ABSTRACT
Acromegaly is a chronic, debilitating condition caused by excessive secretion of growth
hormone (GH). The average incidence of acromegaly is approximately 3.3 per million
each year with a prevalence of approximately 60 per million.[1]
[2] GH-secreting adenomas account for 20% of functional adenomas; 75% of GH adenomas
are macroadenomas. In the majority of cases, the condition results from benign pituitary
adenomas or, rarely, from ectopic production of GH-releasing hormone (GHRH). Ectopic
production of GHRH may be from carcinoid, islet cell, and other tumors and may be
identified histologically by hyperplasia of somatotrophs or biochemically by elevated
circulating levels of GHRH. Excessive GH results in phenotypic changes including acral
enlargement, soft tissue swelling, and facial coarsening. Other features include sweating,
menstrual irregularity, headache, arthritis, carpal tunnel syndrome, diabetes, hypertension,
cardiac dysfunction, loss of libido, galactorrhea, visual field defects, obstructive
sleep apnea, and colonic neoplasia.[1]
[3]
[4]
[5]
[6]
[7] The mortality for acromegalic patients is two to three times higher than that of
the general population, but with appropriate reduction of GH hypersecretion, it tends
to shift into the normal range.[8] Treatment is directed to normalizing GH secretion, eradicating or stabilizing the
pituitary tumor, preserving normal pituitary function, and managing any associated
complications of GH hypersecretion. The treatment modalities available include transsphenoidal
surgery, pharmacotherapy, and radiation or combination therapy. This article provides
an update of the pathophysiology of GH hypersecretion in acromegaly, the newly defined
diagnostic criteria and the end point for a cure for acromegaly, and new developments
in pharmacotherapy and radiotherapy.
KEYWORDS
Acromegaly - pituitary adenoma - transsphenoidal surgery
