Acromegaly

Acromegaly is chronic growth hormone excess arising after the growth plates have fused, so the skeleton thickens rather than lengthens. More than nine in ten cases are a benign somatotroph adenoma of the anterior pituitary. The clinical picture follows from years of elevated IGF-1 acting on bone and connective tissue: enlarging hands and feet, coarsened features and prognathism, thickened skin, arthropathy, obstructive sleep apnoea, hypertension and a cardiomyopathy. The same adenoma before epiphyseal closure produces gigantism instead.

It is rare, a few new cases per million people each year, and slow to diagnose because the changes accrue over a decade. Diagnosis is biochemical: an IGF-1 above the age-adjusted reference range, confirmed by failure of growth hormone to suppress below the assay-specific cut-off during a 75 g oral glucose load. Untreated mortality was historically around double that of matched populations and normalises once the biochemistry is controlled. Treatment is transsphenoidal surgery first, then somatostatin analogues, pegvisomant, or radiotherapy.

Acromegaly is the reference case for what sustained supraphysiological growth hormone does over years, which is why it appears in any discussion of deliberately raised IGF-1. It supplies dose-response evidence no trial in healthy people will ever generate: the same axis pushed hard for long enough yields glucose intolerance, joint destruction, cardiac remodelling and an excess of colonic neoplasia.

Two misreadings recur. The first is using a single random growth hormone level to rule the condition in or out, which is meaningless given pulsatile secretion, since a healthy person can sit transiently above an acromegalic trough. The second is the mirror claim in secretagogue marketing, that because a user will not develop acromegaly the syndrome is irrelevant to them.