline (dopamine agonist): modestly effective, particularly if co-secreting prolactin. Lower cost, oral
- Pasireotide LAR: second-generation SRL for SRL-resistant cases. Risk of hyperglycaemia
3
Radiotherapy
- Stereotactic radiosurgery (e.g. Gamma Knife): second/third-line for residual disease
- Slow onset of effect (months to years). Risk of hypopituitarism (up to 50% at 10 years)
- Continue medical therapy until biochemical control achieved
4
Complication management
- Diabetes/hypertension: standard management
- OSA: CPAP, may improve with GH normalisation
- Colonoscopy surveillance every 3–5 years
- DEXA scan: osteoporosis screening if hypogonadal
- Cardiovascular risk: aggressive management
Complications
- Cardiovascular: Acromegalic cardiomyopathy (biventricular hypertrophy, diastolic dysfunction, arrhythmias), hypertension (35%), accelerated atherosclerosis — leading cause of death
- Diabetes mellitus: GH promotes insulin resistance — up to 30% develop frank diabetes
- Colorectal polyps and cancer: 2–3× increased risk — colonoscopy at diagnosis and regular surveillance
- Obstructive sleep apnoea: Up to 80% — macroglossia + pharyngeal soft tissue overgrowth
- Carpal tunnel syndrome: ~50% — from soft tissue/periosteal overgrowth
- Arthropathy: Weight-bearing joints particularly affected. Irreversible even after GH normalisation
- Hypopituitarism: From tumour mass effect on normal pituitary — may require hormone replacement
UKMLA Exam Tips
- 1Screening test = IGF-1. Confirmatory test = OGTT with GH (failure to suppress <1 mcg/L). Know both
- 2IGF-1 is a better marker than random GH (GH is pulsatile; IGF-1 reflects 24 h GH activity)
- 3Acromegaly features: increased hat/ring/shoe size, coarsened facial features, sweating, carpal tunnel, OSA, diabetes, hypertension
- 4Skin tags in acromegaly correlate with colonic polyps — colonoscopy screening mandatory
- 5Surgery cure rates depend on tumour size: micro >80%, macro 40–60%. Medical therapy if surgery fails
- 6Bitemporal hemianopia = pituitary macroadenoma compressing optic chiasm — always check visual fields
- 7GH is a COUNTER-regulatory hormone → acromegaly causes insulin resistance → diabetes
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