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.
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.
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.
Key medicines
Long-acting somatostatin receptor ligandUse the current product-specific intramuscular or deep-subcutaneous specialist regimen and titrate at labelled intervals from IGF-1, symptoms and tolerability.
PegvisomantInitiate and titrate subcutaneous treatment only through the current specialist commissioning policy, using age-adjusted IGF-1 rather than growth hormone to guide effect.