Acromegaly: Difference between revisions
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== Medications == | == Medications == | ||
*Somatostatin analogs- somatostatin inhibits endocrine cells, including GH-secreting cells of the pituitary gland. Somatostatin analogs (SSAs) mimic the GH-suppressing effects of the body's own somatostatin.<ref name="Fleseriu">4.</ref> SSAs are one of the most common medications prescribed for acromegaly. There are currently three SSAs approved in the US: short-acting octreotride, octreotride LAR, and Somatuline Depot.<ref name="Fleseriu">2.</ref> Most common adverse events are glucose intolerance, and gallbladder and sludge stones.<ref name="Fleseriu">4.</ref> | |||
*Dopamine agonists- leads to GH suppression in a portion of acromegaly patients. Interestingly, this medication stimulates GH release in healthy patients.<ref name="Fleseriu">4.</ref> Advantages of this medication are relatively low cost, oral administration, and no hypopituitarism associated with medication. However, the medication is only effective at lowering GH and IGF-1 to safe levels in approximately 10% of patients, and potentially causes cardiac valvular damage.<ref name="Fleseriu">4.</ref> | |||
*Growth hormone receptor agonists- blocks the GH signal for IGF-1 production. More effective for patients with higher levels of IGF-1, and demonstrated a more favorable influence on glycemic control.<ref name="Fleseriu">4.</ref> Adverse events often associated with growth hormone receptor agonists are compromised liver function and reactions at the injection site.<ref name="Fleseriu">4.</ref> | |||
== Diagnostic Tests/Lab Tests/Lab Values == | == Diagnostic Tests/Lab Tests/Lab Values == |
Revision as of 05:22, 19 March 2011
Original Editors - Alex Kent from Bellarmine University's Pathophysiology of Complex Patient Problems project.
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Definition/Description
[edit | edit source]
Acromegaly is a rare systemic disease which affects the entire body.[1] It is characterized by a hypersecretion of growth hormone (GH) which the body is unable to regulate.[2] GH facilitates growth of muscles, internal organs, and bones, as well as stimulating secretion of its target hormone insulin-like growth factor 1 (IGF-1).[1] ,[3] The extremely high levels of GH and IGF-1 which typify acromegaly cause tissue enlargement and metabolic changes that result in visible deformity as well as an increase in mortality.[2][4] The disease often begins between the ages of 30 and 50, and has an insidious onset and slow progression, often delaying diagnosis until later stages of the disease.[2][3]
Prevalence[edit | edit source]
- The prevalence of acromegaly is approximately 40-70 cases per million persons.[2][4]
- However, new research suggests that the prevalence may be as high as 77 cases per million persons.[4]
- The annual incidence of acromegaly is approximately is 3-4 new cases per million persons.[4]
Characteristics/Clinical Presentation[edit | edit source]
Acromegaly affects many of the body's systems, and various signs and symptoms develop over a period of several years.[5] They range from subtle changes to notable disfigurement.[2]
Clinical Presentation[2][3][5][6]:
- Hand and foot enlargement
- Hyperhydrosis- increased perspiration
- Increased skin thickness
- Darkening and thickening of body hair
- Frontal skull bossing- an abnormally heavy brow and prominent forehead
- Widening of the maxilla accompanied by separation of the teeth
- Jaw malocclusion and overbite
- Soft tissue enlargement
- Skeletal overgrowth and thickening causing many areas to appear swollen
- Deep and husky voice due to thickening of cartilage in the larynx
- Ventilatory dysfunction
- Weight gain
- Joint pain
- Sleep apnea
- Acne
- Vision problems
Associated Co-morbidities[edit | edit source]
IGF-1, the target molecule of GH, enables many of the growth-promoting actions of GH; GH itself is also a regulator of mineral, lipid, and carbohydrate metabolism.[6] Therefore the elevated levels of GH and IGF-1 which are characteristic of acromegaly excessive soft tissue growth, swelling of internal organs, and musculoskeletal, neurological, and metabolic comorbidities.[6]
- Hypertension
- Arrhythmias
- Valvulopathy
- Cardiomyopathy
- Hypertrophy (biventricular or asymmetric septal)
- Congestive heart failure
- Obstructive sleep apnea
- Macroglossia
- Upper airway obstruction
- Ventilatory dysfunction
- Upper airway obstruction
