30. Pathophysiology of Acromegaly
Pathophysiology of Acromegaly
GH secretion from the anterior pituitary and subsequent release of IGF-I from the liver act in concert to stimulate somatic growth1
The GH/IGF-I pathway is tightly regulated by multiple feedback mechanisms1
Growth hormone–releasing hormone (GHRH) stimulates GH release
The hypothalamic peptide somatostatin (SRIF) is the primary inhibitor of GH secretion2,3
Ghrelin, derived from the gastrointestinal tract, also stimulates GH secretion
More than 95% of people with acromegaly have an underlying GH-secreting somatotroph tumor1,2
GH hypersecretion increases synthesis and release of IGF-I, leading to accelerated somatic growth and metabolic dysfunction
Rarely, patients may have a peripheral GH-secreting tumor, such as a pancreatic neoplasm
Hypersecretion of GH from pituitary adenomas has a number of direct and indirect effects that contribute to the clinical manifestations of acromegaly
GH has a direct effect on glucose metabolism, which can lead to glucose intolerance or frank diabetes mellitus1,2
GH release and stimulated increase in IGF-I contribute to tissue growth on several levels, including increased synthesis of protein and growth of bone and soft tissues1,2
Pathophysiology of Acromegaly
GH secretion from the anterior pituitary and subsequent release of IGF-I from the liver act in concert to stimulate somatic growth1
The GH/IGF-I pathway is tightly regulated by multiple feedback mechanisms1
Growth hormone–releasing hormone (GHRH) stimulates GH release
The hypothalamic peptide somatostatin (SRIF) is the primary inhibitor of GH secretion2,3
Ghrelin, derived from the gastrointestinal tract, also stimulates GH secretion
More than 95% of people with acromegaly have an underlying GH-secreting somatotroph tumor1,2
GH hypersecretion increases synthesis and release of IGF-I, leading to accelerated somatic growth and metabolic dysfunction
Rarely, patients may have a peripheral GH-secreting tumor, such as a pancreatic neoplasm
Hypersecretion of GH from pituitary adenomas has a number of direct and indirect effects that contribute to the clinical manifestations of acromegaly
GH has a direct effect on glucose metabolism, which can lead to glucose intolerance or frank diabetes mellitus1,2
GH release and stimulated increase in IGF-I contribute to tissue growth on several levels, including increased synthesis of protein and growth of bone and soft tissues1,2