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]
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[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
