Acromegaly and gigantism !
Too much growth hormone, almost always from a benign pituitary tumour. In adults it enlarges the hands, feet and face; in children it causes gigantism.
Updated 2026-11-01
Structures involved
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In embryology
In the clinical exam
Why it happens
- Hypertrophy: physiologic and pathologic
- Growth hormone and IGF-1
- Measuring hormones: stimulation and suppression tests
- Pituitary: adenohypophysis and neurohypophysis
What it is
A chronic disease caused by excess growth hormone (GH) and its mediator IGF-1, nearly always from a GH-secreting pituitary adenoma. Before the growth plates close it causes gigantism (excessive height); after closure it causes acromegaly (enlargement of bones and soft tissues).
Who gets it
Rare, with an insidious course: diagnosis is often delayed by many years, and in Latin American series most tumours are already macroadenomas when found. Affects men and women similarly, usually diagnosed in middle age.
Causes
- GH-secreting pituitary adenoma (somatotroph adenoma) in almost all cases
- Rarely ectopic GHRH secretion by a neuroendocrine tumour
- Inherited syndromes: MEN 1, McCune-Albright syndrome, Carney complex, familial isolated pituitary adenoma
Risk factors
- Family history of pituitary tumours or MEN 1
- Genetic syndromes listed above (rare)
Pathophysiology
GH acts mainly through IGF-1 made in the liver, which drives growth of bone, cartilage and soft tissues. GH also opposes insulin, causing insulin resistance and diabetes, and promotes sodium retention and hypertension. The enlarging adenoma can compress the optic chiasm and the normal pituitary.
Classification
- Gigantism: GH excess before epiphyseal closure
- Acromegaly: GH excess after epiphyseal closure
- By tumour size: microadenoma under 10 mm, macroadenoma 10 mm or more
Symptoms and signs
- Enlarged hands and feet (larger ring and shoe size)
- Coarse facial features: prominent brow and jaw (prognathism), widened teeth spacing, large nose and tongue
- Excessive sweating, oily thick skin and skin tags
- Joint pain, carpal tunnel syndrome and snoring with sleep apnoea
- Headache and visual field defects
- In children, accelerated growth and very tall stature
Diagnosis
- Clinical
- Compare old photographs, look for acral and facial changes, measure blood pressure and examine visual fields. In children, plot height on growth charts.
- Tests
- Serum IGF-1 is the screening test; failure of GH to suppress during an oral glucose tolerance test confirms the diagnosis. Other pituitary hormones, prolactin, glucose and HbA1c are checked.
- Imaging
- Pituitary MRI to locate and size the adenoma. Echocardiography, sleep study and colonoscopy are used to look for complications.
Differential diagnosis
- Constitutional tall stature (in children)
- Familial coarse features or pachydermoperiostosis
- Hypothyroidism (thick skin and coarse features)
- Marfan syndrome and Klinefelter syndrome as causes of tall stature
- Ectopic GHRH secretion
Goal of treatment
Normalise IGF-1 and GH, remove or control the tumour, protect vision and pituitary function, and treat cardiovascular, metabolic and joint complications.
Treatment
- Surgical
- Transsphenoidal resection of the adenoma is first-line and can cure many microadenomas.
- Medical
- When surgery fails or is not possible: somatostatin analogues (octreotide, lanreotide), the GH receptor antagonist pegvisomant, and sometimes cabergoline.
- Procedure
- Radiotherapy (conventional or stereotactic) for residual tumour not controlled by medicine.
- Follow-up
- Periodic IGF-1, MRI, visual fields and screening for diabetes, hypertension, heart disease, sleep apnoea and colon polyps.
Drugs for this condition
Complications
- Hypertension, cardiomyopathy and heart failure
- Type 2 diabetes from insulin resistance
- Obstructive sleep apnoea
- Arthropathy and carpal tunnel syndrome
- Colonic polyps and colorectal cancer
- Hypopituitarism and visual loss
Prognosis
Untreated, cardiovascular and respiratory disease shorten life expectancy. With biochemical control, mortality approaches that of the general population, although bone and joint changes do not fully reverse.
Prevention
- No primary prevention; earlier recognition of facial and acral changes shortens diagnostic delay
- Screening of relatives in familial syndromes such as MEN 1
Test yourself
Think of the answer, then tap the question to see it.
What is the best screening test for acromegaly?
Serum IGF-1, which reflects integrated GH secretion.
Which test confirms acromegaly?
Failure of GH to suppress during an oral glucose tolerance test.
What is the first-line treatment of a GH-secreting adenoma?
Transsphenoidal surgical resection; somatostatin analogues and pegvisomant are used if it is not curative.
What is the most common cause of death in untreated acromegaly?
Cardiovascular disease (hypertension, cardiomyopathy and heart failure).
What determines whether GH excess causes gigantism or acromegaly?
Whether the epiphyseal growth plates are still open (gigantism) or already closed (acromegaly).
Related conditions
- Pituitary adenoma
- Type 2 diabetes mellitus
- Arterial hypertension
- Heart failure
- Obstructive sleep apnoea
- Carpal tunnel syndrome
- Colorectal polyps and hereditary polyposis syndromes (FAP, Lynch)
- Multiple endocrine neoplasia (MEN 1, 2A, 2B)
- Hypopituitarism (incl. Sheehan syndrome and pituitary apoplexy)
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Acromegaly (MedlinePlus Medical Encyclopedia (U.S. National Library of Medicine), 2025); Gigantism (MedlinePlus Medical Encyclopedia (U.S. National Library of Medicine), 2025).
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