The somatic growth and metabolic dysfunction associated with acromegaly result from excess secretion of GH and subsequent elevation of circulating and locally produced insulin-like growth factor-1 (IGF-1). In healthy individuals, GH secretion is under the dual regulation of growth hormone–releasing hormone (GHRH) and somatostatin, with variations in the secretion of somatostatin being the primary mode of regulation.2
The interaction of GHRH and somatostatin, as well as fluctuations in levels of somatostatin, regulate GH secretion. Hypersecretion of GH and IGF-1 may be caused primarily by GH-secreting adenoma(s) of the pituitary resulting from clonal expansion of a single mutated cell.2
GH-secreting tumors have a large number of receptors for somatostatin and thus are frequently responsive to therapy with analogs of somatostatin, such as octreotide.2,3
Adapted with permission from Melmed.2
GH, growth hormone; GHRH, growth hormone–releasing hormone; IGF-1, insulin-like growth factor-1; SRIF, somatotropin-releasing inhibitory factor.
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References:
1. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, US Department of Health and Human Services. Acromegaly. Bethesda, MD: National Institutes of Health; 2008. NIH publication 08-3924. 2. Melmed S. Acromegaly. N Engl J Med. 1990;322(14):966-977. 3. Lamberts WJ, van der Lely AJ, de Herder WW, Hofland LJ. Octreotide. N Engl J Med. 1996;334(4):246-254.
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