- Insulin resistance
- Impaired glucose metabolism
- Diabetes mellitus
- Organ enlargement
- Colon polyps
- Fluid retention
- Renal failure
Musculoskeletal:[2]
- Arthropathy/osteoarthritis
- Carpal tunnel syndrome
- Osteopenia
Medications[edit | edit source]
- Somatostatin analogs- somatostatin inhibits endocrine cells, including GH-secreting cells of the pituitary gland. Somatostatin analogs (SSAs) mimic the GH-suppressing effects of the body's own somatostatin.[4] SSAs are one of the most common medications prescribed for acromegaly. There are currently three SSAs approved in the US: short-acting octreotride, octreotride LAR, and Somatuline Depot.[4] Most common adverse events are glucose intolerance, and gallbladder and sludge stones.[4]
- Dopamine agonists- leads to GH suppression in a portion of acromegaly patients. Interestingly, this medication stimulates GH release in healthy patients.[4] Advantages of this medication are relatively low cost, oral administration, and no hypopituitarism associated with medication. However, the medication is only effective at lowering GH and IGF-1 to safe levels in approximately 10% of patients, and potentially causes cardiac valvular damage.[4]
- Growth hormone receptor agonists- blocks the GH signal for IGF-1 production. More effective for patients with higher levels of IGF-1, and demonstrated a more favorable influence on glycemic control.[4] Adverse events often associated with growth hormone receptor agonists are compromised liver function and reactions at the injection site.[4]
Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]
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Etiology/Causes[edit | edit source]
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Systemic Involvement[edit | edit source]
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Medical Management (current best evidence)[edit | edit source]
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Physical Therapy Management (current best evidence)[edit | edit source]
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Alternative/Holistic Management (current best evidence)[edit | edit source]
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Differential Diagnosis[edit | edit source]
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Case Reports/ Case Studies[edit | edit source]
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Resources
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Recent Related Research (from Pubmed)[edit | edit source]
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References[edit | edit source]
see adding references tutorial.
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1. Vance M. Acromegaly: a fascinating pituitary disorder. Neurosurg Focus 2010;29(4):1. Cite error: Invalid
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tag; name "Vance" defined multiple times with different content - ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 2. Cordero RA, Barkan AL. Current diagnosis of acromegaly. Rev Endocr Metab Disord 2008;9:13-19. Cite error: Invalid
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tag; name "Cordero" defined multiple times with different content - ↑ 3.0 3.1 3.2 3.Merck Manual Home Edition. Acromegaly and gigantism: pituitary gland disorders. http://www.merckmanuals.com/home/print/sec13/ch162e.html (Accessed March 11 2011). Cite error: Invalid
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tag; name "Merck" defined multiple times with different content - ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.Fleseriu M, Delashaw JB, Cook DM. Acromegaly: a review of current medical therapy and new drugs on the horizon. Neurosurg Focus 2010;29(4):E15. Cite error: Invalid
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tag; name "Fleseriu" defined multiple times with different content - ↑ 5.0 5.1 5.2 5.3 5. Reid TJ, Post KD, Bruce JN, Kanibir MN, Reyes-Vidal CM, Freda PU. Features at diagnosis of 324 patients with acromegaly did not change from 1981 to 2006: acromegaly remains under-recognized and under-diagnosed. Clinical Endocrinology 2010;72:203-208. Cite error: Invalid
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tag; name "Reid" defined multiple times with different content - ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.Melmed S. Acromegaly pathogenesis and treatment. J. Clin. Invest 2009;119:3189-3202. Cite error: Invalid
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