Synopsis
Recognise chronic growth-hormone excess, confirm it with valid biochemistry, and coordinate tumour treatment and systematic complication reduction.
- Acromegaly is usually caused by a growth-hormone-secreting pituitary adenoma; excess insulin-like growth factor 1 drives gradual soft-tissue, skeletal and metabolic change after epiphyseal closure.
- Compare old photographs, ring and shoe size, facial contour, dentition, voice, sweating and hand symptoms because the patient and clinician may normalise a phenotype that evolved over years.
- Measure age-adjusted IGF-1 first when suspicion is credible; repeat a discordant result and consider nutrition, hepatic or renal disease, poorly controlled diabetes, pregnancy, oral oestrogen and assay factors.
- An oral glucose tolerance test assessing growth-hormone suppression can resolve uncertainty, but interpretation must use the laboratory's validated assay and endocrine protocol rather than a universal cut-off.
- Dedicated pituitary MRI follows biochemical confirmation, with formal visual fields for optic pathway contact and a complete assessment of the remaining pituitary axes.
- Transsphenoidal surgery is usual first-line treatment for a resectable adenoma; postoperative biochemistry determines whether surveillance, repeat surgery, medicine or radiotherapy is appropriate.
- Long-acting somatostatin receptor ligands, cabergoline and the growth-hormone receptor antagonist pegvisomant have distinct biochemical, tumour and safety monitoring profiles and require specialist selection.
- Control of hormone excess does not erase established risk: actively assess blood pressure, glucose, sleep apnoea, cardiovascular disease, arthropathy, vertebral fracture, thyroid disease and colorectal risk.
- Sudden severe headache, visual deterioration, ophthalmoplegia or haemodynamic illness suggests pituitary apoplexy or acute cortisol deficiency and overrides the routine acromegaly pathway.
Key red flags
Thunderclap or rapidly severe headache with visual loss, ophthalmoplegia, vomiting or reduced consciousness may be pituitary apoplexy and needs emergency hydrocortisone assessment, MRI and pituitary-neurosurgical contact.
Hypotension, hyponatraemia, hypoglycaemia, profound weakness or recurrent vomiting in a patient with a large pituitary tumour can indicate ACTH deficiency and requires immediate glucocorticoid protection.
Rapidly worsening acuity or field loss indicates threatened vision from tumour or haemorrhage and warrants same-day specialist assessment rather than routine endocrine follow-up.
Chest pain, syncope, decompensated heart failure or a significant arrhythmia needs acute cardiovascular management alongside endocrine review because acromegalic cardiomyopathy can be clinically important.
Severe daytime sleepiness with safety-critical driving or perioperative airway concern requires prompt sleep and anaesthetic planning, not reassurance based on eventual tumour treatment.
Investigation priorities
Screen for integrated growth-hormone action and provide the main biochemical treatment target.
Management branches
Progressive acral or facial change, characteristic complications or an incidental pituitary lesion creates credible suspicion.
- Document longitudinal physical change, associated morbidity, medicines, pregnancy or oestrogen exposure and the symptoms of pituitary compression or deficiency.
- Measure age-adjusted IGF-1 and repeat a borderline or discordant result after addressing reversible physiological, systemic and assay influences.
- Use the local oral glucose growth-hormone suppression protocol when confirmation is required; do not substitute one random growth-hormone sample.
- After biochemical confirmation, arrange dedicated MRI, vision assessment when indicated, complete pituitary profiling and referral to a pituitary multidisciplinary team.